Datasets:

InMedData

/

Cardio_v1

like 1

Ventricular high-rate episodes in pacemaker diagnostics identify a high-risk subgroup of patients with tachy-brady syndrome.

The purpose of this study was to evaluate the frequency and clinical significance of ventricular high-rate (VHR) episodes (ventricular rate &gt;162 bpm) in patients with symptomatic bradycardia and paroxysmal atrial fibrillation (AF).</AbstractText>Newer pacemakers have enhanced diagnostic features that permit detection and storage of detailed information about the frequency, duration, and time of onset of multiple episodes of AF, atrial tachycardia (AT), and ventricular tachycardia (VT). However, the prevalence and prognostic value of AF associated with rapid ventricular rates in the pacemaker population are unknown.</AbstractText>We prospectively followed 125 patients who received a Medtronic AT 500/501 pacemaker for symptomatic bradycardia and paroxysmal AF.</AbstractText>AF recurred in 112 patients (90%) during 22 +/- 8 months of follow-up. A total of 1,324 VHR episodes occurred in 38 patients (30%). Episodes with available electrograms (n = 560) were reviewed and classified as AF (n = 279; 50%), AT (n = 266; 47%) or VT (n = 15; 3%). AF burden was higher in patients with VHR episodes (median 1.9 vs 0.2 hours/day; P &lt; .001). After controlling for AT/AF burden and heart disease, VHR episodes were a significant independent predictor of hospitalization for cardiovascular symptoms (odds ratio 2.92, 95% confidence interval 1.33-6.38; P = .007). Heart rate control improved over time in the cohort, and the frequency of VHR episodes decreased during follow-up (P &lt; .001).</AbstractText>VHR episodes documented in the pacemaker diagnostics identify a high-risk subgroup of patients with AF. Monitoring VHR episodes may be useful for identifying pacemaker patients with AF who require more vigilant monitoring, additional investigations, and/or additional interventions.</AbstractText>

Deaths associated with implantable cardioverter defibrillator failure and deactivation reported in the United States Food and Drug Administration Manufacturer and User Facility Device Experience Database.

The aim of this study was to understand the causes of implantable cardioverter defibrillator (ICD) failure and complications so that adverse events, including unnecessary death, can be prevented.</AbstractText>Sudden death may occur if an ICD fails to treat life-threatening ventricular arrhythmias.</AbstractText>The United States Food and Drug Administration Manufacturer and User Facility Device Experience Database was searched for ICD devices and the search term "death." The search yielded 212 death events involving 100 ICD pulse generator and lead models from five manufacturers. These death events were associated with (A) ICD devices for which pulse generator interrogation data and/or the results of the manufacturers analysis of returned devices were available; (B) ICD devices for which neither interrogation data nor the results of the manufacturer's analysis were reported; and (C) normally functioning ICDs that had been deactivated.</AbstractText>(A) A total of 103 (69%) of 150 death events were associated with defective pulse generators or high-voltage leads. Most (34/42 [81%]) apparently sudden or arrhythmic death events were associated with high-voltage lead failure; other deaths were related to pulse generator failure (8/42 [19%]) caused by electronic component defects. (B) A total of 21 of 51 death events were related to a manufacturer's recall; all deaths were arrhythmic but without allegation of device failure. (C) Eleven death events occurred in patients whose pulse generators were found to be off or deactivated; these devices appeared to have been deactivated accidentally or by exposure to magnetic fields, or they were not reactivated after elective surgery.</AbstractText>ICD device failure and unintended pulse generator deactivation have resulted in unnecessary deaths. Although these deaths may be infrequent, improved devices and follow-up techniques are needed. The magnet deactivation feature probably is unsafe, and health professionals and patients should be cautioned.</AbstractText>

A 25-year control of idiopathic ventricular fibrillation with electrophysiologic-guided antiarrhythmic drug therapy.

The case of a 28-year-old man with recurrent syncope and multiple documented episodes of idiopathic ventricular fibrillation is reported. Recurrent syncope suggesting a self-terminating ventricular tachyarrhythmia occurred after 1 month of amiodarone therapy, and ventricular fibrillation was inducible at electrophysiologic study. After addition of quinidine, no significant ventricular arrhythmias could be induced. Similar results were found during a repeat electrophysiologic study performed 23.5 years later. During a 25-year period, the patient has remained arrhythmia-free on combined antiarrhythmic medication with quinidine and amiodarone.

Recurrent ventricular fibrillation secondary to aortic valve tumor.

The case of a patient with recurrent ventricular fibrillation secondary to an aortic tumor is reported. Ventricular fibrillation occurs secondary to ischemia, arrhythmia, or congenital disease, or it may be an idiopathic event. Irreversible and recurrent situations require placement of an implantable cardioverter defibrillator (ICD). A patient with recurrent syncope secondary to documented ventricular fibrillation without a clear mechanism and a negative electrophysiologic study underwent ICD placement. A cardiac papillary fibroelastoma at the aortic valve subsequently was found. Cardiac tumors in the aortic valve can obstruct the coronary arteries, secondarily causing ischemia and ventricular fibrillation. Such a mechanism must be considered in the differential diagnosis of sudden death.

Biventricular pacing reduces the induction of monomorphic ventricular tachycardia: a potential mechanism for arrhythmia suppression.

The aim of the present study was to evaluate in a prospective randomized fashion the electrophysiologic effects of acute biventricular (BV) pacing. We hypothesized that (1) the local coupling interval in the left ventricle in response to right-sided ventricular premature beats is prolonged when BV pacing is applied during the drive train compared with right ventricular (RV) pacing, and (2) BV programmed electrical stimulation (PES) decreases the induction of ventricular arrhythmias compared with standard RV-PES, regardless of the presence of intraventricular conduction delay.</AbstractText>Previous studies have suggested that BV pacing might decrease the frequency of ventricular arrhythmias; however, the mechanism of arrhythmia suppression remains unclear.</AbstractText>Eighteen patients with coronary artery disease were randomized to RV-PES or BV-PES with a repeat study using the other pacing mode. The RV effective refractory periods were measured during RV-PES and BV-PES. In addition, the local LV S(1)-S(2) coupling interval was measured at 600/450 ms and 400/350 ms during RV-PES and BV-PES.</AbstractText>BV-PES had no effect on RV effective refractory periods. On the other hand, the local LV S(1)-S(2) coupling intervals increased significantly during BV-PES compared with RV-PES (P &lt; .0001). Ventricular tachycardia was induced in six patients using RV-PES but in only one patient with BV-PES (RR = 83%, P = .01). No difference was observed in the induction of ventricular fibrillation.</AbstractText>BV-PES significantly reduced the induction of ventricular tachycardia compared to RV-PES, with no significant effect on ventricular fibrillation induction. Our findings may help explain the reduced incidence of ventricular arrhythmias noted with chronic BV pacing.</AbstractText>

Trends in treated ventricular fibrillation out-of-hospital cardiac arrest: a 17-year population-based study.

The aims of this study were to describe the trends of ventricular fibrillation (VF) out-of-hospital cardiac arrest in Rochester, Minnesota, since 1985 and to determine coexistent trends in implantable cardioverter defibrillator (ICD) placement and termination of potentially lethal ventricular arrhythmias that might explain, at least in part, a declining incidence trend.</AbstractText>The incidence of VF out-of-hospital cardiac arrest treated by emergency medical services (EMS) personnel has declined over the past decade. Because VF out-of-hospital cardiac arrest occurs primarily in the setting of severe coronary artery disease, primary and secondary prevention strategies may account in part for the decline. In particular, ICD use in large primary and secondary prevention clinical trials in patients at high risk of sudden death has demonstrated that these devices improve survival.</AbstractText>All residents of the City of Rochester, Minnesota, who presented with a VF out-of-hospital cardiac arrest from 1985 to 2002, identified and treated by EMS, were included in the study. In addition, residents of the City of Rochester who received their first ICD implant from 1989 to 2002 were identified. From the ICD records, general demographics, etiology of heart disease, comorbid medical disease, and indication for ICD placement were abstracted. Follow-up data obtained from this population included ICD shocks, the underlying rhythm disturbance, and death.</AbstractText>The overall incidence of EMS-treated VF out-of-hospital cardiac arrest in Rochester during the study period was 17.1 per 100,000 [95% confidence interval (CI) 15.1-19.4]. The incidence has decreased significantly (P &lt; 0.001) over the study period: 1985-1989: 26.3/100,000 (95% CI 21.0-32.6), 1990-1994: 18.2/100,000 (95% CI 14.1-23.1), 1995-1999: 13.8/100,000 (95% CI 10.4-17.9), 2000-2002: 7.7/100,000 (95% CI 4.7-11.9). One hundred ten patients received an ICD. The placement of ICDs also has increased dramatically over the past 10 years: 1990-1994: 5.0/100,000 to 2000-2002: 20.7/100,000 (P &lt; 0.001). ICDs terminated VF or fast ventricular tachycardia (&lt;270 ms) in 22 patients. Termination of these potentially fatal arrhythmias has shown a trend toward an increase over the study period: 1990-1994: 1.1/100,000 to 2000-2002: 3.5/100,000 (P = 0.06).</AbstractText>The incidence of VF out-of-hospital cardiac arrest is declining. In contrast, the rates of ICD placement and ICD termination of ventricular tachycardia or VF are markedly increasing. Sudden death preventive strategies are multifactorial. These observations suggest that ICD termination of potentially lethal ventricular arrhythmias may contribute to the lower incidence of VF out-of-hospital cardiac arrest.</AbstractText>

Randomized pilot study of a new atrial-based minimal ventricular pacing mode in dual-chamber implantable cardioverter-defibrillators.

We hypothesized that a new minimal ventricular pacing mode (MVP) that provides AAI/R pacing with ventricular monitoring and back-up DDD/R pacing as needed during AV block (AVB) would significantly reduce cumulative percent ventricular pacing compared to DDD/R.</AbstractText>Conventional DDD/R mode often results in high cumulative percent ventricular pacing that may adversely affect ventricular function and increase risk of heart failure and atrial fibrillation.</AbstractText>MVP was made operational in 30 patients with DDD/R implantable cardioverter-defibrillators (ICDs) and no history of AVB. Patients were randomized to one week each in DDD/R and MVP. Holter monitor recordings (ECG, intracardiac electrograms, and event markers) and device diagnostics were analyzed for cumulative % atrial paced (Cum%AP), cumulative percent ventricular pacing, and frequency and duration of DDD/R pacing back-up. Diaries were used to report symptoms.</AbstractText>Age of the study population was 61 years +/- 12 years and 83% were male. Baseline PR interval was 204 ms +/- 32 ms and programmed AV intervals (DDD/R) were 200 ms +/- 50 ms (paced)/167 ms +/- 54 ms (sensed). Cum%AP was similar between MVP and DDD/R (47.9 +/- 37 vs 46.3 +/- 36). Cumulative percent ventricular pacing was significantly lower in MVP vs DDD/R (3.79 +/- 16.3 vs 80.6 +/- 33.8, P &lt; .0001). Back-up DDD/R pacing during MVP operation due to transient AVB occurred in 10% of patients (9.3 +/- 7.4 [range 1-15] episodes/patient-day, duration 39.7 minutes +/- 156 minutes). Fifteen percent of AV intervals during MVP operation exceeded 300 ms. No significant symptoms were reported during MVP operation.</AbstractText>MVP dramatically reduced cumulative percent ventricular pacing compared to DDD/R while maintaining AV synchrony and providing sensor-modulated atrial pacing support. Intermittent oscillations between MVP and DDD/R during transient AV block appeared safe and well tolerated.</AbstractText>

Diagnostic information in implantable devices that pertain to endpoints in atrial fibrillation studies.

Implantable devices can store significant information about physiologic parameters relating to rhythm and rate control. The primary objective of our analysis was to evaluate the relationship between changes in these parameters and changes in clinical outcomes in patients with atrial tachyarrhythmias (AT). Because the present guidelines do not provide quantitative definition of rhythm and rate control, we used the percent of time in AT and frequency of such episodes as measures of rhythm control. Rate control was measured as the percent of time spent at a ventricular rate &gt;120 beats/min, as well as the median ventricular rate during AT. Analysis was conducted in 643 patients with a history of AT and bradycardia receiving pacemakers to evaluate whether changes in these parameters were correlated with changes in cardiac hospitalization rates and SF-36 and symptom checklist scores. All patients were followed at 1, 4, and 7 months postimplant, during which rhythm and rate control data were collected. Positive correlation was observed between changes in cardiac hospitalization rate and changes in AT burden, as well as frequency of AT (P = 0.01, r = 0.08 for each). Changes in SF-36 or symptom checklist scores did not correlate with changes in rhythm and rate control measures. This patient cohort had relatively asymptomatic atrial fibrillation (symptom checklist frequency and severity scores of 14.3 +/- 9.5 and 11.5 +/- 7.9, respectively), and this may have contributed to the lack of correlation with SF-36 and symptom scores. Data stored in implantable devices offer a unique opportunity to monitor parameters of rhythm as well as rate control in patients with AT. In patients implanted with pacemakers for management of bradyarrhythmias who have a history of AT, a significantly positive but weak correlation was observed between changes in rhythm control measures (AT burden and frequency) and changes in cardiac hospitalization rate.

Ventricular rate control as an endpoint for treatment of atrial fibrillation.

Interest in the use of rate control as an endpoint for managing atrial fibrillation likely will increase given the results of recent randomized clinical trials. As an endpoint, rate control has favorable attributes of ease of measurement and clear numerical definitions. Pharmacologic rate control is achieved in approximately 80% of patients in large clinical trials. Ablation and pacing may achieve rate control in all patients. Rate control has been shown to improve quality of life over pretreatment status. However, several issues regarding the use of rate control as an endpoint are unsettled. Technical issues concerning when and how to measure heart rate remain. The current definitions of rate control are lacking in scientific foundation and demonstration of clinical relevance. Heart rate control during exercise may be difficult to achieve in many patients despite control at rest. Finally, the relationship of rate control to some important clinical outcomes has not been established.

Are there alternatives to mortality as an endpoint in clinical trials of atrial fibrillation?

Although atrial fibrillation (AF) is associated with an increased risk of death in many cohort studies and, therefore, is an endpoint of interest in trials of management of AF, the frequency of occurrence is low. Arrhythmia suppression as a surrogate endpoint for mortality in trials of rhythm management has a bad reputation. Recently, rehospitalization has been suggested as a possible surrogate for mortality in patients with potentially lethal ventricular arrhythmias. The prospect of alternatives to mortality in studies of patients with AF has been explored in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial. That analysis suggested that hospitalization for cardiovascular reasons (CV hospitalization) in patients such as those enrolled in AFFIRM may have many characteristics of a good surrogate for mortality. Furthermore, modeling based on the AFFIRM research plan and using CV hospitalization in a composite endpoint with death from all causes as an alternative to death alone provides ample power to detect even modest differences (&gt;/=15%) with substantial reduction of the number of subjects that need to be enrolled. However, there are limitations in the AFFIRM data on these points. More research is needed to define suitable alternatives to death as an endpoint for trials in a broad spectrum of patients with AF.

The coronary sinus: passive bystander or source of arrhythmia?

The coronary sinus provides access to the epicardial space of the heart allowing ablation of epicardial accessory pathways, foci of ventricular arrhythmia, and arrhythmogenic areas such as the vein or ligament of Marshall. In addition, its musculature may form atrioventricular accessory connections, participate in macroreentrant atrial arrhythmias, and generate foci of microreentrant atrial tachycardia and fibrillation. Thus, the coronary sinus may serve both as a bystander to arrhythmia circuits as well as an original source of cardiac arrhythmia.

Epicardial organization of human ventricular fibrillation.

The objective of this study was to test the hypothesis that on the epicardium of the in vivo human heart, ventricular fibrillation (VF) consists of chaotic small wavefronts that constantly change paths.</AbstractText>Despite the significance of VF to cardiovascular mortality, little is known about the wavefronts that constitute VF in humans.</AbstractText>In 9 patients undergoing cardiac surgery, a single VF episode was induced by rapid pacing immediately after institution of cardiopulmonary bypass while recordings were made from 504 electrodes spaced 2 mm apart in a 20 cm(2) plaque held against the anterior left ventricle epicardium. A total of 26 segments of VF, each 2 s long, were analyzed. A computer algorithm identified individual wavefronts and classified them into groups that followed similar activation sequences.</AbstractText>The mean activation rate was 5.8 +/- 1.8 (mean +/- SD) cycles/s. The wavefronts during each epoch were grouped into 9.4 +/- 7.1 different activation pathways, and 8.3 +/- 2.3 wavefronts followed each pathway. Individual wavefronts spread to activate an area of 5.1 +/- 3.0 cm(2) in the mapped region. The majority of the wavefronts propagated into the mapped region and/or propagated out of the mapped region into adjacent tissue, suggesting that the wavefronts were larger than 5.1 cm(2). Reentry was identified in only 16 of the 26 (62%) 2-s segments, always completed &lt;2 cycles, and lasted for 9.5 +/- 6.6% of these 16 epochs, which is 5.8% of the total duration of all the segments analyzed.</AbstractText>VF wavefronts on the human epicardium are usually large, repeatedly follow distinct pathways, and only occasionally reenter. If these results for the left ventricular epicardium are representative of those for the entire ventricular mass, they do not support the hypothesis that human VF consists of small, constantly changing wavefronts, but rather suggest that there is significant organization of human VF.</AbstractText>

Temporary overdriving pacing as an adjunct to antiarrhythmic drug therapy for electrical storm in acute myocardial infarction.

A-55-year-old man with diabetes mellitus was admitted to hospital because of chest pain. He was diagnosed as anterior acute myocardial infarction and treated with stent placement. After 7 days, ventricular fibrillation occurred because of a subacute reocclusion and balloon angioplasty was performed. Despite reperfusion therapy, intraaortic balloon pumping, antiarrhythmic drugs and beta-blocker, ventricular tachycardia or fibrillation relapsed and cardioversion was performed 29 times during 32 h. Temporary overdrive atrioventricular sequential pacing was initiated and the malignant arrhythmia finally disappeared. Even after stoppage of 25 h overdride pacing, it never recurred. Temporary overdrive pacing is an easy and feasible therapy for a drug-resistant electrical storm associated with AMI and should be performed in the early stage.

Combined effects of nifekalant and lidocaine on the spiral-type re-entry in a perfused 2-dimensional layer of rabbit ventricular myocardium.

Spiral re-entry plays the principal role in the genesis of ventricular tachycardia and ventricular fibrillation (VT/VF). The specific I(Kr) blocker, nifekakant (NIF) has, often in combination with lidocaine (LID), recently been used in Japan to prevent recurrent VT/VF, but the combined effects of these drugs on spiral re-entry had never been investigated.</AbstractText>A ventricular epicardial sheet was obtained from 13 Langendorff-perfused rabbit hearts by means of a cryoprocedure, and epicardial excitations were analyzed with a high-resolution optical mapping system. Nifekakant (0.5 micromol/L) caused significant prolongation of action potential duration (APD) and LID (3 micromol/L) attenuated the APD prolongation without affecting the conduction velocity. VT were induced in 6 hearts by cross-field stimulation, and single- or double-loop spirals circulating around variable functional block lines were visualized during the VT. Nifekakant reduced VT cycle length and caused early termination in association with destabilization of the spiral dynamics (prolongation of functional block line, frequent local conduction block, and extensive meandering). These modifications of spiral-type re-entrant VT by NIF were prevented by addition of LID.</AbstractText>The effects of NIF on the spiral excitations are reversed by LID. This interaction should be taken into account when these drugs are used in combination to treat VT/VF.</AbstractText>

Idiopathic right ventricular outflow tract tachycardia induced during acute episode of atrial fibrillation.<Pagination><StartPage>150</StartPage><EndPage>153</EndPage><MedlinePgn>150-3</MedlinePgn></Pagination><Abstract><AbstractText>Tachycardia-induced tachycardia is a rare condition. We report a case in which an episode of paroxysmal atrial fibrillation led to right ventricular outflow tract tachycardia. We also analyse all potential mechanisms that might contribute to the coexistence of these two different arrhythmias in the same patient.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fragakis</LastName><ForeName>Nikolaos</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>2nd Department of Cardiology, G Papanikolaou Hospital, Thessaloniki, Greece. nfrag@panafonet.gr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papadopoulos</LastName><ForeName>Nikolaos</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Cliousis</LastName><ForeName>Vassilios</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Katsaris</LastName><ForeName>George</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Hellenic J Cardiol</MedlineTA><NlmUniqueID>101257381</NlmUniqueID><ISSNLinking>1109-9666</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001281" MajorTopicYN="N">Atrial Fibrillation</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004554" MajorTopicYN="N">Electric Countershock</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="Y">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D035583" MajorTopicYN="N">Rare Diseases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013611" MajorTopicYN="N">Tachycardia, Atrioventricular Nodal Reentry</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>4</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>7</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>4</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15847137</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15846675</PMID><DateCompleted><Year>2005</Year><Month>07</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>21</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1469-493X</ISSN><JournalIssue CitedMedium="Internet"><Issue>2</Issue><PubDate><Year>2005</Year><Month>Apr</Month><Day>18</Day></PubDate></JournalIssue><Title>The Cochrane database of systematic reviews</Title><ISOAbbreviation>Cochrane Database Syst Rev</ISOAbbreviation></Journal>Pharmacological cardioversion for atrial fibrillation and flutter.

Tachycardia-induced tachycardia is a rare condition. We report a case in which an episode of paroxysmal atrial fibrillation led to right ventricular outflow tract tachycardia. We also analyse all potential mechanisms that might contribute to the coexistence of these two different arrhythmias in the same patient.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fragakis</LastName><ForeName>Nikolaos</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>2nd Department of Cardiology, G Papanikolaou Hospital, Thessaloniki, Greece. nfrag@panafonet.gr</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Papadopoulos</LastName><ForeName>Nikolaos</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Cliousis</LastName><ForeName>Vassilios</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Katsaris</LastName><ForeName>George</ForeName><Initials>G</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D002363">Case Reports</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Hellenic J Cardiol</MedlineTA><NlmUniqueID>101257381</NlmUniqueID><ISSNLinking>1109-9666</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001281" MajorTopicYN="N">Atrial Fibrillation</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004554" MajorTopicYN="N">Electric Countershock</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="Y">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005500" MajorTopicYN="N">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D035583" MajorTopicYN="N">Rare Diseases</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013611" MajorTopicYN="N">Tachycardia, Atrioventricular Nodal Reentry</DescriptorName><QualifierName UI="Q000150" MajorTopicYN="Y">complications</QualifierName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000628" MajorTopicYN="N">therapy</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>4</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>7</Month><Day>6</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>4</Month><Day>26</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15847137</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15846675</PMID><DateCompleted><Year>2005</Year><Month>07</Month><Day>19</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>21</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1469-493X</ISSN><JournalIssue CitedMedium="Internet"><Issue>2</Issue><PubDate><Year>2005</Year><Month>Apr</Month><Day>18</Day></PubDate></JournalIssue><Title>The Cochrane database of systematic reviews</Title><ISOAbbreviation>Cochrane Database Syst Rev</ISOAbbreviation></Journal><ArticleTitle>Pharmacological cardioversion for atrial fibrillation and flutter.</ArticleTitle><Pagination><StartPage>CD003713</StartPage><MedlinePgn>CD003713</MedlinePgn></Pagination><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Atrial fibrillation is the commonest cardiac dysrhythmia. It is associated with significant morbidity and mortality. There are two approaches to the management of atrial fibrillation: controlling the ventricular rate or converting to sinus rhythm in the expectation that this would abolish its adverse effects.<AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">To assess the effects of pharmacological cardioversion of atrial fibrillation in adults on the annual risk of stroke, peripheral embolism, and mortality.<AbstractText Label="SEARCH STRATEGY" NlmCategory="METHODS">We searched the Cochrane Controlled Trials Register (Issue 3, 2002), MEDLINE (2000 to 2002), EMBASE (1998 to 2002), CINAHL (1982 to 2002), Web of Science (1981 to 2002). We hand searched the following journals: Circulation (1997 to 2002), Heart (1997 to 2002), European Heart Journal (1997-2002), Journal of the American College of Cardiology (1997-2002) and selected abstracts published on the web site of the North American Society of Pacing and Electrophysiology (2001, 2002).<AbstractText Label="SELECTION CRITERIA" NlmCategory="METHODS">Randomised controlled trials or controlled clinical trials of pharmacological cardioversion versus rate control in adults (&gt;18 years) with acute, paroxysmal or sustained atrial fibrillation or atrial flutter, of any duration and of any aetiology.<AbstractText Label="DATA COLLECTION AND ANALYSIS" NlmCategory="METHODS">One reviewer applied the inclusion criteria and extracted the data. Trial quality was assessed and the data were entered into RevMan.<AbstractText Label="MAIN RESULTS" NlmCategory="RESULTS">We identified two completed studies AFFIRM (n=4060) and PIAF (n=252). We found no difference in mortality between rhythm control and rate control relative risk 1.14 (95% confidence interval 1.00 to 1.31). Both studies show significantly higher rates of hospitalisation and adverse events in the rhythm control group and no difference in quality of life between the two treatment groups. In AFFIRM there was a similar incidence of ischaemic stroke, bleeding and systemic embolism in the two groups. Certain malignant dysrhythmias were significantly more likely to occur in the rhythm control group. There were similar scores of cognitive assessment. In PIAF, cardioverted patients enjoyed an improved exercise tolerance but there was no overall benefit in terms of symptom control or quality of life.<AbstractText Label="AUTHORS' CONCLUSIONS" NlmCategory="CONCLUSIONS">There is no evidence that pharmacological cardioversion of atrial fibrillation to sinus rhythm is superior to rate control. Rhythm control is associated with more adverse effects and increased hospitalisation. It does not reduce the risk of stroke. The conclusions cannot be generalised to all people with atrial fibrillation. Most of the patients included in these studies were relatively older (&gt;60 years) with significant cardiovascular risk factors.

Pre-operative atrial fibrillation as the key determinant of outcome of mitral valve repair for degenerative mitral regurgitation.

To examine the impact of pre-operative atrial fibrillation (AF) on the outcome of mitral valve repair (MVR) for degenerative mitral regurgitation (MR).</AbstractText>Among 392 patients with moderate to severe MR who underwent MVR between 1991 and 2002, 283 patients with isolated degenerative MR were followed for 4.7+/-3.3 years. Of 27 deaths, nine were due to cardioembolic events and four were due to left ventricular (LV) dysfunction. When compared with patients with pre-operative AF, those with sinus rhythm (SR) had better survival (96+/-2.1 vs. 87+/-3.2% at 5 years, P=0.002) and higher cardiac event-free rates (96+/-2.0 vs. 75+/-4.4% at 5 years, P&lt;0.001). In patients with pre-operative SR, observed and expected survival were similar (P=0.811). Cox multivariable regression analysis confirmed AF [P=0.027, adjusted hazard ratio (AHR) 2.9] and age as independently predictive of survival, and AF (P=0.002, AHR 3.1), New York Heart Association Class, and LV fractional shortening as independently predictive of cardiac event.</AbstractText>Death due to LV dysfunction was not frequent and cardioembolic events due to AF were the leading cause for cardiac death. Pre-operative AF became a strong independent predictor of survival and morbidity. Patients with pre-operative SR had excellent prognosis. The benefits of preventing cardioembolic events due to AF validate the indication of MVR for patients with high risk for AF.</AbstractText>

Effect of cardiac resynchronization therapy on inducibility of ventricular tachyarrhythmias in cardiac arrest survivors with either ischemic or idiopathic dilated cardiomyopathy.

We evaluated whether long-term cardiac resynchronization therapy affects the inducibility of ventricular tachyarrhythmias in relation to reverse remodeling in cardiac arrest survivors with either ischemic or idiopathic dilated cardiomyopathy. Clinical, electrophysiologic, and echocardiographic data of 18 patients were obtained before and after 6 months of cardiac resynchronization.

ECG repolarization waves: their genesis and clinical implications.

The electrocardiographic (ECG) manifestation of ventricular repolarization includes J (Osborn), T, and U waves. On the basis of biophysical principles of ECG recording, any wave on the body surface ECG represents a coincident voltage gradient generated by cellular electrical activity within the heart. The J wave is a deflection with a dome that appears on the ECG after the QRS complex. A transmural voltage gradient during initial ventricular repolarization, which results from the presence of a prominent action potential notch mediated by the transient outward potassium current (I(to)) in epicardium but not endocardium, is responsible for the registration of the J wave on the ECG. Clinical entities that are associated with J waves (the J-wave syndrome) include the early repolarization syndrome, the Brugada syndrome and idiopathic ventricular fibrillation related to a prominent J wave in the inferior leads. The T wave marks the final phase of ventricular repolarization and is a symbol of transmural dispersion of repolarization (TDR) in the ventricles. An excessively prolonged QT interval with enhanced TDR predisposes people to develop torsade de pointes. The malignant "R-on-T" phenomenon, i.e., an extrasystole that originates on the preceding T wave, is due to transmural propagation of phase 2 reentry or phase 2 early afterdepolarization. A pathological "U" wave as seen with hypokalemia is the consequence of electrical interaction among ventricular myocardial layers at action potential phase 3 of which repolarization slows. A physiological U wave is thought to be due to delayed repolarization of the Purkinje system.

Factors associated with poor survival in women experiencing cardiac arrest in a rural setting.

The purpose of this study was to determine whether gender differences exist in the characteristics and outcomes for out-of-hospital cardiac arrest (OHCA) occurring in a rural setting.</AbstractText>In urban settings, women have a lower incidence of OHCA than men but otherwise a comparable survival for ventricular fibrillation (VF) OHCA. Whether OHCA gender differences exist in rural settings is not clear.</AbstractText>The study consisted of a prospective collection and analysis of nontraumatic, adult OHCA prompting a 911 call in six rural Indiana counties.</AbstractText>Over an average period of 2.2 years, 138 women and 250 men experienced OHCA (annual incidence rate: 56.4 per 100,000 men and 29.3 per 100,000 women). Women were older, less likely to experience OHCA in a public setting, more likely to be in an extended care facility, and less likely to have a witnessed arrest than were men. Women were less likely to present with an initial rhythm of VF than men (33.3% vs 53.6%, P &lt; .001). Women in VF had a longer time interval from 911 call to first shock compared with men. Women had poorer survival to hospital discharge for all OHCA (2.2% vs 7.2%, P = .04) and VF OHCA (2.2% vs 13.4%, P = .05) compared with men. After age adjustment, female gender remained associated with a poorer OHCA survival outcome. With adjustment for all significant arrest characteristics, female gender was no longer associated with survival.</AbstractText>In a rural population, women suffering OHCA have a dismal survival rate likely because of multiple unfavorable arrest characteristics.</AbstractText>

Long-term results after ablation of infarct-related ventricular tachycardia.

The purpose of this study was to assess the long-term effects of ablation of infarct-related ventricular tachycardia (VT) and the subsequent requirement for implantable cardioverter-defibrillator (ICD) therapy.</AbstractText>The long-term consequences after initially successful catheter ablation of infarct-related VT remain unclear.</AbstractText>Forty patients who presented with infarct-related VT were studied using noncontact mapping to guide ablation.</AbstractText>One hundred forty VTs were mapped using the noncontact mapping system, including 36 (25.7%) clinical VTs. An endocardial exit site was determined in 100% of VT circuits, diastolic endocardial activity in 77 VTs (55%), and complete circuits in 24 VTs (17.1%). Eighty-one VTs (57.9%) were targeted for ablation, of which 67 (82.7% of targeted) were successfully ablated, including 27 clinical VTs (75% of clinical). Documented recurrence of an ablated VT occurred in 7.5% of patients over 36.3 +/- 21.0 months of follow-up. Episodes of new or recurrent, nontargeted VT or ventricular fibrillation (VF) occurred in 37.5% and VT recurrence without documentation of cycle length in 5%. In patients with ICDs, mean shock frequency was reduced from 6.8 +/- 7.3 per month in the year prior to ablation to 0.05 +/- 0.12 per month after ablation, over 24.7 +/- 18.9 months of follow-up (P &lt; .0001).</AbstractText>In patients with infarct-related VT, noncontact mapping-guided VT ablation is associated with a high procedural success rate, and VT recurrence necessitating ICD therapy delivery is significantly reduced. However, only 42.5% of patients remain free from VT/VF 3 years after ablation. Catheter ablation for infarct-related VT is indicated as an adjunctive therapy in patients with symptomatic VT but cannot substitute for ICDs and antiarrhythmic drugs.</AbstractText>

Defibrillation threshold testing: is it really necessary at the time of implantable cardioverter-defibrillator insertion?

The purpose of this study was to (1) determine how often implantable cardioverter-defibrillator (ICD) system modifications were needed to obtain an adequate safety margin for defibrillation, (2) identify how often and for what indications defibrillation threshold (DFT) testing was not performed, and (3) identify factors predicting the need for modification.</AbstractText>Ventricular fibrillation (VF) typically is induced at the time of ICD insertion. Although DFT testing often is minimized, a safety margin of 10 J has been utilized as a standard of care. However, current devices offer technology such as biphasic waveforms and high outputs, and the need for testing has been questioned.</AbstractText>We reviewed the records of the last 1,139 patients undergoing initial ICD placement, generator replacement, or revision.</AbstractText>Seventy-one patients (6.2%) were identified as having an unacceptably high DFT (&lt;10 J safety margin) requiring intervention, and some required &gt;1 modification. Use of a high-output device alone was not enough to obtain an adequate DFT in 48% (34/71) of patients who required modifications (3% of the total population). No arrhythmia inductions were performed in 54 patients (4.7%) because of well-defined clinical conditions. Patients who required system modification had a lower ejection fraction, were younger, were less likely to have coronary artery disease, were more likely to be undergoing upgrade/generator replacement, and were more likely to be taking amiodarone. Long-term mortality was not different between the group of patients who required modification compared with those who did not (17% vs 20%, P = NS).</AbstractText>Routine VF induction and documentation of effective defibrillation still remains a reasonable part of ICD placement because an inadequate safety margin may occur in &gt;6% of patients. The incidence of patients who were inappropriate for testing based on well-defined clinical conditions is small (&lt;5%) in this unselected large series. Although some clinical features may predict the need for system modification, additional studies are needed to better define "acceptable efficacy" of ICDs in preventing sudden death prior to altering these standards in selected patients.</AbstractText>

[Plasma Nt-proBNP concentration during heart failure therapy].

To study the changes of plasma Nt-proBNP levels obtained at multi-time-points during heart failure patients underwent treatment and the relationship between the concentrations to the patients' clinical improvements.</AbstractText>Forty heart failure patients and 41 normal control patients were chosen. The heart function and clinical characteristics were evaluated. The plasma level of Nt-proBNP was measured with ELISA method.</AbstractText>The plasma Nt-proBNP levels were higher in heart failure group comparing to the control group significantly and gradually fell down in the progression of treatment, along with the improvement of clinical characteristics. The plasma Nt-proBNP levels at the admission were negatively correlated to the therapeutic reaction. The Nt-proBNP levels of patients died or with ventricular fibrillation during admission were higher than others and were apt to elevate during treatment but without statistic significant.</AbstractText>The plasma Nt-proBNP level can be the biochemical indicator of monitoring to heart failure patients in long term treatment.</AbstractText>

Effect of incessant ventricular tachyarrhythmias on serum endothelin and big-endothelin levels.

Endothelin-1 (ET-1) is a potent endogenous arrhythmogenic substance. The aim of our study was to investigate the changes of serum ET-1 and big-endothelin levels in patients suffering from spontaneous, incessant ventricular tachyarrhythmias. The 11 consecutive patients' (mean age, 59 +/- 11 years) underlying diseases were ischemic heart disease, valvular heart disease, dilated cardiomyopathy, primary electrical disease, and arrhythmogenic right ventricular dysplasia in five cases, three cases, one case, one case, and one case, respectively. The mean ejection fraction was 39 +/- 14%, New York Heart Association functional status was I, II, and III in two cases, four cases, and five cases, respectively. Ventricular tachycardias (VT) were detected in five patients, ventricular fibrillation (VF) in three patients, and VT + VF in three patients. VTs terminated spontaneously in two cases. Six patients required multiple external cardioversion/defibrillation shocks, while implantable cardioverter defibrillators terminated all sustained arrhythmias successfully in four cases. Blood samples were collected during arrhythmias and 24 hours (control) following the last VT/VF episode. Serum ET-1 and big-endothelin levels were measured with western blot analysis after immunoprecipitation. Serum ET-1 and big-endothelin levels were significantly higher during the last VT/VF compared with the control period (ET-1, 65.8 +/- 26.8 fmol/mL versus 53.9 +/- 22.3 fmol/mL, P &lt; 0.05; big-endothelin, 115.2 +/- 39.3 fmol/mL versus 89.2 +/- 25.1 fmol/mL, P &lt; 0.05). There was a negative correlation between the age and big-endothelin level measured at both times (during VT/VF, r = 0.94, P &lt; 0.05; control, r = 0.91, P &lt; 0.05). In conclusion, serum big-endothelin and ET-1 levels were significantly higher during incessant VT/VF, which can be a cause of multiple arrhythmia recurrence.

Effects of experimental diabetes on endothelin-induced ventricular arrhythmias in dogs.

Endothelin-1 (ET-1) is known to have a direct arrhythmogenic effect in the mammalian heart. Diabetes mellitus is accompanied by a series of endothelial and cardiac disfunctions; however, little is known about ET-1-induced direct arrhythmias in diabetes mellitus. Therefore, we infused ET-1 (33 pmol/min) into the left anterior descending coronary artery of 28 mongrel dogs, and measured basic hemodynamic parameters, coronary flow and an electrocardiogram. Diabetes mellitus was induced by alloxan (Group 4) and experiments were carried out 8 weeks later. Metabolically healthy dogs served as controls (Group 2). In a further control group, local hyperglycemia was induced by intracoronary glucose infusion (Group 3). ET-1 infusion induced prolongation of the QT-time and frequency-adjusted QT-time in all groups. Other electrophysiological parameters were comparable between the groups. This was followed by the occurence of ventricular premature beats, coupled extra-beats and later sustained ventricular tachycardia. Most of the experiments were terminated by ventricular fibrillation. The onset of arrhythmias was shorter in diabetic dogs as compared with control and locally hyperglycemic animals (18 +/- 8 minutes versus 24 +/- 8 minutes and 30 +/- 28 minutes, P &lt; 0.05). However, there was no difference in the number of ventricular fibrillations, and the total elapsed time until the termination of the experiments. Therefore, the diabetic heart seems to be more prone to ET-1-induced arrhythmias and this is probably not a result of locally high glucose concentrations.

Changes of endothelin-1 and big endothelin-1 levels and action potential duration during myocardial ischemia-reperfusion in dogs with and without ventricular fibrillation.

Myocardial ischemia-reperfusion is associated with increased production of endothelin-1 (ET-1). Moreover, exogenous ET-1 has arrhythmogenic properties. Our aim was to investigate the correlation between endogenous ET-1, big ET-1 levels and epicardial monophasic action potential duration during myocardial ischemia-reperfusion in anesthetized dogs. Thirty-minute myocardial ischemia was followed by a 90-minute reperfusion period in 18 mongrel dogs. The total incidence of ventricular fibrillation (VF) during ischemia and reperfusion was 11.1% and 33.3%, respectively. During ischemia, the monophasic action potential duration at 90% repolarization (MAPD90) decreased significantly (control versus ischemia, 30 minutes, 224.7 +/- 7.1 ms versus 173.8 +/- 7.6 ms; P &lt; 0.05), while during reperfusion a significant prolongation of MAPD90 was observed (ischemia, 30 minutes versus reperfusion, 30 minutes, 173.8 +/- 7.6 ms versus 249.7 +/- 9.9 ms, P &lt; 0.05). During reperfusion ET-1 and big ET-1 levels increased significantly in the coronary sinus and femoral artery (control versus reperfusion, 90 minutes: coronary sinus ET-1, 15.1 +/- 1.4 fmol/mL versus 22.3 +/- 1.1 fmol/mL; big ET-1, 14.7 +/- 1.9 fmol/mL versus 27.4 +/- 2.3 fmol/mL; P &lt; 0.05). The ET-1 concentration increased to a higher level during ischemia in dogs with VF compared with dogs surviving ischemia-reperfusion (non-VF versus VF: control, 15.1 +/- 1.3 versus 15.2 +/- 1.3; ischemia, 30 minutes, 17.6 +/- 1.2 fmol/mL versus 22 +/- 1.6 fmol/mL; P &lt; 0.05), demonstrating a trend of correlation between endothelin levels and development of VF (P = 0.07). ET-1 and big ET-1 levels increased during reperfusion and in the VF group during ischemia; however, there was no correlation between endothelin levels and MAPD90.

Myofiberbreak-up: a marker of ventricular fibrillation in sudden cardiac death.

Electrophysiologically, ventricular fibrillation is defined as a "chaotic, random, asynchronous electrical activity of the ventricles due to repetitive re-entrant excitation and/or rapid focal discharge". To this point its morphological equivalent has not been defined.</AbstractText>Several groups of different diseases and types of accidental death in normal subjects were studied. A complete autopsy was performed and the hearts were examined in 432 cases. A total of 16 myocardial samples per heart were processed for histological examination and sections were stained by haematoxylin and eosin or by specific stains. The frequency, location and extent of myocellular segmentation (stretching and/or rupture) of intercalated discs and associated changes of myocardial bundles and single myocells were investigated. A quantitative analysis was performed and the data were processed for statistical evaluation.</AbstractText>The frequency of MFB was maximal in coronary (88%) and Chagas (76%) groups followed by the intracranial brain haemorrhage group (52%). The extent of myofiberbreak-up was maximal in coronary/Chagas groups followed by intracranial haemorrhage and transplant groups.</AbstractText>No correlation was seen between gender, age, heart weight, degree of coronary atherosclerosis, myocardial fibrosis, survival and MFB. If our postulate is correct, finding MFB in the myocardium might allow the diagnosis of a malignant arrhythmia followed by cardiac arrest due to ventricular fibrillation even in the absence of clinical information (sudden death out-of-hospital).</AbstractText>

Automatic impedance monitoring and patient alert feature in implantable cardioverter defibrillators: being alert for the unexpected!

Recent advances in implantable cardioverter defibrillator (ICD) technology have enabled implementation of an automatic monitoring feature in ICDs that provides daily measurements of several technical parameters such as battery status, pacing, and high-voltage impedance. The system alerts the patient with an audible alarm to contact the physician in case the measured parameters are not within normal limits. Early detection of intermittent and potentially serious complications justifies routine use of this feature. This report describes a patient with an ICD who died suddenly due to ventricular fibrillation, which was not appropriately treated by the device. The cause of device malfunction was most likely an intermittent lead fracture that was not detected by the automatic impedance monitoring and alert feature of this device. Based on these data, potential benefits and theoretical pitfalls of automatic impedance monitoring and alert features are discussed.

Role of streptomycin-sensitive stretch-activated channel in chest wall impact induced sudden death (commotio cordis).

Deaths secondary to low-energy impacts to the precordium in young individuals (commotio cordis) have been reported with increasing frequency. In a swine model, baseball impacts induce ventricular fibrillation when directed at the center of the left ventricle during the vulnerable portion of repolarization just prior to the T-wave peak. It has been hypothesized that activation of stretch-sensitive channels could be crucial for this electrophysiological phenomenon. In this study, a nonselective stretch-activated cation channel was pharmacologically blocked prior to chest blows to determine whether this channel represents a possible pathway by which commotio cordis events occur.</AbstractText>In a randomized and blinded experiment, 12 swine (mean 17.1 +/- 2.5 kg) received either 2-g streptomycin intramuscularly (mean serum concentration 115 +/- 18 muM) or sterile water prior to chest impact. Each animal received six precordial impacts with a baseball propelled at 40 mph.</AbstractText>There was no significant difference in the frequency of induced VF in the animals administered streptomycin (10 of 19 impacts: 53%) compared to those control animals receiving only sterile water (10 of 31: 32%) (P = 0.15). However, the magnitude of ST segment elevation was less in the streptomycin-treated animals (19 +/- 19 mV) versus controls (61 +/- 46 mV) (P = 0.015).</AbstractText>Streptomycin did not alter the frequency of ventricular fibrillation in our commotio cordis model, indicating that the stretch-activated channel is not implicated in the genesis of chest blow-induced cardiac arrest. However, streptomycin did reduce ST elevation following impact suggesting that the stretch-activated channel may play a role in ST segment elevation following chest wall blows.</AbstractText>

Regional variation in capture of fibrillating swine left ventricle during electrical stimulation.

While it has been shown that electrical stimulation can capture a region of myocardium during ventricular fibrillation (VF), the ideal location to stimulate to maximize capture of the fibrillating in vivo left ventricle (LV) is not known. We previously demonstrated a mean directionality to the propagation of VF wavefronts in swine from posterior to anterior LV. We hypothesized that this directionality of VF wavefronts would affect capture of the LV epicardium while stimulating during VF.</AbstractText>In seven open-chest swine, during different VF episodes, electrical stimulation was performed singly or simultaneously from two lines of 26 epicardial electrodes, one on the posterior LV adjacent to the posterior descending coronary artery and another on the anterior LV adjacent to the left anterior descending coronary artery. Mapping was performed between the line of stimulating electrodes with 768 recording electrodes 2-mm apart. The incidence and extent of epicardium captured by stimulation through the lines of stimulating electrodes were determined in the mapped region. Capture occurred during 67% of 78 VF episodes. Capture from the posterior LV line was achieved in 88% of the episodes and from the anterior LV line in 44% of the episodes (P = 0.001). The maximum amount of myocardium captured was also much greater for stimulating from the posterior as compared to the anterior LV line (232 +/- 168 mm(2) vs 64 +/- 124 mm(2), P = 0.003). A significant part of the variability in capture was related to the direction of the mean VF wavefront velocity vector in each animal (r = 0.84, P &lt; 0.05).</AbstractText>Electrical stimulation from the posterior LV resulted in a greater incidence and extent of LV capture than stimulation from the anterior LV. A significant component of the variability in capture is related to the mean direction of VF wavefronts.</AbstractText>

Short QT syndrome and atrial fibrillation caused by mutation in KCNH2.

The short QT syndrome is a newly described clinical entity characterized by the presence of a short QT interval associated with cardiac tachyarrhythmias including sudden cardiac death at a young age in otherwise healthy individuals. A genetic basis has been identified linking the disease to mutations in KCNH2 in the familial forms and a mutation in KCNQ1 in a sporadic form of the disease.</AbstractText>We identified a family with short QT syndrome with a high incidence of paroxysmal atrial fibrillation in their members and no known history of sudden cardiac death. QT interval ranged from 225 to 240 ms within normal heart rate ranges in the affected individuals. Programmed electrical stimulation (PES) was performed in all affected members, which revealed a remarkably short atrial and ventricular refractory period, and inducibility of atrial and ventricular fibrillation. Treatment with propafenone has maintained the individuals free of atrial fibrillation to date. Genetic analysis identified a missense mutation (C to G substitution at nucleotide 1764) which resulted in the amino acid change (N588K) in KCNH2. This mutation had been previously described in two other families with a high incidence of sudden cardiac death.</AbstractText>Our study confirms that N588K is a hotspot for familial form of the short QT syndrome. The disease is clinically heterogeneous, as indicated by the fact that, in the three families with the same mutation, there is a wide range of symptoms, varying from atrial to ventricular fibrillation and sudden death. While the implantation of a defibrillator appears warranted due to the inducibility at PES, the clinical follow-up provides indication that the class Ic agent propafenone could be effective to prevent episodes of paroxysmal atrial fibrillation.</AbstractText>

Clinical and electrophysiological characteristics of Brugada syndrome caused by a missense mutation in the S5-pore site of SCN5A.

Brugada syndrome is an inherited cardiac disorder caused by mutations in the SCN5A gene encoding the cardiac sodium channel alpha-subunit, and potentially leads to ventricular fibrillation and sudden death. We report a case of a novel SCN5A mutation associated with Brugada syndrome. A 51-year-old man suffered from recurrent nocturnal syncopal attacks due to polymorphic ventricular tachycardia. His electrocardiogram showed ST-segment elevation in V1-V3 leads, but there was no evidence of structural heart disease. DNA sequence analysis of SCN5A in this patient revealed a missense mutation (R282H) in the S5-pore region of domain I. This mutational change was not present in 100 healthy Japanese controls. In the patient's family, a 36-year-old brother had died suddenly. Genetic analysis identified two other carriers of the R282H mutation, who had ST-segment elevation and slightly increased QRS widths, but they experienced no syncopal episodes or ventricular fibrillation. Electrophysiological investigation of the R282H mutant channel expressed in cultured cells showed a severe reduction in sodium current density and a mild positive shift of activation curve. R282H did not enhance intermediate inactivation. Single-channel conductance of R282H was slightly decreased compared with WT. The electrophysiological characteristics of the R282H channel are suggested to be closely related to the clinical phenotype of Brugada syndrome.

[Nifekalant hydrochloride as an effective treatment for postoperative ischemic heart disease].

We experienced 2 effective cases of nifekalant hydrochloride. One patient was 76-year-old female who underwent emergent coronary artery bypass grafting (CABG) because of unstable angina pectoris (AP) and ventricular fibrillation (Vf). Her cardiac function had been decreased preoperatively due to old myocardial infarction (OMI). One day after CABG, she revealed sustained ventricular tachycardia (VT) and Vf. Although administrations of neither lidocaine hydrochloride nor magnesium sulfate were effective, nifekalant hydrochloride finally stopped the life-threatening arrhythmia without hypotension. Another patient was 77-year-old male who underwent CABG and Dor operation. His cardiac function also had been decreased due to OMI. He revealed VT attack at midnight 3 days after operation. VT attack still appeared at next 2 midnight under lidocaine hydrochloride infusion, but finally it has disappeared after starting a drip infusion of nifekalant hydrochloride. Nifekalant hydrochloride is quite useful as a new therapeutic strategy for uncontrollable VT and Vf and for the patient who has a reduced left ventricular function because it has an inotropic effect.

[Infarct exclusion for postinfarction left ventricular free wall rupture with severe congestive heart failure].

A 70-year-old man was transferred to our hospital with severe congestive heart failure and ventricular arrhythmia due to acute myocardial infarction. He had experienced chest pain 3 weeks previously and was admitted to another hospital for dyspnea, where he required assist ventilation, 1 week prior to the transfer. An echocardiogram revealed a broad anteroseptal infarction and very poor left ventricular function with an ejection fraction (EF) of 22%. He remained in a severe congestive heart failure condition despite a full administration of catecholamines. Coronary angiogram findings revealed an occlusion of the proximal left anterior descending coronary artery and 1 week later severe hypotension was suddenly presented. An echocardiogram showed pericardial effusion with signs of cardiac tamponade. A pericardiocentesis was performed and hemodynamic improvement was obtained for a short time, after which the patient underwent urgent open heart surgery. During the operation, exclusion of the anteroseptal akinetic area using an oval patch was performed under a cardiopulmonary bypass and ventricular fibrillation. Severe cardiac failure remained postoperatively and the patient could not be weaned from cardiopulmonary bypass, therefore, we implanted a percutaneous cardiopulmonary support (PCPS) and started intraaortic balloon pumping (IABP). The patient was weaned from PCPS at 26 days after surgery and from IABP at 30 days. Following hospital release, he has continued to do well without heart failure for 39 months after the operation.

Safe performance of magnetic resonance imaging on a patient with an ICD.

This is a report on a patient with an implanted cardioverter defibrillator (ICD) who intentionally underwent magnetic resonance imaging (MRI) of a malignant brain tumor. To avoid inadequate detection of ventricular tachycardia (VT) or ventricular fibrillation (VF), the ICD was inactivated by programming the VT-detection and VT/VF-therapy status off. The patient came through the protocol safely and without any difficulty or discomfort. There was no arrhythmic event. MRI affected neither programmed data nor the function of the ICD system.

Transcoronary ablation of septal hypertrophy does not alter ICD intervention rates in high risk patients with hypertrophic obstructive cardiomyopathy.

Transcoronary ablation of septal hypertrophy (TASH) is safe and effectively reduces the intraventricular gradient in patients with hypertrophic obstructive cardiomyopathy (HOCM). To analyze the potential of anti- and proarrhythmic effects of TASH, we studied the discharge rates of implanted cardioverter defibrillators (ICD) in patients with HOCM who are at a high risk for sudden cardiac death.</AbstractText>ICD and TASH were performed in 15 patients. Indications for ICD-implantation were secondary prevention in nine patients after resuscitation from cardiac arrest with documented ventricular fibrillation (n = 7) or sustained ventricular tachycardia (n = 2) and primary prevention in 6 patients with a family history of sudden deaths, nonsustained ventricular tachycardia, and/or syncope. All the patients had severe symptoms due to HOCM (NYHA functional class = 2.9).</AbstractText>During a mean follow-up time of 41 +/- 22.7 months following the TASH procedure, 4 patients had episodes of appropriate discharges (8% per year). The discharge rate in the secondary prevention group was 10% per year and 5% in the group with primary prophylactic implants. Three patients died during follow-up (one each of pulmonary embolism, stroke, and sudden death).</AbstractText>In conclusion, on the basis of ICD-discharge rates in HOCM-patients at high risk for sudden death, there is no evidence for an unfavorable arrhythmogenic effect of TASH. The efficacy of ICD treatment for the prevention of sudden cardiac death in HOCM could be confirmed, however, mortality is high in this cohort of hypertrophic cardiomyopathy patients.</AbstractText>

Atrial pacing should be used more frequently in sinus node disease.

Single lead atrial (AAI(R)) pacing for sick sinus syndrome provides physiological pacing and is less expensive than a dual chamber system. Compared with ventricular-based pacing, it maintains the normal cardiac depolarization sequence, is associated with less atrial fibrillation and heart failure, and avoids pacemaker syndrome. We sought whether it is possible to select patients for AAI(R) pacing with a low likelihood of subsequent ventricular pacing, and whether this approach was cost-effective.</AbstractText>A retrospective review was conducted of AAI(R) pacemaker implantations. Patients requiring a further procedure for insertion of a ventricular lead (for DDD(R) or VVI(R) pacing) were compared with those who remained atrially paced.</AbstractText>2.7% (117 of 4,366) of implants were AAI(R), compared with less than 1% overall for New Zealand and Australia. During follow-up of 3.5 (2.3, 7.7) years, insertion of a ventricular lead was required in 14 (12%), and was more likely in those with pre-existing PR interval &gt;0.20 seconds (odds ratio 7.8, P = 0.003) or left bundle branch block (LBBB, odds ratio 17, P = 0.037). Right bundle branch block, left anterior fascicular block, or history of paroxysmal atrial fibrillation were not more frequent in the group requiring ventricular pacing, and preimplantation Wenckebach point was not different. The most efficient strategy was initial AAIR implantation in all except those with LBBB or PR interval &gt;0.20 seconds. Compared with routine DDDR implantation, cost was reduced by 20%, with a 1.4% annual incidence of further procedures.</AbstractText>AAIR is the appropriate pacing choice for sick sinus syndrome without LBBB or PR interval &gt;0.20 seconds.</AbstractText>

Clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003).

To identify clinical, echocardiographic, and electrocardiographic abnormalities in Boxers with cardiomyopathy and echocardiographic evidence of left ventricular systolic dysfunction.</AbstractText>Retrospective study.</AbstractText>48 mature Boxers.</AbstractText>Medical records were reviewed for information on age; sex; physical examination findings; and results of electrocardiography, 24-hour ambulatory electrocardiography, thoracic radiography, and echocardiography.</AbstractText>Mean age of the dogs was 6 years (range, 1 to 11 years). Twenty (42%) dogs had a systolic murmur, and 9 (19%) had ascites. Congestive heart failure was diagnosed in 24 (50%) dogs. Seventeen (35%) dogs had a history of syncope. Mean fractional shortening was 14.4% (range, 1% to 23%). Mean left ventricular systolic and diastolic diameters were 4.5 cm (range, 3 to 6.3 cm) and 5.3 cm (range, 3.9 to 7.4 cm), respectively. Twenty-eight (58%) dogs had a sinus rhythm with ventricular premature complexes (VPCs), and 20 had supraventricular arrhythmias (15 with atrial fibrillation and 5 with sinus rhythm and atrial premature complexes). Sixteen of the dogs with supraventricular arrhythmias also had occasional VPCs. Morphology of the VPCs seen on lead II ECGs was consistent with left bundle branch block in 25 dogs, right bundle branch block in 8, and both in 11.</AbstractText>Results suggest that Boxers with cardiomyopathy and left ventricular dysfunction frequently have arrhythmias of supraventricular or ventricular origin. Whether ventricular dysfunction was preceded by electrical disturbances could not be determined from these data, and the natural history of myocardial disease in Boxers requires further study.</AbstractText>

Electrophysiological concept of ventricular defibrillation mechanism.

Sudden cardiac death is a major health problem in most industrialized countries around the world including Thailand. It is mainly caused by ventricular fibrillation (VF). Currently, defibrillation is the only effective clinical treatment of this fatal arrhythmia. Although defibrillation mechanism has been investigated extensively for many decades, its definite mechanism is still debated. It is known that understanding the basic mechanism of defibrillation is essential to develop better treatment of VF: In the present article, seven hypotheses commonly proposed as the mechanism of ventricular defibrillation are reviewed. Since research in the field of defibrillation mechanism is dynamic, the present review is to update the information to clinicians and basic investigators on the mechanism of defibrillation available to date.

[Cardiac resynchronization therapy and arrhythmias].

Cardiac resynchronization therapy (CRT) is now considered an established therapy for patients with chronic heart failure in the presence of a wide QRS complex. Though proarrhythmic effects have been described in a few cases, CRT did not increase the frequency of ventricular tachyarrhythmias in prospective studies. In patients on CRT therapy, persistent atrial fibrillation sometimes converts back to sinus rhythm, possibly dependent on the duration of atrial fibrillation.

Respiratory medications and the risk of cardiac arrhythmias.

Medications used to treat respiratory diseases include beta-adrenoceptors, antimuscarinics, inhaled and oral corticosteroids, and theophyllines. Most of these drugs have been associated indirectly with cardiac rhythm disorders, but epidemiologic evidence is limited.</AbstractText>To evaluate the association between respiratory drugs and the occurrence of rhythm disorders among patients with asthma and those with chronic obstructive pulmonary disease, we conducted a case-control study nested in a population-based cohort of individuals 10-79 years of age and registered in the U.K. General Practice Research Database after 1 January 1994. The analysis included 710 confirmed cases and 5000 controls frequency-matched to cases by age (interval of 1 year) and sex.</AbstractText>No increased risk of arrhythmias overall was found among users of inhaled steroids (relative risk = 1.0; 95% confidence interval = 0.8-1.3). Short-term use of theophylline was weakly associated with arrhythmia (1.8; 1.0-3.3). An increased risk was found among users of oral steroids, and the relative risk was greater at the beginning of therapy (2.6; 2.0-3.5). The risk of atrial fibrillation was increased, especially for short-term use of oral steroids (2.7; 1.9-3.8), and a weak association was seen for theophyllines, especially short-term use (1.8; 0.9-3.7). Supraventricular tachycardia was associated with long-term use of oral steroids (2.1; 0.8-5.7), long-term use of antimuscarinics (1.7; 0.7-4.1), and short-term use of theophylline (4.0; 0.9-18.1). Ventricular arrhythmias were associated with oral steroids (3.2; 0.8-13.3) and beta-adrenoceptors (7.1; 0.8-65.9).</AbstractText>Oral steroids and theophylline were the therapeutic groups associated with risk of developing atrial fibrillation, especially with new courses of therapy. Results from this study also are consistent with certain suspected dysrhythmic effects of theophyllines, with supraventricular tachycardia associated with antimuscarinics, and with ventricular arrhythmias associated with beta-adrenoceptors.</AbstractText>

Clinical and echocardiographic determinants of long-term survival after surgical myectomy in obstructive hypertrophic cardiomyopathy.

Surgical myectomy has been the standard treatment for patients with drug-refractory obstructive hypertrophic cardiomyopathy. The clinical and echocardiographic predictors of long-term survival and freedom from cardiovascular morbidity after myectomy have been unclear.</AbstractText>We studied a consecutive cohort of 338 adult patients (age at operation 47+/-14 [range 18 to 77] years, 60% male) who underwent myectomy at our institution. Preoperative resting left ventricular outflow tract (LVOT) gradient was 66+/-32 mm Hg (range 5 to 158 mm Hg). Early postoperative mortality was 1.5% (5 deaths): 4 deaths occurred between 1978 and 1992, and 1 death occurred between 1993 and 2002. During long-term follow-up, 83% of patients reported an improvement to functional class I or II. The majority of patients (98%) had no resting LVOT gradient. Long-term survival was excellent, with 98+/-1% survival at 1 year, 95+/-1% at 5 years, and 83+/-3% at 10 years after myectomy. Multivariable Cox regression analysis identified 5 predictors of overall mortality: (1) age &gt; or =50 years at surgery (hazard ratio [HR] 2.8, 95% CI 1.5 to 5.1, P=0.001), (2) female gender (HR 2.5, 95% CI 1.5 to 4.3, P=0.0009), (3) history of preoperative atrial fibrillation (HR 2.2, 95% CI 1.2 to 4.0, P=0.008), (4) concomitant CABG (HR 3.7, 95% CI 1.7 to 8.2, P=0.001), and (5) preoperative left atrial diameter &gt; or =46 mm (HR 2.9, 95% CI 1.6 to 5.4, P=0.0008). Significant predictors of late major cardiovascular events found on multivariable analysis were (1) female gender (HR 3.3, 95% CI 2.0 to 5.4, P&lt;0.0001), (2) history of preoperative atrial fibrillation (HR 1.9, 95% CI 1.1 to 3.3, P=0.02), and (3) preoperative left atrial diameter &gt; or =46 mm (HR 2.5, 95% CI 1.5 to 4.3, P=0.0008).</AbstractText>Myectomy provides excellent relief for LVOT obstruction in patients with hypertrophic cardiomyopathy. Preoperative clinical and echocardiographic variables can predict long-term outcome after myectomy.</AbstractText>

P wave signal averaged ECG and chemoreflexsensitivity in paroxysmal atrial fibrillation.

Detailed analysis of the QRS-complex and autonomic dysfunction can identify patients at risk to suffer from ventricular arrhythmias. To determine whether patients at risk for paroxysmal atrial fibrillation (PAF) could be identified while in sinus rhythm, a P wave triggered signal averaged ECG and an analysis of the autonomic function by chemoreflexsensitivity (CHRS) were examined. The ratio between the difference of RR intervals in the ECG and the venous partial pressure of oxygen before and after 5-min oxygen inhalation was measured for the determination of CHRS. We examined 224 patients (group A) who suffered from PAF, 250 patients (group B) without arrhythmic history and 30 young volunteers (group C). The filtered P wave duration (FPD) was significantly longer in group A than in group B (140.9+/-21.0 vs. 118.2+/-9.4 ms, p&lt;0.0001) or C (105.2+/-14.1 ms, p&lt;0.0001) while the root mean square voltage of the last 20 ms of the P wave (RMS 20) was significantly lower in group A than in group B (2.68+/-1.12 vs. 4.06+/-1.57 microV, p&lt;0.0001) or C (3.97+/-1.36 microV, p&lt;0.0001). Atrial late potentials (ALP) were defined as a FPD&gt;120 ms and a RMS 20&lt; or =3.5 microV. ALP could identify patients of group A with a specificity of 78% and a sensitivity of 83%. Patients with PAF (2.32+/-1.15 ms/mm Hg) showed a significantly lower CHRS than group B (4.14+/-1.58 ms/mm Hg, p&lt;0.0001) or group C (4.98+/-1.51 ms/mm Hg, p&lt;0.0001). The sensitivity for the presence of atrial fibrillation was 71% for a CHRS below 3.0 ms/mm Hg with a specificity of 70%. A combination of both methods showed a specificity of 85% and a sensitivity of 65% when ALP and pathological CHRS were present. The results of our study suggest that risk of atrial fibrillation could be detected by P wave signal averaged ECG and CHRS. An analysis of CHRS seems to be an appropriate method to demonstrate a neurovegetative imbalance, which might be one possible trigger mechanism.

[Nibentan -- a drug for pharmacological cardioversion of persistent atrial fibrillation].

To assess efficacy of a potassium channel blocker nibentan for pharmacological cardioversion of persistent atrial fibrillation. Method. Nibentan (1% solution) was infused intravenously after 3 weeks of warfarin pretreatment to 31 patients with duration of atrial fibrillation from 4 weeks to 15 months.</AbstractText>Sinus rhythm was restored in 24 patients. Mean dose of nibentan was 0.119+/-0.02 mg/kg. Proarrhythmic effects (paroxysmal or nonsustained polymorphic ventricular tachycardia) and substantial suppression of sinus rhythm automatism were registered in 3 and 3 patients, respectively.</AbstractText>Nibentan is highly effective in persistent atrial fibrillation. It can be recommended for inhospital use in intensive care facilities.</AbstractText>

Cariporide potentiates the effects of epinephrine and vasopressin by nonvascular mechanisms during closed-chest resuscitation.

The efficacy of vasopressor therapy during closed-chest resuscitation is limited and decreases over time. We previously reported that sodium-hydrogen exchanger isoform-1 inhibition during ventricular fibrillation (VF) using cariporide ameliorates ischemic contracture and enhances the efficacy of chest compression. We currently investigated whether cariporide could potentiate pressor responses to epinephrine and vasopressin.</AbstractText>VF was induced and left untreated for 12 min in two series of 16 rats each. Chest compression was then started and the depth adjusted within the initial 2 min to attain an aortic diastolic pressure between 26 and 28 mm Hg. In one series, rats received boluses of epinephrine (150 microg/kg); in the other series, rats received boluses of vasopressin (0.8 U/kg) to maintain the aortic diastolic pressure &gt; 25 mm Hg. Within each series, rats were randomized to receive a 3 mg/kg bolus of cariporide or 0.9% NaCl immediately before starting chest compression. Defibrillation was attempted at 20 min of VF (8 min of chest compression).</AbstractText>Cariporide prompted higher and more sustained coronary perfusion pressures in both the epinephrine group (37 +/- 5 mm Hg vs 29 +/- 7 mm Hg, p &lt; 0.05) and the vasopressin group (36 +/- 5 mm Hg vs 28 +/- 6 mm Hg +/- SD, p &lt; 0.02) even though fewer additional vasopressor doses were required. After resuscitation, cariporide-treated rats had less ventricular ectopic activity, better hemodynamic function, and improved survival scores. In separate experiments, in situ perfusion of the aorta excluded a vascular-mediated effect of cariporide.</AbstractText>Cariporide enhanced the hemodynamic efficacy of vasopressor agents and improved resuscitation outcomes probably as a result of enhanced forward blood flow without effect on the peripheral vasculature.</AbstractText>

Impact of congestive heart failure and left ventricular systolic function on the prognostic significance of atrial fibrillation and atrial flutter following acute myocardial infarction.

Reports on the prognostic importance of atrial fibrillation following myocardial infarction have provided considerable variation in results. Thus, this study examined the impact of left ventricular systolic function and congestive heart failure on the prognostic importance of atrial fibrillation in acute myocardial infarction patients that might explain previous discrepancies.</AbstractText>The study population was 6676 patients consecutively admitted to hospital with acute myocardial infarction. Information on the presence of atrial fibrillation/flutter, left ventricular systolic function and congestive heart failure were prospectively collected. Mortality was followed for 5 years.</AbstractText>In patients with left ventricular ejection fraction&lt;0.25, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.8 (1.1-3.2); p&lt;0.05) but not an increased 30-day mortality. In patients with 0.25&lt;or=left ventricular ejection fraction&lt;or=0.35, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.7 (1.3-2.3); p&lt;0.001) and an increased 30-day mortality (OR=1.7 (1.3-2.2); p&lt;0.001). In-hospital and 30-day mortality was not increased in patients with left ventricular ejection fraction&gt;0.35. In patients with congestive heart failure, atrial fibrillation/atrial flutter was associated with an increased in-hospital mortality (OR=1.5 (1.2-1.9); p&lt;0.001) and increased 30-day mortality (OR=1.4 (1.1-1.7); p&lt;0.001) but not in patients without congestive heart failure. In hospital survivors, atrial fibrillation/atrial flutter was associated with an increased long-term mortality in all subgroups except those with left ventricular ejection fraction&lt;0.25.</AbstractText>Atrial fibrillation/atrial flutter is primarily associated with increased in-hospital mortality in heart failure patients. Long-term mortality is increased in all subgroups except those with left ventricular ejection fraction&lt;25%.</AbstractText>

Left ventricular aneurysm repair: early survival.

The aim of this study was to evaluate the early survival in patients submitted to left ventricular (LV) repair and concomitant myocardial revascularization.</AbstractText>We retrospectively reviewed the records of 51 patients who were submitted to LV repair and concomitant myocardial revascularization between January 1998 and June 2003. Of 51 patients (44 males with a mean age of 60+/-9.2 years, and 7 females with a mean age of 61+/-6.5 years), 29 (56.9 %) were submitted to the McCarthy technique, 16 (31.3 %) to the technique that was described by Jatene and modified by Dor, and 6 (11.8%) to the Cooley technique (linear repair). The mean preoperative LV ejection fraction was 36.5+/-7.7 %, the mean preoperative LV end-diastolic diameter was 61.8+/-3.9 mm, the mean preoperative LV end-systolic diameter was 49.9+/-5.1 mm, the mean preoperative interventricular septal thickness was 9.7+/-1.7 mm, and finally, the mean posterior wall thickness was 8.9+/-1 mm. The mean follow-up was 30.7+/-23.4 months (range 11-82 months).</AbstractText>One patient died during surgery (1.9%) and one early postoperatively (1.9%). The causes of death were respectively irreversible ventricular fibrillation and low cardiac output syndrome. The overall survival at follow-up was 98% (49 patients). One patient died during follow-up of myocardial infarction. At follow-up, all patients presented with improved clinical symptoms, and had a better mean NYHA functional class with respect to the preoperative value (3.3+/-0.3 vs 2.0+/-0.5, p &lt; 0.05). Besides, the mean CCS angina class decreased in all patients (3.4+/-0.2 vs 1.9+/-0.3, p &lt; 0.05). The average LV ejection fraction increased from 36.3+/-7.7 to 44.3+/-4.9% (p &lt; 0.001), the average LV end-diastolic diameter decreased from 61.7+/-3.9 to 55.5+/-5.6 mm (p &lt; 0.001), and the average LV end-systolic diameter decreased from 49.9+/-5.1 to 40.4+/-5.1 mm (p &lt; 0.001). No statistically significant difference was found between the preoperative and postoperative data regarding the interventricular septal thickness (9.7+/-1.7 vs 10.3+/-1.6 mm, p = NS), and the posterior wall thickness (9.7+/-1 vs 8.8+/-1.3 mm, p = NS).</AbstractText>LV aneurysm repair and concomitant myocardial revascularization may be performed with an acceptable surgical risk and a good early survival.</AbstractText>

Clinical evaluation of an inspiratory impedance threshold device during standard cardiopulmonary resuscitation in patients with out-of-hospital cardiac arrest.

To determine whether an impedance threshold device, designed to enhance circulation, would increase acute resuscitation rates for patients in cardiac arrest receiving conventional manual cardiopulmonary resuscitation.</AbstractText>Prospective, randomized, double-blind, intention-to-treat.</AbstractText>Out-of-hospital trial conducted in the Milwaukee, WI, emergency medical services system.</AbstractText>Adults in cardiac arrest of presumed cardiac etiology.</AbstractText>On arrival of advanced life support, patients were treated with standard cardiopulmonary resuscitation combined with either an active or a sham impedance threshold device.</AbstractText>We measured safety and efficacy of the impedance threshold device; the primary end point was intensive care unit admission. Statistical analyses performed included the chi-square test and multivariate regression analysis. One hundred sixteen patients were treated with a sham impedance threshold device, and 114 patients were treated with an active impedance threshold device. Overall intensive care unit admission rates were 17% with the sham device vs. 25% in the active impedance threshold device (p = .13; odds ratio, 1.64; 95% confidence interval, 0.87, 3.10). Patients in the subgroup presenting with pulseless electrical activity had intensive care unit admission and 24-hr survival rates of 20% and 12% in sham (n = 25) vs. 52% and 30% in active impedance threshold device groups (n = 27) (p = .018, odds ratio, 4.31; 95% confidence interval, 1.28, 14.5, and p = .12, odds ratio, 3.09; 95% confidence interval, 0.74, 13.0, respectively). A post hoc analysis of patients with pulseless electrical activity at any time during the cardiac arrest revealed that intensive care unit and 24-hr survival rates were 20% and 11% in the sham (n = 56) vs. 41% and 27% in the active impedance threshold device groups (n = 49) (p = .018, odds ratio, 2.82; 95% confidence interval, 1.19, 6.67, and p = .037, odds ratio, 3.01; 95% confidence interval, 1.07, 8.96, respectively). There were no statistically significant differences in outcomes for patients presenting in ventricular fibrillation and asystole. Adverse event and complication rates were also similar.</AbstractText>During this first clinical trial of the impedance threshold device during standard cardiopulmonary resuscitation, use of the new device more than doubled short-term survival rates in patients presenting with pulseless electrical activity. A larger clinical trial is underway to determine the potential longer term benefits of the impedance threshold device in cardiac arrest.</AbstractText>

Reprogramming of the human atrial transcriptome in permanent atrial fibrillation: expression of a ventricular-like genomic signature.

Atrial fibrillation is associated with increased expression of ventricular myosin isoforms in atrial myocardium, regarded as part of a dedifferentiation process. Whether reexpression of ventricular isoforms in atrial fibrillation is restricted to transcripts encoding for contractile proteins is unknown. Therefore, this study compares atrial mRNA expression in patients with permanent atrial fibrillation to atrial mRNA expression in patients with sinus rhythm and to ventricular gene expression using Affymetrix U133 arrays. In atrial myocardium, we identified 1434 genes deregulated in atrial fibrillation, the majority of which, including key elements of calcium-dependent signaling pathways, displayed downregulation. Functional classification based on Gene Ontology provided the specific gene sets of the interdependent processes of structural, contractile, and electrophysiological remodeling. In addition, we demonstrate for the first time a prominent upregulation of transcripts involved in metabolic activities, suggesting an adaptive response to increased metabolic demand in fibrillating atrial myocardium. Ventricular-predominant genes were 5 times more likely to be upregulated in atrial fibrillation (174 genes upregulated, 35 genes downregulated), whereas atrial-specific transcripts were predominantly downregulated (56 genes upregulated, 564 genes downregulated). Overall, in fibrillating atrial myocardium, functional classes of genes characteristic of ventricular myocardium were found to be upregulated (eg, metabolic processes), whereas functional classes predominantly expressed in atrial myocardium were downregulated (eg, signal transduction and cell communication). Therefore, dedifferentiation with adoption of a ventricular-like signature is a general feature of the fibrillating atrium.

Propranolol intoxication revealing a Brugada syndrome.

This is the first report of Brugada syndrome revealed by beta-blocker intoxication. A 24-year-old healthy man ingested propranolol (2.28 g) to commit suicide. After early gastric lavage, electrolytes, cardiac enzymes, chest X-ray, and echocardiography were normal. Dosages of psychotropic drugs were negative. ECG showed a typical coved-type pattern of Brugada syndrome. Follow-up showed partial ECG normalization of the discrete saddleback-type pattern. The ajmaline- test confirmed Brugada syndrome. These ECG modifications may be explained by the stabilizing membrane effect of high concentration of propranolol and/or inhibition of ICaL. This case illustrates the possible deleterious effects of beta-blockers in patients with Brugada syndrome.

An autopsy case of Brugada syndrome with significant lesions in the sinus node.

A 30-year-old man with Brugada syndrome died suddenly. The heart weighed 380 g. The left ventricular wall showed mild thickening, and marked fatty tissue deposition was noted in the right ventricular outflow tract. Neither ventricle was enlarged. Contraction band necrosis was diffuse in both ventricles. In the ventricles no cardiac muscle cell hypertrophy or atrophy, or significant interstitial fibrosis was observed. In the sinus node the number of nodal cells was reduced by half, with fatty tissue and fibrosis prominent. But no lesions were evident in the right bundle branch.

Unsuccessful internal defibrillation in Brugada syndrome: focus on refractoriness and ventricular fibrillation cycle length.

In patients with Brugada syndrome, implantable cardioverter defibrillator (ICD) is the only reliable treatment to prevent sudden death though, in some cases, internal defibrillation may be unsuccessful. The aim of this study was to examine the determinants of defibrillation failure, with a focus on electrophysiologic characteristics.</AbstractText>The study included 51 patients treated with ICD: 22 with Brugada syndrome and 29 with structural heart disease (SHD). The prevalence of defibrillation energy requirement precluding the programming of a 10-J safety margin, the mean right ventricular effective refractory period (ERP), and mean induced ventricular fibrillation cycle length (VFCL) from the stored ICD electrograms, were compared between the two patient groups.</AbstractText>High defibrillation requirements were observed in 18% of patients with Brugada syndrome versus 0% of patients with SHD. However, the patients with SHD had larger heart size than those with Brugada syndrome. Mean VFCL and mean ERP were both significantly shorter in patients with Brugada syndrome than in patients with SHD, and ERP and VFCL were significantly correlated.</AbstractText>Patients with Brugada syndrome have a high prevalence of high defibrillation energy requirement, and short ventricular ERP and VFCL.</AbstractText>

[Semiautomatic external defibrillation: use inside a hospital].

The electric rhythm which provokes the majority of the cases of sudden death is ventricular fibrillation, and the only effective measure to reestablish spontaneous circulation consists in administering a precocious electrical discharge, or defibrillation. Time is a fundamental factor since the possibilities tor survival are practically nil it defibrillation is applied 10 to 12 minutes after the patient suffers his/her attack. Therefore, in recent years, the use of semiautomatic external defibrillators has been promoted. These small, low-cost, easy to handle apparatuses are designed so that the first person who detects a cardio-respiratory arrest can defibrillate, whether or not that person is a trained medical technician. Bearing in mind that in our hospitals nurses are in close contact with patients 24 hours a day nurses become the most appropriate professional to utilize these devices once they have received minimum training and instruction in the use of semiautomatic external defibrillators which will qualify and authorize nurses to do so.

Plasma concentration of atrial natriuretic peptide is related to the duration of atrial fibrillation in patients with advanced heart failure.

Plasma concentration of atrial natriuretic peptide (ANP) is elevated in patients with atrial fibrillation (AF) and in patients with chronic heart failure (CHF).Aim. To assess ANP level in patients with permanent AF and advanced CHF.</AbstractText>The study group consisted of 41 patients (27 males, mean age 62+/-8 years) with AF of a mean duration of 8.8 months. Twenty six (63%) patients were in NYHA class II, and 15 (37%) - in NYHA class III or IV. All patients underwent clinical and echocardiographic evaluation as well as ANP plasma concentration assessment. Multiple regression analysis was used to identify factors which determine ANP plasma concentration.</AbstractText>Mean ANP plasma concentration was 52.4+/-22.7 pg/ml in the whole study group; 38.6+/-10.8 pg/ml in NYHA class II patients and 74.9+/-18.7 pg/ml in NYHA class III-IV subjects (p&lt;0.0001). Among echocardiographic parameters, patients with NYHA class III or IV had significantly lower left ventricular ejection fraction and greater left atrial volume than patients with NYHA class II (32% versus 56%, p&lt;0.0001 and 101.0+/-23.8 cm(3) versus 83.4+/-16.1 cm(3), p&lt;0.006, respectively). Multiple regression analysis revealed a significant negative correlation between AF duration and ANP level (p=0.0013) in a group of patients with NYHA class III or IV and identified AF duration as an independent predictor of ANP plasma concentration in this group of patients.</AbstractText>ANP plasma concentration in patients with persistent AF and advanced CHF is determined by AF duration - the longer the AF duration the lower the ANP level.</AbstractText>

Role of postoperative use of adrenergic drugs in occurrence of atrial fibrillation after cardiac surgery.

Use of adrenergic (inotropic and vasopressor) drugs is common after cardiac surgery.</AbstractText>The study was undertaken to evaluate the role of postoperative adrenergic drug use as a predictor of postoperative atrial fibrillation (AF) after cardiac surgery.</AbstractText>The study population consisted of 199 patients post cardiac surgery. Postoperative adrenergic drug use and the baseline and clinical variables were analyzed as possible predictors of postoperative AF.</AbstractText>Of 199 patients, postoperative AF occurred in 59 patients (incidence 30%). The adrenergic drugs were used in 127 (64%) patients. Postoperative AF occurred in 49 of the 127 patients (39%) with and in 10 of the 72 patients (14%) without adrenergic drug use (p &lt; 0.01). By univariate analyses, postoperative adrenergic drug use, age, left ventricular hypertrophy, left atrial size, valve surgery, aortic valve replacement, cross clamp time, bypass time, postoperative ventricular pacing, and hours in intensive care unit were predictors of development of postoperative AF. Atrial pacing was a predictor of freedom from developing AF. By multivariate logistic regression analysis, adrenergic drug use was an independent predictor of postoperative AF (odds ratio [OR] 3.35, 95% confidence interval [CI] 1.38-8.12, p = 0.016). Two other independent predictors were valve surgery (OR 2.88, 95% CI 1.31-6.35, p = 0.002) and age (OR 10.73, 95% CI 10.37-11.10, p = 0.0001). Adrenergic drug use, valve surgery, ventricular pacing, and age were predictors of time duration from surgery to the occurrence of AF. Drugs with predominantly beta1-adrenergic receptor affinity were associated with a higher incidence of postoperative AF (dopamine 44%, dobutamine 41% vs. phenylepherine 20%, p = 0.001).</AbstractText>Use of adrenergic drugs is an independent predictor of postoperative AF after cardiac surgery.</AbstractText>

[What do we actually know about out-of-hospital cardiac arrest?].

Each year at least 300,000 people in the United States and 8000 to 10,000 people in Switzerland suffer from out-of-hospital cardiac arrest, mostly due to ventricular fibrillation. Early defibrillation provides definitive treatment for most of cardiac arrest victims. Semi-automatic external defibrillators are easy to handle devices allowing to deliver an early electric shock and can be successfully used by lay people following minimal training. Newer strategies of defibrillation designed to respond faster to out-of-hospital cardiac arrest, including public access defibrillation, as well as improvement of each link of the chain of survival appears as the best strategy for the management of out-of-hospital cardiac arrest.

A comparison of cardiac resynchronization by sequential biventricular pacing and left ventricular pacing to simultaneous biventricular pacing: rationale and design of the DECREASE-HF clinical trial.

The first generation of cardiac resynchronization therapy (CRT) devices approved for the treatment of heart failure used simultaneous biventricular (BiV) pacing to achieve ventricular resynchronization. Left ventricular pacing alone and sequential BiV pacing also show promise as alternative ways to deliver CRT, but have not been studied together in a large randomized trial.</AbstractText>The Device Evaluation of CONTAK RENEWAL 2 and EASYTRAK 2: Assessment of Safety and Effectiveness in Heart Failure (DECREASE-HF) Trial is a randomized, double-blind, 3-arm study of patients in New York Heart Association Class III or IV with an ejection fraction of 35% or less and a QRS duration &gt; or =150 ms. Patients are randomized to receive either left ventricular pacing, simultaneous BiV pacing, or sequential BiV pacing.</AbstractText>The study uses a novel composite endpoint that combines peak oxygen consumption and left ventricular end systolic dimension, thus combining a measure of symptomatic improvement (peak oxygen consumption) with a physiologic measure of ventricular reverse remodeling (left ventricular end systolic dimension) into a single composite score. Additionally, the safety and effectiveness of the CONTAK RENEWAL 2/4/4HE/EASYTRAK 2 system will be evaluated using: heart failure-related adverse events; system-related complications; left ventricular lead-related complications; detection time of induced ventricular fibrillation; and left ventricular lead performance (pacing threshold, pacing impedance, and R-wave amplitude).</AbstractText>

Prolonged repolarization after ventricular assist device support is associated with arrhythmias in humans with congestive heart failure.

Recent observations indicate that the QTc interval often increases in the early postoperative period (&lt;1 week) after mechanical unloading of severely failing hearts with a left ventricular assist device (LVAD). The present study examined whether early changes in ventricular repolarization after LVAD placement are associated with ventricular arrhythmias.</AbstractText>An electrocardiogram was obtained within 4 days before LVAD placement, &lt;12 hours after LVAD placement, and weekly thereafter. Patient records were reviewed for documented ventricular tachycardia (VT) or ventricular fibrillation (VF) for 1 week preoperatively and the first 2 weeks postoperatively. Differences in QTc interval between patients with and without VT were evaluated. Ten of 17 patients enrolled (59%) had VT or VF after LVAD placement. Of these, 4 required therapeutic intervention because of clinical instability or symptoms. The change in the QTc (DeltaQTc) between the preoperative and immediate postoperative period was significantly different among patients with VT/VF compared with patients without VT/VF (+23 ms vs. -68 ms, P &lt; .001).</AbstractText>The early period after initiation of LVAD support of the failing human heart is associated with a relatively high incidence of significant ventricular arrhythmias after LVAD placement. Beyond the impact of myocardial inflammation and wound healing occurring after all LVAD implants, early postoperative increases in the QTc interval after cardiac unloading appear to predispose to ventricular arrhythmias.</AbstractText>

Congestive heart failure and atrial fibrillation: rhythm versus rate control.

The incidence both of heart failure and atrial fibrillation is steadily increasing in the United States' population, and these conditions frequently coexist in the same patient. It is likely that the onset of one of these disorders leads to the onset and propagation of the other through multiple mechanisms. Several studies have investigated the prognosis of patients with both conditions, but a definitive conclusion regarding outcomes such as mortality and quality of life has yet to be determined.</AbstractText>Evidence demonstrating the improvement of left ventricular function and other hemodynamic parameters with the restoration and maintenance of sinus rhythm does exist. beta-blockade, angiotensin-converting enzyme inhibition, and aldosterone antagonism have been shown to improve survival in patients with heart failure. However, the efficacy of these therapies in patients with coexisting atrial fibrillation has not been adequately assessed. Furthermore, these therapies do not directly address the issue of rhythm management. The use of several antiarrhythmic medications and device therapy is becoming more frequent in the management of this subset of patients. Recent investigations of antiarrhythmic treatment have assessed outcomes such as survival, quality of life, exercise tolerance, and maintenance of sinus rhythm. Data from these studies suggest that antiarrhythmic therapy may be efficacious in such patients. Device therapy is another alternative which has been demonstrated to be at least as beneficial as medical therapy.</AbstractText>Both retrospective and prospective studies of antiarrhythmic therapy and device therapy have demonstrated promising results. Several studies are ongoing and will provide more insight into the management of such patients.</AbstractText>

An arrhythmia classification system based on the RR-interval signal.

This paper proposes a knowledge-based method for arrhythmic beat classification and arrhythmic episode detection and classification using only the RR-interval signal extracted from ECG recordings.</AbstractText>A three RR-interval sliding window is used in arrhythmic beat classification algorithm. Classification is performed for four categories of beats: normal, premature ventricular contractions, ventricular flutter/fibrillation and 2 degrees heart block. The beat classification is used as input of a knowledge-based deterministic automaton to achieve arrhythmic episode detection and classification. Six rhythm types are classified: ventricular bigeminy, ventricular trigeminy, ventricular couplet, ventricular tachycardia, ventricular flutter/fibrillation and 2 degrees heart block.</AbstractText>The method is evaluated by using the MIT-BIH arrhythmia database. The achieved scores indicate high performance: 98% accuracy for arrhythmic beat classification and 94% accuracy for arrhythmic episode detection and classification.</AbstractText>The proposed method is advantageous because it uses only the RR-interval signal for arrhythmia beat and episode classification and the results compare well with more complex methods.</AbstractText>

Infarct morphology identifies patients with substrate for sustained ventricular tachycardia.

We sought to evaluate whether infarct size characterization by cardiac magnetic resonance imaging (MRI) is a better predictor of inducible ventricular tachycardia (VT) than left ventricular ejection fraction (LVEF).</AbstractText>Inducibility of VT at electrophysiologic study (EPS) and low LVEF can identify patients with a substrate for VT. Magnetic resonance imaging has been shown to identify, with high precision, areas of myocardial infarction and may therefore be a better tool to evaluate for a substrate for VT.</AbstractText>We studied 48 patients with known coronary artery disease who were referred for EPS using cine and gadolinium-enhanced MRI. Wall motion and infarct characteristics were determined blindly and compared among patients with no inducible ventricular arrhythmias (n = 21), those with inducible monomorphic VT (MVT, n = 18), and those with either inducible polymorphic VT or ventricular fibrillation (n = 9).</AbstractText>Patients with MVT had larger infarcts than patients who did not have inducible arrhythmias (mass: 49 +/- 5 g [SE] vs. 28 +/- 5 g, p &lt; 0.005; surface area: 172 +/- 15 cm(2) vs. 93 +/- 14 cm(2), p &lt; 0.0005). Patients with polymorphic VT/fibrillation had intermediate values (mass: 36 +/- 7 g; surface area: 115 +/- 22 cm(2)). Ejection fraction was inversely related to infarct mass and surface area, with R(2) values ranging from 0.21 to 0.27. Logistic regression and receiver-operating characteristic analysis demonstrated that infarct mass and surface area were better predictors of inducibility of MVT than LVEF.</AbstractText>Infarct surface area and mass, as measured by cardiac MRI, are better identifiers of patients who have a substrate for MVT than LVEF. Further evaluation of infarct size characterization by cardiac MRI as a predictor of sudden cardiac death is warranted.</AbstractText>

Depression as a predictor for appropriate shocks among patients with implantable cardioverter-defibrillators: results from the Triggers of Ventricular Arrhythmias (TOVA) study.

We sought to examine the relationship between symptoms of depression and shock-treated ventricular arrhythmias among implantable cardioverter-defibrillator (ICD) patients.</AbstractText>Depression predicts mortality in patients with coronary artery disease (CAD), but whether this is via an increased risk of fatal ventricular arrhythmias is unclear.</AbstractText>We prospectively analyzed data on symptoms of depression and risk of ventricular arrhythmia (ventricular tachycardia/ventricular fibrillation [VT/VF]) resulting in ICD discharge in the Triggers of Ventricular Arrhythmias (TOVA) study. Symptoms were assessed by the Center for Epidemiologic Studies-Depression (CES-D) scale. Scores of 16 to 26 and &gt; or =27 represented mild and moderate/severe depression, respectively. The Cox and Anderson-Gill proportional hazards models were used to test for associations among all patients and patients with CAD.</AbstractText>Among 645 patients with baseline assessments, 90 (14%) were mildly depressed and 25 (3.9%) were moderately to severely depressed. Moderate/severe depression was associated with time to first shock for VT/VF (hazard ratio [HR] 3.2, 95% confidence interval [CI] 1.1 to 9.9) and all shocks for VT/VF including recurrent episodes (HR 3.2, 95% CI 1.2 to 8.6). Among the 476 CAD patients, the association with time to first shock (HR 6.4, 95% CI 1.9 to 21.1) and all shocks (HR 8.3, 95% CI 2.9 to 23.3) remained. The risk of shock for VT/VF was associated with depression severity in the total population (p for trend = 0.02) and among patients with CAD (p &lt; 0.01), even after controlling for multiple confounders.</AbstractText>More severe symptoms of depression predict shocks for VT/VF among ICD patients. The elevated risk of VT/VF among patients with CAD and depression suggests that arrhythmia may contribute significantly to total mortality in this subgroup.</AbstractText>

The prognostic importance of left ventricular outflow obstruction in hypertrophic cardiomyopathy varies in relation to the severity of symptoms.

The aim of this study was to investigate whether the prognostic importance of left ventricular (LV) outflow obstruction in hypertrophic cardiomyopathy (HCM) is influenced by other predictors of morbidity and mortality.</AbstractText>It remains unknown whether the effect of outflow obstruction on clinical outcome in HCM is influenced by other determinants of survival.</AbstractText>We assessed the impact of severity of symptoms, LV wall thickness, atrial fibrillation, and age on the prognostic importance of outflow obstruction in a large HCM population.</AbstractText>Of 526 consecutive HCM patients, 141 (27%) had outflow obstruction. During a follow-up of 4.5 +/- 4.1 years, 34 patients died of HCM. The incidence of cardiovascular death was significantly higher among patients with LV obstruction than among those without obstruction (relative risk [RR] = 2.14; p = 0.02). The prognostic power of the outflow gradient changed in relation to severity of symptoms (p = 0.024). At initial evaluation, LV obstruction was a significant predictor of cardiovascular mortality only in New York Heart Association (NYHA) functional class I to II patients (hazard ratio [HR] = 2.38; p = 0.025). During follow-up, at time of development of severe symptoms, the outflow gradient lost its prognostic significance (HR = 1.18; p = 0.66), whereas NYHA functional class III to IV was associated with an eight-fold increase in risk of cardiovascular mortality (HR = 7.90; p &lt; 0.001).</AbstractText>In patients with HCM, the prognostic importance of LV outflow obstruction varies in relation to the severity of symptoms. In patients with mild or no symptoms, obstruction is an important predictor of cardiovascular death. After development of severe symptoms, NYHA functional class becomes the dominant marker of prognosis independently of the presence of an outflow gradient.</AbstractText>

N-Terminal-proBNP (NT-proBNP) as an indicator of cardiac dysfunction. A study in patients presenting with suspected cardiac disorders.

Natriuretic peptides represent a novel diagnostic tool in the assessment of cardiac dysfunction.</AbstractText>A total of 473 consecutive referred patients presenting to 18 cardiologists for the assessment of their cardiac state were recruited for the study. Patients received a medical history, a physical examination an electrocardiogram and an echocardiogram where left ventricular ejection fraction was recorded.</AbstractText>NT-proBNP was found to correlate with left ventricular ejection fraction (LVEF), level of symptoms (NYHA classification), history of angina pectoris (AP) and myocardial infarction (AMI). Atrial fibrillation (AF) and thyroid dysfunction as well as renal impairment were shown to influence NT-proBNP levels.</AbstractText>The study supports the hypothesis that NT-proBNP determination contributes to the assessment of patients presenting to cardiologists.</AbstractText>

The effect of tirofiban and clopidogrel pretreatment on outcome of old saphenous vein graft stenting in patients with acute coronary syndromes.

In spite of developments in interventional cardiology, the success rate of saphenous vein graft stenting is still low in patients with acute coronary syndromes. In this study, we aimed at finding out the effect of pretreatment with Tirofiban, a glycoprotein IIb/IIIa inhibitor, and clopidogrel, an adenosine diphosphate antagonist, on the outcome of saphenous vein graft stenting in patients with acute coronary syndrome. A total of 47 patients, who had lesions in saphenous vein grafts and acute coronary syndrome, could be randomized to treated group (n = 24), who received Tirofiban and clopidogrel for 48 hours before the intervention, and untreated group (n = 23), who did not receive Tirofiban and clopidogrel. In the untreated group, the intervention was performed just after the coronary angiography. All patients underwent stenting as the standard intervention. The groups were compared by Mann-Whitney's U-test or Chi-Square test. The level of statistical significance was set at 0.05. There were no significant differences regarding age, gender, and atherosclerotic risk factors between the two groups. In treated group, precutaneous coronary intervention was successful in all patients and no-reflow phenomenon occurred in only one patient. The rate of no-reflow or slow-flow phenomenon was significantly lower in treated group (one patient vs 9 patients, p = 0.004). One patient in untreated group experienced ventricular fibrillation, which was converted to sinus rhythm after defibrillation. During short-term follow-up, there were no acute myocardial infarction, coronary bypass surgery or death in both groups. There was no major bleeding. Minor bleeding was more frequent in treated group, but it did not achieve statistical significance (3 vs 1; p = 0.322). In conclusion, pretreatment with tirofiban and clopidogrel before percutaneous coronary intervention might result in better immediate outcomes in old saphenous vein grafts without any significant increase in bleeding complications.

Effects of oxypeucedanin on hKv1.5 and action potential duration.

A furocoumarin derivative, oxypeucedanin, was purified from Angelica dahurica, and its effects on the human Kv1.5 (hKv1.5) channel and on the cardiac action potential duration (APD), were examined using the patch-clamp technique and the conventional microelectrode technique. Oxypeucedanin inhibited the hKv1.5 current in a concentration-dependent manner, with an IC(50) value of 76 nM, while it had no effect on human eag-related gene (HERG) current. Oxypeucedanin induced an initial fast decline of hKv1.5 current during depolarizations. The inhibition of hKv1.5 channel by oxypeucedanin was voltage-dependent, especially at depolarizing pulses between -40 and 0 mV which corresponds to the voltage range of the channel's opening. Oxypeucedanin also slowed the deactivation time course, resulting in a tail crossover phenomenon. Additionally, oxypeucedanin prolonged the APD of rat atrial and ventricular muscles in a dose-dependent manner. These results suggest that oxypeucedanin is a kind of open-channel blocker of the hKv1.5 channel and it prolongs the APD; therefore, it is an excellent candidate as an antiarrhythmic drug for atrial fibrillation.

[Importance of critical events training for anesthesiology residents: experience with computer simulator.].

Because of monitoring and drugs evolution, there has been a decrease in the incidence of critical events during anesthetic procedures. Despite this low frequency, critical event training for Anesthesiology residents remains important. This study aimed at evaluating Anesthesiology residents' critical care skills during computer-simulated anesthesia.</AbstractText>Seventeen anesthesiology residents (first and second year) and 5 anesthesiology instructors were evaluated. Using the Anesthesia Simulator Consultant (2.0 - 1995/Anesoft) simulations of ventricular fibrillation (VF) and anaphylactic reaction (AR) were performed. After simulation, results of each participant were printed and approaches to solve predetermined critical events were evaluated and scored. Participants have evaluated the simulator by filling out a questionnaire.</AbstractText>There were no significant differences in means obtained by groups, but there has been a trend toward better performance of second year residents and Anesthesiology instructors during VF simulation. There has been a trend toward better performance of Anesthesiology instructors during AR simulation.</AbstractText>Critical events management training should be the focus during residents and anesthesiologists training. Computer simulation could be a way to carry out such training.</AbstractText>

Estimation of cardiac event risk by MDCT.

Coronary calcifications are specific markers for coronary atherosclerosis. The amount of coronary calcium is related to the likelihood of vulnerable plaques. Vulnerable plaques may rupture and may result in sudden coronary thrombus formation, occlusion, ischemia and ventricular fibrillation and finally cardiac death. Therefore, it is reasonable to believe that the risk of cardiac events can be assessed by the quantification of the extent of coronary calcium. However, until now, the predictive value of coronary calcium and the advantage over conventional risk factors has not yet been proven by any prospective cohort study. In practice uncertainty exists in the group of patients with an intermediate risk for cardiac events. In this particular cohort it is likely that the assessment of coronary atherosclerosis may help in the decision to initiate or discard a specific therapy. For this purpose it has been suggested to replace the Framingham age score by a score corrected by the amount of coronary calcium. Follow-up investigations may be helpful in the short term to determine the efficiency of different therapeutical options. To determine a significant progression of the amount of coronary calcium, the absolute mass should be determined in a period of 1 year.

Surgical ventricular restoration in end-stage ischemic cardiomyopathy patients.

Surgical ventricular restoration (SVR) has generally been contraindicated in patients with an ejection fraction (EF) &lt;20%, with pulmonary arterial (PA) pressure &gt;60 mm Hg, and being treated with inotropic agents.</AbstractText>The patients in this study were 6 men and 5 women 50 to 78 years of age (mean, 62.4 years). Three patients were in New York Heart Association (NYHA) class III with an EF &lt;30%. Eight patients were in NYHA class IV with EF &lt;20%, PA pressure &gt;70 mm Hg, and left ventricular asynergy. Three patients had had recent myocardial infarction (MI) with shock and multiple organ failure. Three patients had mitral regurgitation, 1 patient had ventricular septal defect (VSD), 4 patients had diabetes mellitus, and 5 had morbid obesity. All patients underwent intraoperative transesophageal echocardiography and were being treated with milrinone or nesiritide. Seven patients had intraaortic balloon pumps. All patients underwent coronary artery bypass (CAB), receiving 1 to 5 (average, 3.54) grafts per patient. The SVR (Dor) procedure was performed with a Chase Mannequin device. Preoperative end-diastolic volume was 240 to 330 mL, and postoperative volume decreased to 110 to 130 mL. Two patients underwent mitral valve repair, and 1 underwent VSD closure. One patient underwent microwave ablation for atrial fibrillation.</AbstractText>Ten (91%) of 11 patients were discharged home in 10 to 14 days. There was 1 death: A 78-year-old man with acute MI died 43 days later of septic shock due to hemodialysis.</AbstractText>End-stage ischemic cardiomyopathy patients with EF &lt;20% can safely undergo surgery after meticulous preoperative preparation to decrease PA pressure, pulmonary capillary wedge pressure, and peripheral vascular resistance and to increase CO by SVR, CAB, and correction of associated lesions. Mortality was 9% with improved hemodynamics and relief of congestive heart failure in all survivors for 3 to 12 months.</AbstractText>

Ethnicity and variation in prognosis for patients newly hospitalised for heart failure: a matched historical cohort study.

To compare mortality and factors predictive for outcome in age matched white and South Asian cohorts after first admission for heart failure.</AbstractText>Matched historical cohort study.</AbstractText>One National Health Service trust comprising three acute care hospitals.</AbstractText>176 South Asian (mean age 68 (10) years, 45% women) and 352 age and sex matched white (70 (11) years, 42% women) patients hospitalised for the first time with heart failure.</AbstractText>All cause survival, measures of disease severity, and the association of clinical variables with outcome.</AbstractText>Compared with white patients, South Asian patients had similar rates of prior coronary heart disease but more often had prior hypertension (45% v 33%, p = 0.006) and diabetes (46% v 18%, p &lt; 0.0001). Atrial fibrillation (15% v 31%, p = 0.0002) and prior diuretic use (39% v 48%, p = 0.041) were less common among South Asians. Left ventricular function was more often preserved (38% v 23%, p = 0.002) and less often severely impaired (18% v 28%, p = 0.025) among South Asians. During follow up (range 520-1880 days) 73 of 176 (41.2%) South Asian and 167 of 352 (47.4%) white patients died. South Asian ethnicity was associated with lower all cause mortality (odds ratio 0.71, 95% confidence interval 0.53 to 0.96, p = 0.02). Other predictors of outcome (admission age, lower systolic blood pressure, higher creatinine, higher plasma glucose, and lower haemoglobin) were similar in each cohort.</AbstractText>At first hospitalisation, heart failure appears less advanced in South Asians, among whom diabetes and hypertension are more prevalent. Survival is better for South Asian than for white patients. Higher glucose and lower haemoglobin at admission provide useful prognostic information in heart failure.</AbstractText>

Effect of hypothermia on transthoracic defibrillation in a swine model.

Induced hypothermia (H) appears a promising intervention to protect the heart and brain after resuscitation from cardiac arrest. However, the influence of H on transthoracic defibrillation energy requirements is not well documented.</AbstractText>In 39 swine (21.4+/-1.3(S.E.) kg) hypothermia was induced by surrounding the head, thorax and abdomen with ice. The swine were divided into four groups: (1) normothermia (N) followed by severe H (30 degrees C) (n=10), (2) severe H followed by N (n=10), (3) N followed by moderate H (33 degrees C) (n=10) and (4) moderate H followed by N (n=9). After 30s of electrically induced ventricular fibrillation (VF), the swine were defibrillated (biphasic waveform) at energies of 20J, 30J, 50J and 100J in random order in both N and H conditions.</AbstractText>For pigs in Group 1 (N followed by severe H), shock success in terminating VF was higher during hypothermia (odds ratio 4.09 (95% CI: 2.21, 5.58; p&lt;0.0001), despite the fact that impedance rose from 39+/-3Omega (N) to 42+/-3Omega (H) (p&lt;0.001) and current fell from 22+/-8 (N) to 21+/-7A (H) (p&lt;0.001). There were no significant differences in the shock success between N and H for the other groups. Post-defibrillation ventricular asystole occurred less often during hypothermia compared to normothermia (p=0.0002).</AbstractText>Severe H facilitated transthoracic defibrillation in this swine model. Since impedance rose and current fell during H, the improved shock success must be due to a hypothermia-induced change in the mechanical or electrophysiologic properties of the myocardium. Moderate hypothermia did not alter the energy requirement for defibrillation.</AbstractText>

Differences in time to defibrillation and intubation between two different ventilation/compression ratios in simulated cardiac arrest.

During basic life support (BLS) by a two-rescuer-team early defibrillation and ALS procedures should be performed without interruptions of the BLS-ventilation/compression sequence. The objective of this study was to determine the impact of a ventilation/compression ratio of 5:50 versus 2:15 on the time intervals "Start BLS to first shock" and "Start BLS to intubation".</AbstractText>Using a random cross over design 40 experienced paramedics performed a standard BLS/ALS-algorithm according to ILCOR guidelines in a manikin model with ventricular fibrillation (resusci skillreporter anne, Laerdal, Norway) performing both the 2:15 and the 5:50 ventilation/compression ratio. BLS was started with bag/valve/mask ventilation, a semi-automatic defibrillator (corpuls 08/16S) was connected with the manikin, ECG-analysis and three shocks were performed and the tracheal intubation was prepared. Ventilation/compression sequence was only interrupted during ECG-analysis and defibrillation. Expiratory volumes and number of compressions were measured. Variables were compared using paired Students t-test. In addition paramedics were interviewed about work-flow and emotional stress during the tests.</AbstractText>The time interval "Start BLS to first shock" was 78 s (2:15-group) versus 63 s (5:50-group), p&lt;0.0001, the time interval "Start BLS to intubation" was 183 s (2:15-group) versus 150 s (5:50-group), p&lt;0.0001, mean ventilation volumes per minute were 4490 ml (2:15-group) versus 4370 ml (5:50-group), p&gt;0.1, mean number of compressions were 65 min-1. (2:15-group) versus 68 min-1 (5:50-group), p&gt;0.1. The work-flow and emotional stress was appraised by the paramedics to be significantly superior in the 5:50 ratio (p&lt;0.0001).</AbstractText>The ventilation/compression ratio of 5:50 compared with 2:15 during BLS with an unsecured airway reduces the time until the first defibrillation and tracheal intubation was performed without changes in ventilation volume and compressions per minute. The Paramedics stated that the 5:50 ratio improved the work-flow and reduced the emotional stress.</AbstractText>

Risk factors for first-ever ischemic stroke: a hospital-based case-control study in Kaohsiung, Taiwan.

Numerous population-based epidemiological studies have shown the prevalence and strength of vascular risk factors for stroke but little is known about risk factors of stroke in Taiwan. The aim of this study was to identify vascular risk factors in a group of first-ever ischemic stroke patients in Taiwan.</AbstractText>The study consisted of 228 consecutively hospitalized cases of first-ever ischemic stroke and 228 healthy age- and sex-matched control subjects. Conditional logistic regression analyses were performed to evaluate the risk factors.</AbstractText>Significant risk factors included hypertension (odds ratio [OR] 2.7, 95% confidence interval [CI] = 1.53-4.80), atrial fibrillation (OR 14.8, 95% CI = 2.32-94.73), ischemic heart disease (OR 4.4, 95% CI = 1.48-13.38), cigarette smoking (OR 2.3, 95% CI = 1.10-4.96), left ventricular hypertrophy (OR 2.7, 95% CI = 1.18-6.16), and other abnormal electrocardiographic findings (OR 2.1, 95% CI = 1.11-3.80).</AbstractText>Several vascular risk factors of first-ever ischemic stroke were identified. A population-based study involving more vascular risk factors is needed for generalization.</AbstractText>

The new selective I(Ks)-blocking agent HMR 1556 restores sinus rhythm and prevents heart failure in pigs with persistent atrial fibrillation.

Antiarrhythmic drugs for treatment of atrial fibrillation in patients with heart failure are limited by proarrhythmia and low efficacy. Experimental studies indicate that the pure I(Ks) blocking agents chromanol 293b and HMR 1556 prolong repolarization more markedly at fast than at slow heart rates and during beta-adrenergic stimulation. These properties may overcome some of the above quoted limitations.</AbstractText>Ten domestic swine underwent pacemaker implantation (PM) and atrial burst pacing to induce persistent AF. Four days after onset of persistent AF, pigs were randomized to HMR 1556 (30 mg/kg, p.o., 10 days) or placebo. All animals receiving HMR 1556 converted to SR (5.2 +/- 1.9 days), whereas placebo pigs remained in AF. Pigs treated with placebo developed high ventricular rates (297 +/- 5 bpm) and severe heart failure, whereas pigs treated with HMR 1556 remained hemodynamically stable. Left ventricular ejection fraction on the day of euthanization was significantly lower in the placebo compared to the HMR 1556 group (30 +/- 4% vs. 69 +/- 5%, p &lt; 0.005). Similar results were seen with epinephrine levels (placebo 1563 +/- 193 pmol/l vs. HMR 613 +/-196 pmol/l, p &lt; 0.05). Right atrial monophasic action potentials were significantly longer in the HMR 1556 compared to the placebo group (230 +/- 7 ms vs. 174 +/- 13 ms, p &lt; 0.05).</AbstractText>The new I(Ks) blocker HMR 1556 efficiently and safely restores SR and prevents CHF in a model of persistent AF. Restoration of SR is most likely linked to a marked prolongation of atrial repolarization even at high heart rates.</AbstractText>

A randomized controlled trial of magnesium sulfate, in addition to usual care, for rate control in atrial fibrillation.

We examine the safety and efficacy of magnesium sulfate infusion, in addition to usual care, for acute rate reduction in patients with atrial fibrillation and a rapid ventricular response rate.</AbstractText>This was a prospective, randomized, double-blind, placebo-controlled trial of intravenous magnesium sulfate in adult emergency department patients with rapid atrial fibrillation. Study solutions were given in addition to any therapy the treating physician would normally consider appropriate, including the use of standard rate-reduction agents. Patients received either 20 mEq (2.5 g, 10 mmol) magnesium sulfate over a 20-minute period, followed by 20 mEq (2.5 g, 10 mmol) over a 2-hour period intravenously, or placebo.</AbstractText>One hundred ninety-nine patients were randomized, 102 to receive magnesium sulfate and 97 to receive placebo. The antiarrhythmic drug most commonly used by treating physicians was digoxin. Magnesium sulfate was more likely than placebo to achieve a pulse rate of less than 100 beats/min (63 [65%] of 97 versus 32 [34%] of 93, relative risk [RR] 1.89; 95% confidence interval [CI] 1.38 to 2.59; P &lt;.0001) and more likely to convert to sinus rhythm (25 [27%] of 94 patients versus 11 [12%] of 91 patients; RR 2.20; 95% CI 1.15 to 4.21; P =.01). Comparative mean pulse rate reductions in the magnesium sulfate group did not reach predetermined clinical significance levels (&gt; or =15 beats/min reduction) at any of the measured time points. Magnesium sulfate was more likely to be associated with an adverse event (14 [15%] of 95 patients versus 5 [5%] of 92 patients; RR 2.71; 95% CI 1.02 to 7.23; P =.04).</AbstractText>Magnesium sulfate, when used to supplement other standard rate-reduction therapies, enhances rate reduction and conversion to sinus rhythm in patients with rapid atrial fibrillation.</AbstractText>

Clinical, echocardiographic, and hemodynamic characteristics of rheumatic mitral valve stenosis and atrial fibrillation.

Chronic atrial fibrillation (AF) is associated with an increased frequency of embolic events and negative impact on cardiac function, and therefore, an increased morbidity and mortality risk in patients with rheumatic mitral valve stenosis (RMS). In the present study, the clinical, 2-D and Doppler echocardiographic, and left-and right-heart hemodynamic data were evaluated for 92 patients (68 women) with RMS and AF and compared with data from 118 patients (88 women) with RMS with sinus rhythm. The clinical, echocardiographic, and hemodynamic evaluations were performed within 1 to 7 days of each other. Patients with AF were older (45.7+/-13.4 vs 38.6+/-12.0 years, p &lt; 0.01) and had a longer symptomatic period (108.2+/-117.9 vs 50.6+/-53.1 months, p &lt; 0.01) compared with those with sinus rhythm. Most of the patients with AF were in NYHA functional capacity 3-4 (74% vs 19%), whereas most of the patients with sinus rhythm were in NYHA functional capacity 2. Patients with AF had a higher mitral valve score based on morphologic features ranging from 4 to 16 depending on the severity of disease (8.3+/-2.1 vs 6.5+/-1.9, p &lt; 0.01) and greater left ventricular end-diastolic diameter (LVEDD) (52.3+/-8.7 vs 47.7+/-8.7 mm, p &lt; 0.02), and end-systolic diameter (LVESD) (34.4+/-7.5 vs 30.9+/-7.5 mm, p &lt; 0.01). Organic tricuspid valve involvement was diagnosed more frequently in patients with AF (61% vs 32%, p &lt; 0.01). Mild mitral regurgitation was also more frequent in patients with AF (71%vs 51%, p &lt; 0.03). The mitral valve area was similar in patients with and without AF (1.30+/-0.39 vs 1.39+/-0.41 cm2, p &gt; 0.05). Mean diastolic mitral valve gradient and pulmonary artery pressure did not differ in patients with and without AF. Right atrial pressures were higher in patients with AF (7.6+/-3.3 vs 6.3+/-1.9 mm Hg, p &lt; 0.02). The authors suggest that (1) AF occurred in older patients, who had a longer disease process and more serious symptoms; (2) hemodynamic derangements (mitral valve gradient, pulmonary artery pressure) did not differ in patients with and without AF; (3) greater mitral valve score, more tricuspid valve involvement, higher LVEDD, which are suggestive of greater rheumatic activity process were more frequently seen in patients with AF than in those without AF. These findings support the opinion that AF is a marker of widespread rheumatic damage in patients with RMS.

Diltiazem versus amiodarone to prevent atrial fibrillation in coronary surgery.

The prophylactic effect of amiodarone on atrial fibrillation after coronary bypass grafting with extracorporeal circulation was compared with that of diltiazem in two groups of 60 patients each. Patients were monitored continuously for 8 days. The incidence of atrial fibrillation was recorded retrospectively in a control group of 60 patients who received our standard prophylactic regimen of an oral beta blocker. The incidence of postoperative atrial fibrillation was not significantly different in the two test groups: 11.7% for the amiodarone group and 10% for the diltiazem group. The incidence of atrial fibrillation in the control group was 23.3% and the differences were marginally significant when compared to the amiodarone ( p = 0.093) and diltiazem groups ( p = 0.050). The prophylactic use of diltiazem or amiodarone is feasible and safe for patients undergoing coronary bypass, with similar rates of atrial fibrillation.

Minimal access via lower partial sternotomy for congenital heart defects.

To evaluate the invasiveness of a minimal access approach for simple congenital heart defects, and determine whether it can be regarded as a standard operation, 83 patients with an atrial septal defect and 73 with a ventricular septal defect underwent repair through a minimal skin incision and lower partial median sternotomy. There were no operative deaths, severe intraoperative complications, or conversion to full sternotomy. The clinical course of 106 patients was compared with that of 21 treated using a full sternotomy by the same surgeon; there were no significant differences, except in the operative time for ASD patients. The clinical courses of 2 minimal access subgroups (50 patients operated on by residents and 106 treated by the staff surgeon were compared; operative time, bypass time, ventricular fibrillation time (ASD repair), and cardiac arrest time (VSD repair) were significantly shorter in those operated on by the staff surgeon, but there was no difference in clinical course. The minimal access approach produced good cosmetic results, its invasiveness was similar to that of a full sternotomy, and it may be considered a standard operation for pediatric patients with septal defects.

The Gurvich waveform has lower defibrillation threshold than the rectilinear waveform and the truncated exponential waveform in the rabbit heart.

Implantable cardioverter defibrillator studies have established the superiority of biphasic waveforms over monophasic waveforms. However, external defibrillator studies of biphasic waveforms are not as widespread. Our objective was to compare the defibrillation efficacy of clinically used biphasic waveforms, i.e., truncated exponential, rectilinear, and quasi-sinusoidal (Gurvich) waveforms in a fibrillating heart model. Langendorff-perfused rabbit hearts (n = 10) were stained with a voltage-sensitive fluorescent dye, Di-4-ANEPPS. Transmembrane action potentials were optically mapped from the anterior epicardium. We found that the Gurvich waveform was significantly superior (p &lt; 0.05) to the rectilinear and truncated exponential waveforms. The defibrillation thresholds (mean +/- SE) were as follows: Gurvich, 0.25 +/- 0.01 J; rectilinear-1, 0.34 +/- 0.01 J; rectilinear-2, 0.33 +/- 0.01 J; and truncated exponential, 0.32 +/- 0.02 J. Using optically recorded transmembrane responses, we determined the shock-response transfer function, which allowed us to predict the cellular response to waveforms at high accuracy. The passive parallel resistor-capacitor model (RC-model) predicted polarization superiority of the Gurvich waveform in the myocardium with a membrane time constant (taum) of less than 2 ms. The finding of a lower defibrillation threshold with the Gurvich waveform in an in vitro model of external defibrillation suggests that the Gurvich waveform may be important for future external defibrillator designs.

Permanent His-bundle pacing after atrioventricular node ablation in a patient with chronic atrial fibrillation and mitral regurgitation.

Hemodynamic deterioration because of worsening of mitral regurgitation can occur in a small number of patients undergoing atrioventricular node (AVN) ablation and pacing therapy. Patients with moderate mitral regurgitation before ablation seem prone to this complication. Successful permanent His-bundle pacing after AVN ablation was performed in a patient with chronic atrial fibrillation and moderate mitral regurgitation. Pulmonary capillary wedge pressure V-wave amplitude was markedly diminished and the mitral regurgitation area, calculated from the echocardiogram, was decreased by His-bundle pacing compared with that during right ventricular outflow tract or apical pacing.

The genetics of cardiac arrhythmias.

Cardiac rhythm problems result in high levels of morbidity and mortality, with sudden arrhythmic death claiming approximately 300,000 lives in the United States each year. Investigations into the genetic contributions to rhythm and conduction disorders have found genes or loci associated with primary rhythm/conduction disorders such as familial atrial fibrillation and atrio-ventricular block, underscoring the importance of collecting a thorough family history. Combinations of single or multiple genes and environmental risk factors may place only certain family members at risk. Some cardiac muscle problems, such as cardiomyopathy, predispose to arrhythmia and have documented genetic components. Primary health care providers need current knowledge of genetic contributions to rhythm/conduction problems so that family members at risk can be identified early and cared for appropriately. This article provides an overview of the genetic contributions to cardiac rhythm and conduction problems.

The Brugada Syndrome.

In 1992 a syndrome was described consisting of syncopal episodes and/or (resuscitated) sudden death in patients with a structurally normal heart and a characte ristic electrocardiogram (ECG) displaying a pattern resembling a right bundle branch block with ST segment elevation in leads V1 to V3. The disease is genetically determined with an autosomal dominant pattern of transmission in 50% of the familial cases. Several different mutations have been identified affecting the structure, function and trafficking of the sodium channel. The syndrome is ubiquitous. Its incidence and prevalence are difficult to estimate, but this disease may cause 4 to 10 sudden deaths per 10,000 inhabitants per year representing the most frequent cause of natural death in males younger than 50 in South Asia. The disease has been linked to the sudden infant death syndrome (SIDS) and to the sudden unexpected death syndrome (SUDS) by showing that the electrocardiogram and mutations are the same as in Brugada syndrome. The diagnosis is easily made by means of the ECG when it is typical. There exist, however, patients with concealed and intermittent electrocardiographic forms that make the diagnosis difficult. The ECG can be modulated by changes in autonomic balance, body temperature, glucose level and the administration of antiarrhythmic, neuroleptic and antimalaria drugs. Beta adrenergic stimulation normalizes the ECG. Loss of the action potential dome in right ventricular epicardium but not in endocardium underlies the ST segment elevation. Electrical heterogeneity within right ventricular epicardium leads to the development of closely coupled extrasystoles via phase 2 reentry that precipitate ventricular ,fibrillation. Antiarrhythmic drugs do not prevent sudden death in symptomatic or asymptomatic individuals. Implantation of an automatic cardioverter-defibrillator is the only currently proven effective therapy. Patients with frequent electrical storms may even need cardiac transplantation as last resort.

[Cardiac arrest outside hospital: initial and subsequent cardiological management].

The prognosis of cardiac arrest outside hospital is directly related to the initial management. The aim of this work was to evaluate the characteristics of the initial and subsequent cardiological management of victims of cardiac arrest outside hospital with a retrospective analysis of data from the SAMU 35 (Emergency Medical Service, IIIe et Vilaine region) in the period April 1998 - April 2002.</AbstractText>533 non-traumatic cardiac arrests outside hospital were reported in 532 patients (average age 63 +/- 17, 73% male). The cardiac arrest occurred at home in 77% of cases. The initial cardiac rhythm documented was asystole in 63% of cases, ventricular fibrillation (VF) in 30% ventricular tachycardia (VT) in 1% and electromechanical dissociation in 6%. A cardiac aetiology was presumed in 294 (69%) of the 424 resuscitated patients. Among these, 22% (66/294) were admitted to coronary care units, 11% (31) left hospital alive, 8% (24) with no neurological sequelae. The survival rate for patients with cardiac arrest outside hospital in the presence of a witness and for whom the initial rhythm was VF or VT was 21%. The patient's age (&lt;60 years)[OR: 1.05; CI 95%: 1.02-1.07; p &lt; 0.001], rapid arrival of the SAMU (&lt;10 min) [OR: 5.68; CI 95%: 1.42-22.7; p = 0.01] and resuscitation by the witness (OR: 8.26; CI 95%: 3.28-20.83; p &lt; 0.001) were factors predictive of survival in a multivariate analysis. Coronary heart disease remains the principal cause of cardiac arrest in patients admitted to cardiology units (68%), with a recent coronary thrombosis shown in 40% of patients undergoing angiography (16/40).</AbstractText>the prognosis of cardiac arrest outside hospital remains bleak, with a mortality of 90%. The survival rate is higher if the initial management is optimal, associated with bystander resuscitation and an immediate emergency service response allowing rapid defibrillation. Diagnosis and management of acute coronary syndrome in a cardiological setting must be integrated into the strategy.</AbstractText>

Current status of mitral valve repair.

Mitral valve repair is the procedure of choice to treat mitral valve dysfunction. Advantages of mitral valve repair over mitral valve replacement include improved long-term survival, better preservation of left ventricular function, and greater freedom from endocarditis, thromboembolism, and anticoagulant-related hemorrhage. The feasibility and durability of mitral valve repair depend upon the etiology of mitral valve dysfunction. In degenerative and ischemic mitral valve diseases, valve repair is possible in 90% of cases and freedom from reoperation is high. In contrast, rheumatic valves are less amenable to repair and durability is limited. Most isolated valve operations can be performed in a minimally invasive fashion using a partial upper sternotomy. In patients with atrial fibrillation and mitral valve disease, the Maze procedure or pulmonary vein isolation is performed, eliminating atrial fibrillation and the need for long-term anticoagulation.

Pharmacologic therapies for atrial fibrillation.

Pharmacologic therapy for atrial fibrillation may be used for acute cardioversion or ventricular rate control or for long-term therapy to maintain sinus rhythm or control ventricular rates in atrial fibrillation. Therapies must be tailored to elderly patients, with particular attention to structural heart disease, bradycardia, hypotension, and other comorbidities, including renal or hepatic insufficiency. Such considerations may dictate the use or avoidance of certain agents. Other important considerations for elderly patients include challenges associated with anticoagulation and maintaining therapeutic international normalized levels without risk of bleeding. When considering pharmacologic agents for elderly patients, it is also valuable to take into account socioeconomic issues, such as access to medications, adherence to complicated dosing schedules, and availability of appropriate clinical follow-up to assess therapeutic efficacy and adverse reactions to various agents. A carefully constructed therapeutic regimen can provide effective symptom control and atrial fibrillation management for elderly patients.

[Early post-operative arrhythmias in endomyocardial fibrosis or chronic parietal endocarditis in 84 cases studied at the Cardiology Institute of Abidjan].

The authors have studied rhythmic events happened during early post-operative period in 84 operated patients for endomyocardial fibrosis, synonym nowadays to chronic parietal endocarditis, in the Institute of Cardiology of Abidjan (C&#xf4;te d'lvoire), from January 1977 to July 1991. The mean age has been 15.6 +/- 43 years old. Endocardectomy was left in 25 cases, right in 32 and at last bilateral in the 19 others. The surgical way has been a left and/or right atriotomy. Mitral and/ ortricuspide valvular surgery has been always realised. The absolute prevalence of patients having presented one or several arrhythmias, atrial tachycardia and premature ventricular beats. The favouring factors have been the period of exclusion of the aortic root from circulation and number of endomyocardectomy. Atrial fibrillation has been related to auricular volume. Most of nodal arrhythmias have appeared with surgery. Endomyocardial fibrosis surgery has been greatful in rhythmic plan in 16% of patients. Early post-operative arrhythmias have been responsible forone case of the death of the operated patients and they have been present in seven other cases of the death.

[Effect of omega-3 fatty acids on the prevention of atrial arrhythmias].

The effects of omega-3 fatty acids on membrane stabilization are well known. Reduction of ventricular arrhythmias and sudden death has been reported; fewer data exist regarding the effects on atrial arrhythmias. The object of this report is to evaluate the reduction of atrial arrhythmia-fibrillation after treatment with omega-3, in patients with dual-chamber pacemakers.</AbstractText>We have examined 40 patients with paroxysmal atrial tachyarrhythmia recorded at the periodic pacemaker controls. At the study entry, all patients were treated with omega-3 (1 g/die); no changes in the device programmation and in the previous pharmacological therapy were allowed. The devices were interrogated after 4 months of treatment to evaluate the number of episodes and the burden of atrial tachyarrhythmia. At this time, the treatment was discontinued and the patients were reevaluated 4 months later.</AbstractText>Two patients discontinued the treatment complaining of adverse gastroentheric effects. The episodes of atrial tachyarrhythmia in the pre-treatment period resulted 444 +/- 1161, and the burden 3.89% of time; in the treatment period resulted respectively 181 +/- 436 (-59%, p = 0.037) and 1.06% (-67%, p = 0.029). After drug withdrawal, the episodes of atrial tachyarrhythmia raised to 552 +/- 1717 (p = 0.065) and the burden to 2.69% (p = 0.003).</AbstractText>Our data suggest a powerful effect of omega-3 fatty acids in the reduction of atrial tachyarrhythmia-fibrillation in these patients, without significant adverse effects.</AbstractText>

Update in atrial fibrillation.

Atrial fibrillation (AF) is the most common sustained arrhythmia in adults. It is a significant public health problem in the United States where it affects 2.2 million Americans and almost 10% of the population older than 80 years. It should be emphasized that the prevalence of AF increases with advancing age and with worsening cardiac function. AF is an independent risk factor for death and greatly increases the risk for embolic stroke. In addition, this arrhythmia can be associated with hemodynamic instability, tachycardia-induced cardiomyopathy, and systemic embolism. The management of atrial fibrillation today is directed toward the prevention of thromboembolism, control of the ventricular rate and conversion to sinus rhythm. It is the purpose of this review to summarize the most recent information about the clinical implications and treatment of this common rhythm disorder.

Fatal course of parvovirus B19-associated myocarditis in a female liver transplant recipient.

Acute myocarditis may result in severe hemodynamic compromise with fatal outcome. Furthermore, recent studies suggest myocarditis as a major cause of sudden unexpected death. A variety of cardiotropic viral, rickettsial, and bacterial infectious agents have been identified to date. Parvovirus B19 (PVB19) is usually benign in childhood, but it may also cause death due to myocarditis. We present here the case of an adult female who presented with fatigue, dyspnea on exertion, and orthostatic dizziness 8 months after successful liver transplantation. Cardiologic work-up, including left ventricular endomyocardial biopsy, revealed acute myocarditis secondary to PVB19. Since no specific therapy for this virus is available, the patient was treated symptomatically with an angiotensin-converting enzyme inhibitor plus beta-blocker and diuretics. After a period of stabilization, new-onset rapid atrial fibrillation caused acute low-output syndrome within 14 days after hospital admission. The patient eventually died because of refractory cardiogenic shock. In conclusion, to our knowledge this is the first report of PVB19-induced myocarditis confirmed by detection of viral genome in myocardium in a liver transplant recipient.

Charging up the public for automated external defibrillators.

Public training in the use of automated external defibrillators to treat out-of-hospital cardiac arrests has been receiving increased attention. The implementation of public access defibrillation programs has been the most significant intervention to improve survival in decades. Dramatic success came when we placed automated external defibrillators in the hands of the public to be utilized without an Emergency Medical Services response having to occur. The device is simple to operate -- sixth-grade children have demonstrated safe and effective operation. Training should be taken to its elemental level. Cardiopulmonary resuscitation training should not be forgotten; it too should be taken to its simplest form.

Ibutilide for rapid conversion of atrial fibrillation or flutter in a mixed critically ill patient population.

Ibutilide is an intravenous class III antiarrhythmic agent that has been shown to be effective in converting acute onset atrial fibrillation/flutter in stable medical and cardio-surgical patients. Data on its use in critically ill patients are rare. The aim of this open, non-randomized, prospective trial was to assess the potential role of ibutilide for conversion of recent onset atrial fibrillation/flutter in a mixed critically ill ICU-population.</AbstractText>Twenty cardiac-surgical and 17 medical patients with acute tachycardic atrial fibrillation or flutter received up to two 10-min intravenous infusions of 1.0 mg ibutilide.</AbstractText>The cumulative conversion efficacy of ibutilide was 56.8% (21 of 37 patients). The mean time to termination of the arrhythmia was 17.7 +/- 12.5 min (range 4 to 45 min) after the start of the first infusion. Conversion success was significantly higher in medical compared to cardiac-surgical patients (82.4 versus 35.0%, p=.0063). In a multivariate binary stepwise logistic regression analysis adjusted for age, heart rate and reduced left ventricular function, cardiac surgery remained significantly associated with a lower conversion probability (RR, .14; 95%CI, 0.02 to 0.76; p=.0190). Serious, ibutilide-induced ventricular arrhythmias developed in 3/37 patients (8.1%). Two of these 3 patients had a left ventricular ejection fraction &lt; 20%.</AbstractText>Ibutilide is an effective treatment for conversion of acute tachycardic atrial fibrillation/flutter in critically ill patients. Higher efficacy can be expected in medical than cardiac-surgical patients. Ventricular proarrhythmia, especially in patients with severely depressed left ventricular function represents the most important limitation of ibutilide treatment.</AbstractText>

The incidence and timing of major arrhythmias following successful primary angioplasty for acute myocardial infarction.

The potential benefits of direct percutaneous transluminal coronary angioplasty (PTCA) on malignant arrhythmias in the hospital phase of acute myocardial infarction have not yet been established.</AbstractText>We prospectively investigated the incidence and timing of major arrhythmias occurring during direct PTCA and within 24 hours of mechanical reperfusion in 90 consecutive patients with acute myocardial infarction undergoing successful direct PTCA within 12 hours of symptom onset.</AbstractText>Ventricular fibrillation and complete atrioventricular block occurred exclusively during direct PTCA and both resolved in the catheterization laboratory. Holter monitoring showed that ventricular tachyarrhythmias, such as runs of more than 3 extrasystoles, were detectable only during the first 8 hours after direct PTCA.</AbstractText>In our group of patients undergoing successful direct PTCA, no in-hospital life-threatening arrhythmias occurred after this procedure.</AbstractText>

[Cardiology].

The therapeutic acquisition to be retained for 2004 are: 1. The elderly patients with heart failure also should receive beta blocker treatment. The correction of anaemia, aggravating factor in heart failure, improves symptoms and survival of the patient. 2. It remains to prove that the treatment of sleep apnea, which seems to be an additional factor for mortality in cardiovascular diseases, is able to reduce the risk. 3. The interventions in the endocanabino&#xef;d system which regulates weight and metabolic processes might be a promising new therapeutic acquisition. 4. Prevention of coronary disease with lipid lowering drugs is still a major topic, and the trend goes the lower the better. The problems observed with Rofecoxybe and other drug interactions reminds us to be conscious when prescribing multiple drugs. 5. The implantable defibrillator seems to be a life insurance in the event of ventricular fibrillation. However, it is not so easy to identify the patient who might really benefit.

C-reactive protein elevation predicts the occurrence of atrial structural remodeling in patients with paroxysmal atrial fibrillation.

It has been poorly understood whether inflammation may contribute to atrial structural remodeling and increase the propensity for atrial fibrillation (AF) to persist. We investigated the relationship between C-reactive protein (CRP) elevation and the development of atrial remodeling in AF. The study population comprised 50 consecutive paroxysmal AF (PAF) patients and 50 control patients without AF. All patients underwent echocardiography, and high-sensitivity CRP was routinely measured. C-Reactive protein was significantly higher in the patients with PAF than control patients (0.231+/-0.176 mg/dl vs 0.055+/-0.041 mg/dl, P&lt;0.001). Other predictors of elevated CRP included left ventricular mass (P&lt;0.05), left ventricular end-systolic diameter (P&lt;0.05), and left atrial (LA) diameter (P&lt;0.001). In a multivariate analysis, only CRP and LA diameter were independent predictors of PAF. Elevated CRP levels correlated with LA diameter (r=0.489, P&lt;0.001). Left atrial diameter was increased in PAF patients compared with control patients (P&lt;0.001). We found that a longer duration of AF is associated with higher CRP levels and a larger LA diameter (duration &lt;30 days: CRP 0.166+/-0.139 mg/dl, LA diameter 38.4+/-8.0 mm; duration &gt;30 days: CRP 0.345+/-0.181 mg/dl, LA diameter 45.6+/-6.6 mm; P&lt;0.001). In conclusion, longer AF duration is associated with CRP elevation and atrial structural remodeling, as approximated by larger LA diameter. However, CRP elevation, while correlating with LA diameter, was not an independent predictor of atrial structural remodeling. Thus, it remains unclear whether CRP and the inflammatory state are contributory to LA remodeling or whether LA remodeling or AF induces elevation in CRP and inflammation.

Long term complications in single and dual chamber pacing are influenced by surgical experience and patient morbidity.

To determine how short and long term complication rates after pacemaker implantation are influenced by patient morbidity, operator experience, and choice of pacing system.</AbstractText>Retrospective analysis of 1884 patients who received VVI (n = 610), VDD (n = 371), or DDD devices (n = 903) between 1990 and 2001. Follow up period was 64 (34) months. The influence of age, sex, coronary artery disease, myocardial infarction, reduced left ventricular (LV) function, right ventricular (RV) dilatation, atrial fibrillation, device type, and operator experience on operation time and complication rate were analysed.</AbstractText>Operation time was prolonged in patients with coronary artery disease, inferior myocardial infarction, reduced LV function, and RV dilatation. Implantation of DDD pacemakers prolonged operation time, particularly among operators with a low or medium level of experience. The overall complication rate was 4.5%. Sixty seven per cent of these complications occurred within the first three months. Complication rate was increased by age, reduced LV function, and RV dilatation. Implantation of DDD systems led to a higher complication rate (6.3%) than implantation of VVI (2.6%) or VDD pacemakers (3.2%). These differences were present only among operators with a low or medium level of experience.</AbstractText>Operation time and complication rate increased with age, impaired LV function, and RV dilatation. Complication rates were higher with DDD than with VVI or VDD implantation and were excessive among inexperienced but not experienced operators.</AbstractText>

Heart failure in patients with preserved and deteriorated left ventricular ejection fraction.

To determine clinical and prognostic differences between preserved and deteriorated systolic function (defined as left ventricular (LV) ejection fractions &gt; or = 50% and &lt; 50%, respectively) in patients with heart failure satisfying modified Framingham criteria.</AbstractText>Records were studied of 1252 patients with congestive heart failure (CHF) (mean (SD) age 69.4 (11.7) years; 485 women, 767 men) who had been admitted to a cardiology service for CHF in the period 1991-2002 and whose LV systolic function had been echocardiographically evaluated within two weeks of admission. Data were collected on the main clinical findings, supplementary examinations, treatment, and duration of hospitalisation. Whether the patient was alive in the spring of 2003 was evaluated by searching the general archives of the hospital and by telephone survey.</AbstractText>LV systolic function was preserved in 39.8% of patients. Age, female to male sex ratio, and prevalence of atrial fibrillation, valve disease, and other non-ischaemic, non-dilated cardiopathies were all significantly greater in the group with preserved systolic function. New York Heart Association functional class IV, third heart sound, jugular vein congestion, cardiomegaly, radiological signs of lung oedema, pathological Q waves, left bundle branch block, sinus rhythm, ischaemic cardiopathy, and dilated cardiomyopathy were all significantly more prevalent in the group with deteriorated systolic function, as was treatment with angiotensin converting enzyme inhibitors and most other antihypertensive drugs on discharge from hospital. There was no significant difference in survival between the groups with preserved and deteriorated systolic function (either survival regardless of age at admission or in subgroups aged &lt; 75 and &gt; or = 75 years at admission). In the whole group, survival rates after one, three, and five years were 84.0%, 66.7%, and 50.9%, respectively.</AbstractText>In view of the poor prognosis of patients with CHF with preserved LV systolic function, who are currently treated empirically, it is to be hoped that relevant controlled clinical trials under way will afford information allowing optimisation of their treatment.</AbstractText>

[Attempt to assess the risk of recurrence of life-threatening ventricular arrhythmia using simple non-invasive tests].

Baroreflex sensitivity (BRS), as assessed using phenylephrine method, and depressed 24-hour heart rate variability (HRV) have been shown to be powerful predictors of life-threatening ventricular arrhythmias. However, before these tests are widely used, their methodology has to be simplified. The aim of this study was to assess the prognostic value of simple non-invasive BRS parameter (Robbe index, BRS-RI) and short-term HRV, together with left ventricular ejection fraction (LVEF) and late potentials (LP) assessment in patients after myocardial infarction (MI) with documented history of ventricular tachycardia (VT) and ventricular fibrillation (VF).</AbstractText>The observation was conducted on 53 patients after MI with documented VT or VF. They were was divided into two groups: with or without recurrence arrhythmia. During the follow-up malignant ventricular arrhythmia events occurred in 31 patients VT/VF(+), no VT or VF was recorded in the 22 subjects VT/VF(-). In all patients the following parameters were analyzed: BRS-RI (transfer function, 0.07-0.14 Hz), HRV parameters such as: SDNN, rMSSD, pNN50, LF LF (NU), LF/HF. Additionally, LVEF and LP were assessed.</AbstractText>In the VT/VF(+) and VT/VF(-) groups, values of analyzed parameters were: BRS-RI: 4.4 +/- 2.5 and 8.4 +/- 6.1 ms/mm Hg (p=0.03); BRS-RI &lt; or = 3 ms/mm Hg: 8/15 and 2/16 (p=0.02); SDNN: 23.0 +/- 18.0 and 20.0 +/- 11.6 ms (p=0.99); rMSSD: 70.9 +/- 69.8 and 34.1 +/- 30.2 ms (p=0.34); pNN50: 10.7 +/- 14.6 and 4.4 +/- 9.0% (p=0.7); LF: 204.5 +/- 509.7 and 160.7 +/- 265.8 ms2 (p=0.95); LF (NU): 0.5 +/- 0.4 and 0.5 +/- 0.3 (NU) (p=0.77); LF/HF: 1.3 +/- 1.2 and 2.1 +/- 2.2 (p=0.49); LVEF: 32.5 +/- 9.1 and 39.8 +/- 13.3% (p=0.03); LP: 19/24 and 15/19 (p=0.99). The only indices of prognostic values were Robbe-index and LVEF. Their prognostic value in prediction of arrhythmic event occurrence was independent of each other's and of age, time elapsed from MI and number of MI (p=0.007). Non-diagnostic values of BRS-RI were found in 22 patients (42%).</AbstractText>Among the evaluated indices, only LVEF and Robbe-index have prognostic value in prediction of life-threatening ventricular arrhythmia recurrence after myocardial infarction. However, a high percentage of non-diagnostic values obtained in BRS-RI assessment limits the usefulness of this index.</AbstractText>

"W-shaped" volume curve with gated myocardial perfusion single photon emission computed tomography.

Gating errors (GEs) with ECG gated myocardial SPECT (G-SPECT) may occur irrespective of the presence or absence of arrhythmias. We evaluated the impact of GEs on both reconstructed tomograms and left ventricular ejection fraction (LVEF) derived from G-SPECT, and searched for clues to identify these errors.</AbstractText>We studied 2 GE patients, 10 normal subjects (NLs), and 10 atrial fibrillation patients. Stress technetium-99m sestamibi G-SPECT was performed. Left ventricular (LV) contraction was evaluated in the beating slices. LVEF was calculated with G-SPECT using QGS (Cedars-Sinai, Los Angels) and p-FAST (Sapporo Medical University, Japan), and compared with that obtained by echocardiography (ECHO). LV volume curves were created by QGS and p-FAST. The heart rates (HRs) were calculated from the acquired images, and compared with their resting HRs. The mean count density of the myocardium was measured and time-activity curves were created.</AbstractText>In patients with GEs, bi-phasic LV contraction was demonstrated with fading-out towards end-diastole. G-SPECT underestimated LVEF compared to ECHO by 10% or more. The volume curves appeared "W-shaped." The HRs from the images were slower than the resting HRs. The count density decrement from frame #1 to #8 was larger than that of NLs. The time-activity curves were different in shape from those of NLs.</AbstractText>G-SPECT underestimates LVEF in patients with GEs. These errors can be identified with a combination of visual inspection of beating slices, time-volume curves, and time-activity curves. Monitoring the HR is a clue for anticipating and avoiding these errors.</AbstractText>

N-2-mercaptopropionylglycine, a scavanger of reactive oxygen species, does not modify the early antiarrhythmic effect of ischaemic preconditioning in anaesthetised dogs.

The possible involvement of reactive oxygen species (ROS) in the protective effects of ischaemic preconditioning (PC) against arrhythmias was examined in anaesthetised dogs using the ROS scavenger N-2-mercaptopropionylglycine (MPG).</AbstractText>PC was induced in 20 chloralose-urethane anaesthetised dogs by two 5 min occlusions of the left anterior descending (LAD) coronary artery 20 min prior to the prolonged (25 min) ischaemia/reperfusion (I/R) insult. In 10 of these dogs MPG was infused locally into a small side branch of the LAD in a dose of 0.15 mg kg(-1) min(-1), starting 10 min prior to and continuing throughout the entire PC procedure. In another four dogs subjected to preconditioning in the absence and then 2h later in the presence of MPG free radical formation was evaluated by the chemiluminescence method. Eleven dogs, infused with saline and subjected to a 25 min I/R insult, served as controls. A further 9 dogs, which were not preconditioned, were given MPG over a period of 60 min prior to occlusion.</AbstractText>Preconditioning markedly reduced the number of ventricular premature beats (VPBs; 86 +/- 34 v. 377 +/- 78; P &lt; 0.05), the episodes of ventricular tachycardia (VT; 2.0 +/- 0.7 v. 13.6 +/- 4.5; P &lt; 0.05) and the incidences of both VT (60% v. 91%) and ventricular fibrillation (0% v. 82%; P &lt; 0.05) during the prolonged occlusion. Survival (from the combined ischaemia and reperfusion insult) was significantly increased (40% v. 0%; P &lt; 0.05) by PC. MPG did not modify the protective effects of PC, although free radical (mostly superoxide) formation that occurred following PC was abrogated in the presence of MPG. Thus, the number of VPBs (111 +/- 39), VT episodes (1.2 +/- 0.9) and the incidences of VT (20%) and VF (0%) during occlusion were similar to the PC dogs. MPG itself did not significantly modify arrhythmia severity in non-PC dogs.</AbstractText>We conclude that in our canine model of ischaemia/reperfusion the generation of ROS does not play a trigger role in the early PC-induced antiarrhythmic protection.</AbstractText>

Pyrroloquinoline quinone (PQQ) decreases myocardial infarct size and improves cardiac function in rat models of ischemia and ischemia/reperfusion.

As pyrroloquinoline quinone (PQQ) is a redox cofactor in mammals, we asked if it is cardioprotective. Rats were subjected to 2 h of left anterior descending (LAD) coronary artery ligation without reperfusion (model 1, ischemia). In model 2 (ischemia/reperfusion), rats were subjected to 17 or 30 min of LAD occlusion and 2 h of reperfusion. PQQ (15-20 mg/kg) was given i.p., either 30 min before LAD occlusion (Pretreatment) or i.v. at the onset of reperfusion (Treatment). In model 1, PQQ reduced infarct size (10.0 +/- 1.5 vs 19.1 +/- 2.1%, P &lt; 0.01). In model 2, either PQQ Pretreatment or Treatment also reduced infarct size (18.4 +/- 2.3 and 25.6 +/- 3.5% vs 38.1 +/- 2.6%, P &lt; 0.01). PQQ resulted in higher LV developed pressure and LV (+)dP/dt after 1-2 h of reperfusion (P &lt; 0.05), and fewer ventricular fibrillation episodes. PQQ dose (5-20 mg/kg) was inversely related to infarct size. PQQ reduced myocardial tissue levels of malondialdehyde (MDA), an indicator of lipid peroxidation (316 +/- 88 vs 99 +/- 14 nmol/g, P &lt; 0.01). PQQ given either as Pretreatment or as Treatment at the onset of reperfusion is highly effective in reducing infarct size and improving cardiac function in a dose-related manner in rat models of ischemia and ischemia/reperfusion. The optimal dose in this study, which exhibited neither renal nor hepatic toxicity, was 15 mg/kg, but lower doses may also be efficacious. We conclude that PQQ, which appears to act as a free radical scavenger in ischemic myocardium, is a highly effective cardioprotective agent.

Termination of spiral waves during cardiac fibrillation via shock-induced phase resetting.

Multiple unstable spiral waves rotating around phase singularities (PSs) in the heart, i.e., ventricular fibrillation (VF), is the leading cause of death in the industrialized world. Spiral waves are ubiquitous in nature and have been extensively studied by physiologists, mathematicians, chemists, and biologists, with particular emphasis on their movement and stability. Spiral waves are not easy to terminate because of the difficulty of "breaking" the continuous spatial progression of phase around the PSs. The only means to stop VF (i.e., cardiac defibrillation) is to deliver a strong electric shock to the heart. Here, we use the similarities between spiral wave dynamics and limit cycle oscillators to characterize the spatio-temporal dynamics of VF and defibrillation via phase-resetting curves. During VF, only PSs, including their formation and termination, were associated with large phase changes. At low shock strengths, phase-resetting curves exhibited characteristics of weak (type 1) resetting. As shock strength increased, the number of postshock PSs decreased to zero coincident with a transition to strong (type 0) resetting. Our results indicate that shock-induced spiral wave termination in the heart is caused by altering the phase around the PSs, such that, depending on the preshock phase, sites are either excited by membrane depolarization (phase advanced) or exhibit slowed membrane repolarization (phase delay). Strong shocks that defibrillate break the continuity of phase around PSs by forcing the state of all sites to the fast portion of state space, thus quickly leading to a "homogeneity of state," subsequent global repolarization and spiral wave termination.