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Cilnidipine, an N+L-type dihydropyridine Ca channel blocker, suppresses the occurrence of ischemia/reperfusion arrhythmia in a rabbit model of myocardial infarction.

Dihydropyridine Ca channel blockers are widely prescribed for the treatment of hypertension and coronary artery diseases, but it remains unknown whether these agents protect against arrhythmias. We investigated whether cilnidipine, an N+L-type Ca channel blocker, reduces the incidences of ventricular premature beats (VPBs) and, if so, via what mechanisms. Japanese white rabbits underwent 30 min of ischemia and 48 h of reperfusion. Cilnidipine (0.5 or 1.0 microg/kg/min, i.v.) or saline (i.v.) was administered from 30 min before ischemia to 30 min after reperfusion. Electrocardiogram and blood pressure were monitored and the incidences of VPBs were measured. At 48 h after reperfusion, myocardial infarct was measured. Myocardial interstitial noradrenaline levels were determined before, during and after 30 min of ischemia with cilnidipine (0.5 and 1.0 microg/kg/min) or saline. The incidences of VPBs during ischemia and reperfusion were significantly attenuated in the cilnidipine 0.5 group (15.6 +/- 3.1 and 6.8 +/- 1.9 beats/30 min) and in the cilnidipine 1.0 group (10.4 +/- 4.9 and 3.5 +/- 1.0 beats/30 min) compared to the control group (27.2 +/- 4.5 and 24.2 +/- 3.1 beats/30 min), respectively. Myocardial interstitial noradrenaline levels were significantly reduced in the cilnidipine 0.5 and 1.0 groups compared to the control group during ischemia and reperfusion. The antiarrhythmic effect of cilnidipine may be related to the attenuation of cardiac sympathetic nerve activity. This finding may provide new insight into therapeutic strategies for hypertensive patients with ventricular arrhythmias.

Electrocardiographic changes in patients with haemorrhagic fever with renal syndrome.

The purpose of the study was to assess the incidence, type and dynamics of electrocardiography (ECG) alterations in patients with haemorrhagic fever with renal syndrome (HFRS) according to different stages of the disease. 79 patients hospitalized at the University Hospital for Infectious Diseases in Zagreb during the large HFRS outbreak in Croatia in 2002 were retrospectively analysed. HFRS diagnosis was confirmed by enzyme-linked immunosorbent assay. A 12-lead resting ECG was obtained. 30 (38%) patients had abnormal ECG findings, most frequently in the oliguric stage. Increased levels of urea and creatinine were observed in all patients with abnormal ECG, along with abnormal chest X-ray in nearly 50% of cases. Sinus tachycardia was the most frequent ECG disorder in the febrile stage, and bradycardia in the oliguric stage. During the course of disease, some other ECG disorders were recorded: bundle branch conduction defects, non-specific ventricular repolarization disturbances, supraventricular and ventricular extrasystoles, prolonged QT interval, low voltage of the QRS complexes in standard limb leads, atrioventricular block first-degree, and atrial fibrillation. Myocarditis was present in 3 patients. In conclusion, abnormal ECG was found in more than one-third of HFRS patients with the most common findings during the oliguric stage. All ECG changes were transient.

Impact of sinus rhythm restoration and maintenance on left ventricular function and exercise tolerance in patients with persistent atrial fibrillation.

Although early improvement of haemodynamic parameters following successful cardioversion of atrial fibrillation (AF) has been well documented, the long-term benefits of sinus rhythm (SR) restoration are less obvious, mainly due to a high rate of AF relapses.</AbstractText>To determine the impact of SR restoration and maintenance on exercise tolerance and heart failure progression in patients with persistent non-valvular AF during a one year follow-up period.</AbstractText>We studied 104 patients (33 females, 71 males, mean age 60.4+/-7.4 years) with mild to moderate stable heart failure and persistent AF with well-controlled ventricular rate who were scheduled for cardioversion. They underwent submaximal exercise testing 24 hours before cardioversion, as well as 1 and 12 months afterwards. Exercise capacity was determined during symptom-limited exercise testing, according to a modified Bruce protocol. Heart failure symptoms were assessed at the same time-points of follow-up.</AbstractText>SR was presented in 66 (63.5%) patients one year after cardioversion. In patients with SR, a significant improvement in left ventricular (LV) performance, exercise capacity and heart failure symptoms was noted. There was an increase in LV fractional shortening (29.9+/-7.6% vs 35.6+/-9.3%; p&lt;0.001), maximal workload (4.7+/-2.3 vs 8.5+/-3.0 MET; p&lt;0.001), exercise duration (125.3+/-115.3 vs 294.7+/-216.7 sec.; p&lt;0.001), and improvement in the NYHA functional class (p&lt;0.001). No such changes were observed in patients who had AF relapse during follow-up or in those who had unsuccessful cardioversion.</AbstractText>Successful cardioversion of persistent AF resulted in a significant improvement of exercise capacity and a decrease in heart failure symptoms during one year follow-up period only in patients who maintained SR.</AbstractText>

[Massive myocardial hypertrophy in hypertrophic cardiomyopathy: a risk factor for sudden death and high defibrillation threshold during cardioverter-defibrillator implantation].

Two cases of hypertrophic cardiomyopathy with massive hypertrophy and high defibrillation threshold (DFT) are described. A 14-year-old boy, whose single risk factor for sudden death was extreme hypertrophy with maximum interventricular septum (IVS) thickness of 43 mm, survived an episode of ventricular fibrillation. During ICD implantation DFT testing showed energy requirements &gt;30 J and the procedure was aborted. Amiodarone and verapamil treatment was discontinued and treatment with oral sotalol was instituted. After a period of amiodarone washout the procedure was repeated and DFT of 24 J was encountered. An 18-year-old female with massive hypertrophy (IVS thickness=35 mm) and other risk factors for sudden death underwent ICD implantation for primary prevention. During the procedure DFT=20 J and ICD with 30 J maximal output was implanted. An increase in DFT to more than 20 J was encountered during pre-discharge test. Lack of 10 J safety margin warranted ICD system revision and upgrade; during the second procedure DFT was 24 J and ICD with 35 J maximal output was implanted. In summary, in both cases ICDs with 35 J maximal output were successfully implanted.

Implantable defibrillators configured for hybrid therapy of persistent and permanent atrial fibrillation: initial clinical experience with a novel lead system.

Hybrid therapy strategies have combined antiarrhythmic drugs (AAD) with pacemakers, atrio-ventricular defibrillators (AV ICD) or atrial ablation individually. The feasibility combining AAD with dual site RA pacing (DAP) in an AV ICD has not been examined.</AbstractText>We used an AV ICD with a novel lead configuration permitting DAP, antitachycardia pacing (ATP) or atrial shocks (ADF) in patients (pts) with refractory persistent or permanent AF. Hybrid therapy included linear RA ablation and/or focal ablation. Continuous DAP and automatic ATP with patient or physician activated ADF.</AbstractText>24 pts, mean age 66 +/- 10 yrs, with cardiac disease (22 pts), underwent insertion of an AVICD with dual RA leads. 20 patients had concomitant ablative procedures (RA only = 19, RA + LA = 1) and all pts continued previously ineffective AAD. During a follow-up of 2-36 months (mean 17 +/- 8 mos), rhythm control was restored in all pts &amp; maintained long-term in 19 (83%) pts. 8 pts used AF termination therapies successfully. Device datalogs showed no episodes of AF in 6 pts, asymptomatic brief arrhythmias in 4 pts, infrequent paroxysmal AF in 9 pts &amp; persistent AF recurred in 5 pts. AV ICD detection algorithms reliably detected AF or AT in the DAP mode in all pts. Intermittent brief P wave double counting occurred during AT in selected pts. No pt received inappropriate ADF therapy.</AbstractText>1. DAP can be safely incorporated in an AVICD devices for use in an hybrid therapy strategy for AF pts. 2. These devices can be effective for both AF prevention &amp; termination. 3. Long term rhythm control can be achieved and documented by device datalogs in persistent and permanent AF.</AbstractText>

Internal atrial and ventricular defibrillation during electrophysiology procedures.

Over the last twenty years internal defibrillation has evolved from an experimental technique into an important adjunctive procedure in the electrophysiology laboratory. Internal deflbrillation is used for treating persistent atrial fibrillation and refractory ventricular arrhythmias. Atrial defibrillation can be performed with several electrode configurations but generally shocks from 1 to 50 joules are delivered between electrodes placed in the coronary sinus and lateral wall of the right atrium. Ventricular defibrillation is usually performed with electrodes in the right ventricle and superior vena cava, although "unipolar" configurations with an internal ventricular electrode and a skin electrode can be used. Currently, internal deflbrillation can be required in 5-10% of cases within the electrophysiology laboratory and will become more commonly used as electrophysiologists perform more complex catheter ablation procedures.

New technologies of internal defibrillation.

This paper reviews recent research seeking to provide more efficient device oriented treatments for atrial and ventricular fibrillation to improve implantable cardioverter defibrillator (ICD) therapy. Investigators have proposed and tested many innovative technologies that may be included in future ICDs. Amongst the most promising technologies are combined cardiac resynchronization therapy and defibrillation, defibrillation coils in the coronary venous system, critical timing of defibrillation shocks, and pacing during ventricular fibrillation and tachycardia. Atrial defibrillation with ICDs is an area of considerable interest, but is not likely to gain widespread application unless acceptable methods of lowering pain associated with defibrillation shocks are implemented.

Internal defibrillation: where we have been and where we should be going?

Internal cardioversion has been developed as an alternative technique for patients who are resistant to external DC cardioversion of atrial fibrillation (AF) and was found to be associated with higher success rates. It used initially high energies (200-300 J) delivered between an intracardiac catheter and a backplate. Subsequent studies have shown that it is possible to terminate with energies of 1 to 6 Joules, paroxysmal or induced AF in 90 percent of patients and persistent AF in 75 percent of patients, using biphasic shocks delivered between a right atrium-coronary sinus vectors. Consequently, internal atrial defibrillation can be performed under sedation only without the need for general anesthesia. Recently developed external defibrillators, capable of delivering biphasic shocks, have increased the success rates of external cardioversion and reduced the need for internal cardioversion. However, internal defibrillation is still useful in overweight or obese patients, in patients with chronic obstructive pulmonary disease or asthma who are more difficult to defibrillate, and in patients with implanted devices which may be injured by high energy shocks. Low energy internal defibrillation has also proven to be safe and this has prompted the development of implantable devices for terminating AF. The first device used was the Metrix system, a stand-alone atrial defibrillator (without ventricular defibrillation) which was found to be safe and effective in selected groups of patients. Unfortunately, this device is no longer being marketed. Only double chamber defibrillators with pacing capabilities are presently available: the Medtronic GEM III AT, an updated version of the Jewel AF and the Guidant PRIZM AVT. These devices can be patient-activated or programmed to deliver automatically ounce atrial tachyarrhythmias are detected, therapies including pacing or/and shocks. Attempts to define the group of patients who might benefit from these devices are described but the respective role of atrial defibrillators versus other non-pharmacologic therapies for AF, such as surgery and radiofrequency catheter ablation, remains to be determined. Advantages and limitations or atrial defibrillators and approaches to reduce shock related discomfort which may be a concern in some patients, are reviewed. Studies have shown that despite shock discomfort, quality of life was improved in patients with atrial defibrillators and the need for repeated hospitalizations was reduced. The cost of these devices remains a concern for the treatment of a non-lethal arrhythmia. Attention that atrial defibrillators will receive from cardiologists and from the industry in the future, will depend of the long-term results of other non-pharmacological options and of the identification of the group of AF patients which will require restoration and maintenance of sinus rhythm. But there is no doubt that selected subsets of patients with AF could benefit from atrial defibrillation.

Ventricular tachycardia in a neonate with prenatally diagnosed cardiac tumors: a case with tuberous sclerosis.

We report a patient with prenatally diagnosed tuberous sclerosis. Fetal ultrasonography demonstrated multiple cardiac tumors and arrhythmia. After birth, because of frequent supraventricular extrasystoles, the infant was admitted to the neonatal intensive care unit. Findings on 24-hour ambulatory electrocardiogram (ECG) showed frequent supraventricular tachycardia and ventricular tachycardia with four beats as the longest run. At the age of 12 days, he developed cardiopulmonary arrest after crying out. A monitored ECG showed ventricular tachycardia. Twenty minutes after onset, a 12-lead ECG showed ventricular fibrillation, which returned to normal sinus rhythm with repeated DC cardioversion. Oral antiarrhythmic therapy with carteolol hydrochloride was effective. The patient showed no further symptoms after oral medication was initiated and the tumors regressed spontaneously.

Unusual and early hyperglycemia following amiodarone infusion in two infants.

Amiodarone is an effective antiarrhythmic agent that is widely used for tachyarrhythmias, especially ventricular tachycardia and supraventricular tachycardia. It has some mild short-term (e.g., skin rashes, gastrointestinal symptoms, and corneal microdeposits) and long-term side effects (thyroid dysfunction, visual disturbances, pulmonary infiltrates, ataxia, and hepatitis). We present two infants who had hyperglycemia following amiodarone infusion during the early postoperative period.

Levosimendan improves postresuscitation myocardial dysfunction after beta-adrenergic blockade.

In earlier studies, we found that a nonselective beta-adrenergic blocking agent, propranolol, facilitated cardiac resuscitation, reduced postresuscitation myocardial ectopy, and improved postresuscitation survival. However, the potential adverse effects and specifically the negative inotropic actions of propranolol prompted our further investigation of the potential value of a non-beta-adrenergic inotropic drug, levosimendan, in conjunction with propranolol, for minimizing postresuscitation myocardial dysfunction after successful resuscitation from cardiac arrest. Ventricular fibrillation was induced and untreated for 7 minutes in 15 domestic pigs, which were divided into propranolol, propranolol plus levosimendan, and control groups. Propranolol was administered as a bolus dose of 0.1 mg/kg during cardiac arrest. Electrical defibrillation was attempted after 12 minutes of cardiac arrest including 5 minutes of precordial compression. Levosimendan was administered at 10 minutes after successful resuscitation in a dose of 20 microg/kg and followed by infusion of 0.4 microg/kg/min over the ensuing 220 minutes. Propranolol reduced energies or numbers of defibrillatory shocks and postresuscitation myocardial ectopy, and it improved postresuscitation myocardial dysfunction. When levosimendan was added, postresuscitation myocardial contractile function was improved even more.

[Influence of sinus rhythm restoration and maintenance on left ventricle diameter and function in patients with persistent atrial fibrillation--one year follow-up].

Aim of our study was to determine the dynamics of selected echocardiographic parameters after sinus rhythm (SR) restoration and maintenance in pts with persistent nonvalvular atrial fibrillation (AF) during one year follow-up period.</AbstractText>Our study population comprised 104 pts (F/M 33/71; mean age 60.4 +/- 7.4) assigned to SR restoration and maintenance with serial antiarrhythmic drug usage, for whom transthoracic echocardiographic (TTE) variables were recorded prior to, 2 and 12 months after cardioversion (CD). Left ventricle diastolic diameter and fractional shortening were variables of interest.</AbstractText>SR was presented in 66 (63.5%) pts at one year. There was no significant differences in left ventricle diastolic diameter during the follow up. A significant increase in left ventricular fractional shortening (29.9 +/- 6.9% vs 34.5 +/- 8.9%; p &lt; 0.001) was found in pts assigned to the sinus rhythm restoration according to intention-to-treat analysis. Such trend was noted only in pts who maintained SR during the follow up (29.9 +/- 7.6% vs 35.6 +/- 9.3%; p &lt; 0.001).</AbstractText>Among all considered variables only value of left ventricular fractional shortening increased after successful CV of persistent AF in one year follow-up.</AbstractText>

Atrial fibrillation increases production of superoxide by the left atrium and left atrial appendage: role of the NADPH and xanthine oxidases.

Atrial fibrillation (AF) is associated with an increased risk of stroke due almost exclusively to emboli from left atrial appendage (LAA) thrombi. Recently, we reported that AF was associated with endocardial dysfunction, limited to the left atrium (LA) and LAA and manifest as reduced nitric oxide (NO*) production and increased expression of plasminogen activator inhibitor-1. We hypothesized that reduced LAA NO* levels observed in AF may be associated with increased superoxide (O2*-) production.</AbstractText>After a week of AF induced by rapid atrial pacing in pigs, O2*- production from acutely isolated heart tissue was measured by 2 independent techniques, electron spin resonance and superoxide dismutase-inhibitable cytochrome C reduction assays. Compared with control animals with equivalent ventricular heart rates, basal O2*- production was increased 2.7-fold (P&lt;0.01) and 3.0-fold (P&lt;0.02) in the LA and LAA, respectively. A similar 3.0-fold (P&lt;0.01) increase in LAA O2*- production was observed using a cytochrome C reduction assay. The increases could not be explained by changes in atrial total superoxide dismutase activity. Addition of either apocyanin or oxypurinol reduced LAA O2*-, implying that NADPH and xanthine oxidases both contributed to increased O2*- production in AF. Enzyme assays of atrial tissue homogenates confirmed increases in LAA NAD(P)H oxidase (P=0.04) and xanthine oxidase (P=0.01) activities. Although there were no changes in expression of the NADPH oxidase subunits, the increase in superoxide production was accompanied by an increase in GTP-loaded Rac1, an activator of the NADPH oxidase.</AbstractText>AF increased O2*- production in both the LA and LAA. Increased NAD(P)H oxidase and xanthine oxidase activities contributed to the observed increase in LAA O2*- production. This increase in O2*- and its reactive metabolites may contribute to the pathological consequences of AF such as thrombosis, inflammation, and tissue remodeling.</AbstractText>

Emergency call processing and survival from out-of-hospital ventricular fibrillation.

Our aim was to report the effect of the emergency call processing in the dispatching centre on survival from out-of-hospital ventricular fibrillation (VF).</AbstractText>This retrospective cohort study was conducted in Helsinki Emergency Medical Services. All consecutive cases with out-of-hospital bystander witnessed VF of cardiac origin between 1 January 1997 and 31 December 2002 were included. Data were collected prospectively. Call processing times, call numbers per dispatcher and telephone guided cardiopulmonary resuscitation (CPR) were studied. Discharge alive from hospital was used as primary end point.</AbstractText>The study population consisted of 373 cases. Cardiac arrest (CA) was recognised in 296 cases (79.4%) by the dispatcher. Survival to discharge was 37.2% (110/296) if CA was recognised and 28.6% (22/77) if it was not recognised (p=0.1550). When the dispatcher handled &lt;4 VF calls during the study period survival to discharge was 22.1% (17/77) compared to 38.2% (50/131) and 39.4% (65/165) when the call volume was 4-9 or &gt;9 (p=0.0227). The mean time to dispatch a first responding unit (FRU) was 77.1+/-44.3 s. Survival to discharge was 39.4% (65/165) when the FRU dispatching time was &lt;60s and 32.2% (67/208) when dispatching took &gt; or =60 s (p=0.1496). The mean time to CA recognition was 170.2+/-130.1 s. Spontaneous circulation was achieved more rapidly when the time was &lt;150 s (p=0.0426), but there was no difference in survival to discharge. Telephone guided CPR instructions were given in 123 cases (35.5%). Survival to discharge was 43.1% (53/123) when CPR instructions were given and 31.7% (72/223) when they were not given (p=0.0453).</AbstractText>We showed that low CA call numbers per dispatcher is associated with a decreased probability of survival. Giving telephone guided CPR instructions should be promoted as they influence the outcome. Further studies are needed to determine optimal call processing times.</AbstractText>

Left ventricular hypertrabeculation/noncompaction as a cardiac manifestation of Duchenne muscular dystrophy under non-invasive positive-pressure ventilation.

Though cardiac involvement is a frequent finding in patients with Duchenne muscular dystrophy (DMD) at the wheel-chair-bound stage, left ventricular hypertrabeculation (LVHT) has not been reported. The patient is a 28-year-old male with the typical clinical features of end stage DMD. Since the age of 16 years he required ventilatory support by means of non-invasive positive-pressure ventilation (NIPPV), initially intermittently and since age 27 permanently. Since the age of 21 years he developed chronic heart failure, and since age 24 atrial flutter, successfully treated with amiodarone. After discontinuation of amiodarone because of hyperthyroidism, he developed atrial fibrillation. Echocardiography at age 28 revealed mitral insufficiency, enlarged left atrial diameter, and, surprisingly, LVHT. Since LVHT was absent at the initial echocardiographic examination, it was regarded acquired. The case shows that cardiac involvement in DMD may not only comprise rhythm abnormalities, valve abnormalities, and dilative cardiomyopathy, but also LVHT in single cases.

[Effect of atrial fibrillation on left ventricle function in the elderly].

Atrial fibrillation (FA) coexists with heart failure, and its occurrence frequency increases with age. This arrhythmia can precede heart failure as well as can be a consequence of cardiac function deterioration.</AbstractText>The influence of atrial fibrillation on left ventricle (LV) function assessed by echocardiography in the elderly. Investigated group. Study group consists of 30 older patients 75,9 (+/- 4,6) years old with chronic atrial fibrillation, mean duration 319,5 (+/- 292,5) days and 30 younger patients 56,7 (+/- 3,7) years old with atrial fibrillation, mean duration 254,2 (+/- 191,2) days. In control group were 30 persons 74,7 (+/- 5,1) years old with sinus rhythm (SR). In all patients transthoracic (TTE) echocardiography was performed to assess following parameters: end-diastolic diameter of LV (LVEDd), end-systolic diameter of LV (LVESd), fractional shortening of LV (FS LK), stroke volume of LV (SV LK), cardiac output (CO), ejection fraction of LV (EF LK), preejection period of LV (PEP LK), ejection period of LV (LVET), maximal aortic flow velocity (V max LK), maximal velocity of mitral early diastolic flow (E ampl LK), deceleration time of mitral early diastolic flow (E dcct LK). Consequently transoesophageal (TEE) echocardiography was made to record flow in left superior pulmonary vein (LSPV) and following parameters were measured: maximal systolic flow velocity in LSPV (PVS), maximal diastolic flow velocity in LSPV (PVD), integral of systolic flow in LSPV (PVS intg), deceleration time of diastolic flow in LSPV (PVD dcct). During Holter electrocardiographic recording were calculated: maximal heart rate (HR max), minimal heart rate (HR min), mean heart rate (Hr sr).</AbstractText>Older patients with atrial fibrillation characterised significantly lower EF LK and FS LK than younger patients and older patients with sinus rhythm. Most of Doppler echocardiographic parameters recorded from aortic flow as well as measured in left superior pulmonary vein have lower values in older patients with arrhythmia compared to younger ones. LVEDd was significantly greater in older patients with atrial fibrillation than in those with sinus rhythm. E ampl LK was markedly lower in older patients with atrial fibrillation and coexisted with shortening deceleration time of this flow in this group of patients. PVD did not differ in studied groups but deceleration time of this flow similarly to deceleration time of mitral flow was markedly shortened in older group of patients with arrhythmia. HR mean and Hr max in older patients with atrial fibrillation were significantly higher in older patients with atrial fibrillation compared to those without arrhythmia whereas HR min did not differ between mentioned groups. HR mean calculated from 24 hours correlated with poorer hemodynamic parameters of left ventricle.</AbstractText>Atrial fibrillation in the elderly causes greater systolic and diastolic dysfunction of left ventricle compared to younger patients with this kind of arrhythmia. The left ventricle contractility deterioration in older patients with atrial fibrillation correlates with high maximal and mean diurnal heart rate.</AbstractText>

Treatment of arrhythmic storm in implantable defibrillator patients.

A common ICD therapy-related complication is arrhythmic storm (AS). The objective of our study was to define the impact of AS on patients' prognoses in order to compare the total mortality of AS patients with the rest of the group.</AbstractText><AbstractText Label="MATERIAL/METHODS" NlmCategory="METHODS">We studied 138 patients who received ICDs between 1994 and 2001. Patients who experienced one or more arrhythmic storms were statistically compared with patients who had no accumulation of malignant arrhythmia or no episodes.</AbstractText>One thousand four hundred ninety episodes of arrhythmia were analyzed. Arrhythmia recurrence was present in 71% of the patients. The majority of episodes (78%) were ventricular tachycardias and only 3% of episodes were ventricular fibrillation. Seventy percent of all arrhythmic episodes were asymptomatic. The ICD therapy sensitivity was 99.7%. Thirty-eight arrhythmic storms in 19 patients (14%) were observed during follow-up. The occurrence of AS was twice as high among patients with LVEF &lt;35% than the rest of the group (18% vs. 8%). The total survival of patients with AS was significantly lower than that of the ICD patients who did not experience an AS (36.8% vs. 16.8%, p=0.042). All episodes of arrhythmic clusters during the AS were ventricular tachycardias.</AbstractText>Arrhythmic storm is a serious risk marker for cardiac death. Ventricular tachycardia is a basic rhythm disorder of AS episodes and occurs significantly more often than ventricular fibrillation. Arrhythmic storm is responsible for a 4.6 times more frequent re-admission to hospital.</AbstractText>

Atropine aborts bradycardic effect of endotracheally administered vasopressin.

Vasopressin is an alternative drug to adrenaline in intractable ventricular fibrillation. However, vasopressin can cause significant bradycardia, resulting in reduced cardiac output. We investigated whether pre-treatment with atropine abrogates vasopressin-induced bradycardia in a beating-heart canine model.</AbstractText><AbstractText Label="MATERIAL/METHODS" NlmCategory="METHODS">Five adult mongrel dogs received endotracheal vasopressin (1.0 U/kg) with or without endotracheal atropine (0.02 mg/kg) or a placebo (10 ml saline) after being anesthetized and ventilated. Hemodynamic variables and arterial blood gases were determined. Each dog (studied 3 times, one week apart) served as its own control.</AbstractText>Endotracheal vasopressin produced early and significant (p&lt;0.05) bradycardia (from 55+/-7 mmHg to 35+/-5 beats/min) compared with controls, starting one minute post-injection and lasting one hour. In contrast, in atropine-pretreated animals the heart rate increased significantly (p&lt;0.05) for as long as one hour post-atropine and vasopressin administration. In addition, animals treated with vasopressin with or without atropine exhibited a significant rise in diastolic blood pressure (from 83+/-5 to 160+/-15 and from 83+/-3 to 108+/-10 mmHg, respectively). Systolic and mean blood pressures also increased significantly compared with controls. Blood gases remained unchanged in all groups.</AbstractText>Endotracheal administration of vasopressin can cause protracted bradycardia. Pretreatment with atropine can abrogate this effect. We suggest that atropine administration be considered when vasopressin is administered during cardio-pulmonary resuscitation. Further studies are warranted to evaluate the effect of vasopressin and atropine in a closed-chest model of cardio-pulmonary resuscitation.</AbstractText>

Effects of cardiac resynchronization therapy on incidence of atrial fibrillation in patients with poor left ventricular systolic function.

Although the beneficial role of cardiac resynchronization therapy (CRT) in selected patients with heart failure is well proven, its effect on the incidence of atrial fibrillation (AF) is unclear. The present study compared the incidence of AF in 36 consecutive patients with chronic heart failure receiving CRT with its incidence in controls matched for age, gender, and left ventricular ejection fraction but not receiving CRT. The findings suggest that patients with CRT had a significantly lower incidence of AF than controls. Further studies to establish the role of CRT in preventing AF and its mechanisms are warranted.

Benefits, unresolved questions, and technical issues of cardiac resynchronization therapy for heart failure.

This review aims to provide a synthesis of the published evidence regarding the rationale and clinical benefits of cardiac resynchronization therapy (CRT) with implantable atrial-synchronized biventricular pacing (BVP) devices in patients with moderate to advanced heart failure and intra- and interventricular conduction delays. In addition, it addresses clinical and technical issues that have yet to be resolved, such as the selection of the most suitable candidates for CRT; the usefulness of combining BVP with automatic defibrillation backup; the value of CRT in patients with atrial fibrillation; the importance of alternative sites of pacing, such as the atrial septum and the right ventricular (RV) outflow tract; the harmful effects of the long-standing practice of producing an iatrogenic left bundle branch block by conventional RV pacing in patients receiving standard permanent pacemakers; the question of precisely where on the left ventricle optimal pacing is achieved; and the potential applications of CRT in patients with pediatric or congenital heart disease. Considering how major advances have been achieved since the first clinical application of CRT in 1994, one can be optimistic about the future of the electrotherapeutic management of heart failure.

Effects of beta-blockers on implantable cardioverter defibrillator therapy and survival in the patients with ischemic cardiomyopathy (from the Multicenter Automatic Defibrillator Implantation Trial-II).

This study examined the effects of beta blockers on (1) appropriate implantable cardioverter defibrillator (ICD) therapy for ventricular tachycardia (VT) or ventricular fibrillation (VF), (2) inappropriate ICD therapy for atrial fibrillation or supraventricular tachycardia, and (3) survival in 691 patients who received ICDs in the Multicenter Automatic Defibrillator Implantation Trial-II. The study population involved 258 patients who were not receiving beta blockers and 433 who were receiving metoprolol (n = 192), atenolol (n = 58), or carvedilol (n = 182). Patients receiving beta blockers were divided into the upper quartile and lower 3 quartiles of the drug doses they were taking. Patients receiving the higher doses of beta blockers (those in the top quartile of doses) had a significant reduction in the risk for VT or VF requiring ICD therapy compared with patients not receiving beta blockers (hazard ratio 0.48, p = 0.02). The frequency of inappropriate ICD therapy for supraventricular tachyarrhythmias was not significantly different among the 3 treatment groups (p = 0.32). Beta-blocker use at the 2 dosage levels was associated with significant improvement in survival compared with the nonuse of beta blockers (hazard ratios 0.42 to 0.44, p &lt;0.01). In conclusion, beta blockers reduce the risk for VT or VF and improve survival in ICD-treated patients with ischemic cardiomyopathy.

Soft tissue impact characterisation kit (STICK) for ex situ investigation of heart rhythm responses to acute mechanical stimulation.

Both mechanical induction and mechanical termination of arrhythmias have been reported in man. Examples include pre-cordial impacts by sports implements (baseballs, pucks) that can trigger arrhythmias, including ventricular fibrillation, or via the so-called pre-cordial thump, used as an emergency resuscitation measure to convert arrhythmias to normal sinus node rhythm. These interventions have been partially reproduced in experimental studies on whole animals. Relating observations at the system's level to underlying mechanisms has been difficult, however, largely because of: (i) a deficit in efficient and affordable pharmacological agents to selectively target (sub-)cellular responses in whole animal studies, and (ii) the lack of suitable experimental models to study the above responses at intermediate levels of functional and structural integration, such as the isolated heart or cardiac tissue. This paper presents a soft tissue impact characterisation kit (STICK), suitable for quantitative investigations into the effects of acute mechanical stimulation on cardiac electro-mechanical function in rodent isolated heart or tissue preparations. The STICK offers independent control over a range of relevant biophysical parameters, such as impact location and energy, pre-impact projectile speed and contact area, as well as over the timing of a mechanical stimulus relative to the cardiac cycle (monitored via electrocardiogram, ECG, here recorded directly from the cardiac surface). Projectile deceleration upon interaction with the tissue is monitored, contact-free, with a resolution of 175 microm, providing information on tissue deformation dynamics, force, pressure and work of the mechanical intervention. In order to study functional effects of cardiac mechanical stimulation in the absence of tissue damage, impacts must be limited (for juvenile Guinea pig heart) to 2-2.5 mJ in the slack left ventricle (diastolic impact) and 5-10 mJ in contracture (systolic impact), as confirmed by enzyme assay and histological investigation. Impacts, timed to coincide with the early T-wave of the ECG, are capable of triggering short runs of ventricular fibrillation. Thus, the STICK is a suitable tool for the study of acute cardiac mechano-electric feedback effects, caused by short impulse-like mechanical stimulation, at the level of the isolated organ or tissue.

Coronary artery bypass surgery in high-risk patients.

In high-risk coronary artery bypass patients; off-pump versus on-pump surgical strategies still remain a matter of debate, regarding which method results in a lower incidence of perioperative mortality and morbidity. We describe our experience in the treatment of high-risk coronary artery patients and compare patients assigned to on-pump and off-pump surgery.</AbstractText>From March 2002 to July 2004, 86 patients with EuroSCOREs &gt; 5 underwent myocardial revascularization with or without cardiopulmonary bypass. Patients were assigned to off-pump surgery (40) or on-pump surgery (46) based on coronary anatomy coupled with the likelihood of achieving complete revascularization.</AbstractText>Those patients undergoing off-pump surgery had significantly poorer left ventricular function than those undergoing on-pump surgery (28.6 +/- 5.8% vs. 40.5 +/- 7.4%, respectively, p &lt; 0.05) and also had higher Euroscore values (7.26 +/- 1.4 vs. 12.1 +/- 1.8, respectively, p &lt; 0.05). Differences between the two groups were nonsignificant with regard to number of grafts per patient, mean duration of surgery, anesthesia and operating room time, length of stay intensive care unit (ICU) and rate of postoperative atrial fibrillation.</AbstractText>Utilization of off-pump coronary artery bypass graft (CABG) does not confer significant clinical advantages in all high-risk patients. This review suggest that off-pump coronary revascularization may represent an alternative approach for treatment of patients with Euroscore &gt; or = 10 and left ventricular function &lt; or = 30%.</AbstractText>

Cor triatriatum sinistrum: a rare congenital cardiac anomaly presenting in an adult with chronic atrial fibrillation.

Cor triatriatum is a rare congenital cardiac anomaly in which the left atrium is divided into proximal (dorsal or upper) and distal (ventral or lower) chambers by a fibromuscular septum. The upper chamber receives the pulmonary veins and the lower chamber contains the atrial appendage and the mitral valve. The 2 chambers communicate through a defect in the membrane. Cor triatriatum is often associated with other congenital cardiac anomalies. Most frequently, the upper chamber communicates with the right atrium through a patent foramen ovale or atrial septal defect, and the clinical symptoms simulate anomalous pulmonary venous return. Less commonly, the foramen ovale communicates with the distal chamber and the clinical features mimic mitral stenosis. When cor triatriatum is the only abnormality, the clinical findings are also similar to mitral stenosis with development of pulmonary hypertension and subsequent right ventricular hypertrophy and atrial enlargement. The diagnosis is usually made in infancy or childhood, and the lack of treatment results in death in 75% of patients. We report the case of a woman who presented much later in life. The patient was a 57-year-old female with a clinical history of chronic atrial fibrillation who presented to the emergency department because of a "funny sensation" in her chest, though she denied chest pain, nausea, vomiting, or diaphoresis. EKG revealed atrial fibrillation with a rapid ventricular response and a tachycardic rate of 157. She had a therapeutic level of digoxin, and cardiac enzymes were normal. The patient was admitted and placed on Cardizem drip. Serial EKGs remained normal and heart rate control was achieved. On hospital day 2, the patient became dyspneic and cyanotic. She went into cardiac arrest and died.Autopsy revealed cardiomegaly (610 g) with 4-chamber dilatation. A septum divided the left atrium into 2 chambers. The defect in the dividing membrane measured 1 cm in diameter. No other congenital defects were noted. The large size of the defect in the membrane likely accounted for the late onset of symptoms that allowed this patient to survive into adulthood without previous diagnosis or surgical intervention (which is usually required in childhood).

Mechanisms of disease: current understanding and future challenges in Brugada syndrome.

Brugada syndrome is a clinical entity characterized by ST-segment elevation in the right precordial leads (V1-V3) and an episode of ventricular fibrillation in the absence of structural heart disease. Data regarding genotype-phenotype relationships are limited, since SCN5A, the gene encoding the a subunit of the sodium channel, is as yet the only gene linked to Brugada syndrome. Studies of SCN5A mutations responsible for the Brugada phenotype have shown the presence of functional defects in the sodium-channel current. Experimental studies employing arterially perfused right-ventricular wedge preparations have elucidated cellular mechanisms for this phenotype. Data indicate that an accentuated action-potential notch, mediated by a prominent transient outward current and loss of the action-potential dome in the epicardium (but not in the endocardium) of the right ventricle give rise to a transmural voltage gradient, resulting in ST-segment elevation and the induction of ventricular fibrillation. On the basis of cellular mechanisms, it might be possible to normalize the Brugada phenotype by use of therapeutic agents or interventions that decrease net outward currents by decreasing the transient outward current or outward potassium currents, or increasing the L-type inward calcium current or fast sodium current. Interventions that increase net outward currents through raising the transient outward current or outward potassium currents or decreasing the L-type inward calcium current or fast sodium current might aggravate or unmask the Brugada phenotype, resulting in an acquired form of this syndrome. In this review, we discuss future challenges relating to risk stratification, genetic heterogeneity, sex and ethnic differences in Brugada syndrome.

[Assessment of energy-dependent Ca2+ transport in myocardial mitochondria in the ventricular fibrillation: potential diagnostic implication].

The method of evaluation of ATP synthesis from ADP and Ca2+ transport in myocardial mitochondria has been developed. The addition of glutamate to the homogenisation media improved the parameters studied. It was shown that the Ca2+ transport test is highly informative and sensitive for the estimation of heart muscle energetic state.

Stentless bioprostheses in small aortic roots: impact of patient-prosthesis mismatch on survival and quality of life.

Although stentless bioprostheses offer hemodynamic advantages, prosthetic valves of smaller size may provide less reduction of left ventricular hypertrophy and, therefore, affect survival and quality of life.</AbstractText>A total of 303 patients (mean age 75 +/- 7 years) who underwent aortic valve replacement with the stentless Freestyle bioprostheses were followed up. The impact of projected indexed effective orifice area (IEOA) on survival and quality of life (QoL) was determined multivariately by Cox regression and logistic regression analysis.</AbstractText>Independent predictors of survival time were diabetes mellitus (p &lt; 0.001), atrial fibrillation (p = 0.004), male gender (p = 0.015), peripheral vascular disease (p = 0.039), and patient-prosthesis mismatch (PPM, defined as projected IEOA &lt; 0.75 cm2/m2) in patients with aortic regurgitation (p = 0.017). A history of congestive heart failure (p = 0.016), small body mass index (p = 0.01), age &gt; 75 years (p = 0.002) and small projected IEOA (p = 0.016) were identified as predictors of impaired QoL.</AbstractText>PPM and small projected IEOA were identified as independent risk factors for impaired mid-term survival and QoL. As the occurrence of PPM was rare in total root replacements, and the implantation procedure did not increase the operative risk in the present patient population, the recommendation is made to consider this implantation technique if a small projected IEOA is expected.</AbstractText>

An experimental method for the percutaneous induction of a posterolateral infarct and functional ischemic mitral regurgitation.

Appropriate experimental models are needed to study the mechanisms underlying left ventricular (LV) remodeling and functional ischemic mitral regurgitation (IMR). Herein is described an original percutaneous method for inducing a well-defined posterolateral infarct and significant IMR.</AbstractText>Under videofluoroscopic guidance, the second (OM2) and third (OM3) obtuse marginal branches of the circumflex artery of six sheep were selectively and sequentially injected with 100% ethyl alcohol. Transthoracic echocardiography (TTE) was performed before and after alcohol injection, and weekly until sacrifice at 8 +/- 1.3 weeks. The LV endsystolic (LVESD) and end-diastolic (LVEDD) dimensions, interpapillary distance (M1-M2), mitral annulus diameter (MA), and degree of IMR and ischemic tricuspid regurgitation (ITR) were measured.</AbstractText>One animal died from irreversible ventricular fibrillation. In the remaining sheep, a well-defined posterolateral infarct of 22% of the heart mass resulted, followed by 2.8 + IMR and 2.1+ ITR. The mean weight gain was 16%, and all sheep showed signs of heart failure. All echocardiographic parameters were increased: systolic MA by 29%, diastolic MA by 18%, LVEDD by 33%, LVESD by 62%, M1-M2 diastolic by 32%, M1-M2 systolic by 21%, and tethering and tenting distances by 32% and 108%, respectively.</AbstractText>The percutaneous selective injection of 100% ethyl alcohol in OM2 and OM3 resulted in a well-defined posterolateral infarct and significant IMR and ITR. Because it was a percutaneous procedure, this novel, simple and reproducible method did not require a thoracotomy. This model should facilitate the further study of LV remodeling and IMR.</AbstractText>

Effects of percutaneous balloon mitral valvuloplasty on plasma B-type natriuretic peptide in rheumatic mitral stenosis with and without atrial fibrillation.

The study aim was to evaluate the effect of percutaneous balloon mitral valvuloplasty (PBMV) on plasma B-type natriuretic peptide (BNP) levels in patients in sinus rhythm (SR) and with atrial fibrillation (AF).</AbstractText>Thirty patients with rheumatic mitral stenosis who underwent successful PBMV were included in the study. Of these patents, 21 were in SR (SR group) and nine had AF (AF group). Plasma BNP levels were measured using the Triage BNP Test in all patients before, and at 20 min and 24 h after, PBMV. Control levels were measured in eight healthy volunteers.</AbstractText>Basal plasma BNP levels in patients were significantly higher than those in controls (123.5 +/- 69.5 versus 16.4 +/- 7.6 pg/ml, p &lt; 0.01), and correlated with mean left atrial pressure (mLAP; r = 0.441, p &lt; 0.05) and pulmonary artery pressure (PAP; r = 0.488, p &lt; 0.01). No significant difference was observed in BNP levels between the SR and AF groups. In the SR group, BNP levels decreased after PBMV (pre-PBMV 128.7 +/- 75.9 pg/ml; at 20 min, 88.6 +/- 62.0 pg/ml; at 24 h, 43.4 +/- 26.7 pg/ml; respectively, p &lt; 0.05). Changes in plasma BNP (deltaBNP) correlated positively with those in mLAP (deltamLAP) (r = 0.696, p &lt; 0.01) and PAP (deltaPAP) (r = 0.456, p &lt; 0.05). Left ventricular end-diastolic volume (LVEDV) (96.1 +/- 21.6 versus 111.5 +/- 25.2 ml, p &lt; 0.01) and stroke volume (SV) (59.2 +/- 15.8 versus 69.0 +/- 17.9 ml, p &lt; 0.05) augmented accordingly without any changes in left ventricular end-diastolic pressure (LVEDP) (p = NS). In contrast, in group AF, BNP levels remained unchanged (pre-PBMV 111.6 +/- 53.4 pg/ml; at 20 min, 122.0 +/- 68.7 pg/ml; at 24 h, 106.1 +/- 56.2 pg/ml; respectively, p = NS), while LVEDP increased (6.4 +/- 3.6 versus 8.6 +/- 3.2 mmHg, p &lt; 0.01), without any changes in LVEDV and SV (p = NS).</AbstractText>The study results indicate that, in mitral stenosis patients, a high BNP level is associated with high mLAP and PAP. Cardiac rhythm may play an important role in changes of BNP level after PBMV. BNP may be a valid marker to reflect changes in mLAP and PAP after PBMV in patients with SR, but not in those with AF.</AbstractText>

The dynamics of cardiac fibrillation.

Reentry occurs when the electrical wave propagating through the atria or ventricles breaks locally and forms a rotor (also called a scroll wave or functional reentry). If the waves propagating outward from a rotor develop additional wavebreaks (which may form new rotors), fibrillation results. Tissue heterogeneity, exacerbated by electrical and structural remodeling from cardiac disease, has traditionally been considered the major factor promoting wavebreak and its degeneration to fibrillation. Recently, however, dynamic factors have also been recognized to play a key role. Dynamic factors refer to cellular properties of the cardiac action potential and Ca(i) cycling, which dynamically generate wave instability and wavebreak, even in tissue that is initially completely homogeneous. Although the latter situation can only be created in computer simulations, its relevance to real (heterogeneous) cardiac tissue has been unequivocally demonstrated. Dynamic factors are related to membrane voltage (Vm) and Ca(i). Vm factors include electrical restitution of action potential duration and conduction velocity, short-term cardiac memory, and electrotonic currents. Ca(i) factors are related to dynamic Ca(i) cycling properties. They act synergistically, as well as with tissue heterogeneity, to promote wavebreak and fibrillation. As global properties, rather than local electrophysiological characteristics, dynamic factors represent an attractive target for novel therapies to prevent ventricular fibrillation.

Interruptions of chest compressions during emergency medical systems resuscitation.

Survival after nontraumatic out-of-hospital (OOH) cardiac arrest in Tucson, Arizona, has been flat at 6% (121/2177) for the decade 1992 to 2001. We hypothesized that interruptions of chest compressions occur commonly and for substantial periods during treatment of OOH cardiac arrest and could be contributing to the lack of improvement in resuscitation outcome.</AbstractText>Sixty-one adult OOH cardiac arrest patients treated by automated external defibrillator (AED)-equipped Tucson Fire Department first responders from November 2001 through November 2002 were retrospectively reviewed. Reviews were performed according to the code arrest record and verified with the AED printout. Validation of the methodology for determining the performance of chest compressions was done post hoc. The median time from "9-1-1" call receipt to arrival at the patient's side was 6 minutes, 27 seconds (interquartile range [IQR, 25% to 75%], 5 minutes, 24 seconds, to 7 minutes, 34 seconds). An additional 54 seconds (IQR, 38 to 74 seconds) was noted between arrival and the first defibrillation attempt. Initial defibrillation shocks never restored a perfusing rhythm (0/21). Chest compressions were performed only 43% of the time during the resuscitation effort. Although attempting to follow the 2000 guidelines for cardiopulmonary resuscitation, chest compressions were delayed or interrupted repeatedly throughout the resuscitation effort. Survival to hospital discharge was 7%, not different from that of our historical control (4/61 versus 121/2177; P=0.74).</AbstractText>Frequent interruption of chest compressions results in no circulatory support during more than half of resuscitation efforts. Such interruptions could be a major contributing factor to the continued poor outcome seen with OOH cardiac arrest.</AbstractText>

KCNH2-K897T is a genetic modifier of latent congenital long-QT syndrome.

Clinical heterogeneity among patients with long-QT syndrome (LQTS) sharing the same disease-causing mutation is usually attributed to variable penetrance. One potential explanation for this phenomenon is the coexistence of modifier gene alleles, possibly common single nucleotide polymorphisms, altering arrhythmia susceptibility. We demonstrate this concept in a family segregating a novel, low-penetrant KCNH2 mutation along with a common single nucleotide polymorphism in the same gene.</AbstractText>The proband is a 44-year-old white woman with palpitations associated with presyncope since age 20, who presented with ventricular fibrillation and cardiac arrest. Intermittent QT prolongation was subsequently observed (max QTc, 530 ms), and LQT2 was diagnosed after the identification of a missense KCNH2 mutation (A1116V) altering a conserved residue in the distal carboxyl-terminus of the encoded HERG protein. The proband also carried the common KCNH2 polymorphism K897T on the nonmutant allele. Relatives who carried A1116V without K897T were asymptomatic, but some exhibited transient mild QTc prolongation, suggesting latent disease. Heterologous expression studies performed in cultured mammalian cells and using bicistronic vectors linked to different fluorescent proteins demonstrated that coexpression of A1116V with K897T together resulted in significantly reduced current amplitude as compared with coexpression of either allele with WT-HERG. Thus, the presence of KCNH2-K897T is predicted to exaggerate the IKr reduction caused by the A1116V mutation. These data explain why symptomatic LQTS occurred only in the proband carrying both alleles.</AbstractText>We have provided evidence that a common KCNH2 polymorphism may modify the clinical expression of a latent LQT2 mutation. A similar mechanism may contribute to the risk for sudden death in more prevalent cardiac diseases.</AbstractText>

Cardiovascular morbidity and mortality in hypertensive patients with lower versus higher risk: a LIFE substudy.

We hypothesized that losartan was superior to atenolol in reducing cardiovascular events in a lower-risk group (LRG) versus a higher-risk group (HRG) of patients in a Losartan Intervention For Endpoint reduction (LIFE) substudy, independently of blood pressure (BP) reduction. In a post hoc analysis, we designated 4282 patients as LRG on the basis of: (1) no previous cardiovascular disease (coronary, cerebral, peripheral vascular disease); (2) no diabetes; (3) no isolated systolic hypertension; and (4) inclusion of the lowest 3 quartiles of electrocardiographically documented left ventricular hypertrophy. The HRG consisted of 4911 remaining patients who did not qualify for the LRG. In the LRG, losartan was superior to atenolol in reducing stroke: hazard ratio (HR), 0.72 (95% confidence interval [CI], 0.53 to 0.98); new-onset diabetes (HR, 0.74 [95% CI, 0.58 to 0.93]; and new-onset atrial fibrillation: HR, 0.69 (95% CI, 0.51 to 0.92), all P&lt;0.05 but not composite end points or cardiovascular mortality (both P=NS). In the HRG, losartan was superior to atenolol in reducing composite end points: HR, 0.82 (95% CI, 0.71 to 0.94), P&lt;0.01; cardiovascular mortality: HR, 0.77 (95% CI, 0.62 to 0.95), P&lt;0.05; stroke: HR, 0.75 (95% CI, 0.61 to 0.92), P&lt;0.01; new-onset diabetes: HR, 0.76 (95% CI, 0.60 to 0.96), P&lt;0.05; and new-onset atrial fibrillation: HR, 0.71 (95% CI, 0.58 to 88), P&lt;0.05. Test for interaction of treatment with LRG versus HRG was not significant for composite end point, stroke, or atrial fibrillation, but was for cardiovascular mortality (P=0.018). Achieved systolic BP reduction favored losartan over atenolol by -1.8 mm Hg in LRG (P=NS) and -0.7 mm Hg (P=0.001) in HRG, but no significant differences occurred in diastolic or mean BP in either group. In conclusion, losartan compared with atenolol reduces the risk of stroke, new-onset diabetes, and new-onset atrial fibrillation in the LRG and the HRG.

Atrial fibrillation impairs cardiac sympathetic response to baroreceptor unloading in congestive heart failure.

In this study, we investigated for a potential mechanism by which atrial fibrillation (AF) might convey a worse prognosis in congestive heart failure (CHF). Specifically, we aimed to determine whether AF impaired cardiac sympathetic response to baroreceptor unloading in comparison to sinus rhythm (SR) in CHF.</AbstractText>Eighteen CHF patients (ejection fraction 30+/-2%, age 59+/- 2 years), nine in SR and nine in AF, were enrolled. A right heart study and cardiac sympathetic tone assessment by coronary sinus catheter were performed at baseline and after 10 min of 20 degrees and 30 degrees of passive head up tilt (HUT). Filling pressures fell significantly during HUT in both SR and AF groups (AF, P=0.002; SR, P&lt;0.001). The cardiac sympathetic response to HUT was significantly attenuated by AF compared with SR (P=0.014). In conjunction, right atrial appendages were collected from 23 cardiac surgery patients, 12 in SR and 11 in AF to investigate the presence of fibrosis. AF was associated with a significant increase in the collagen density (P=0.025).</AbstractText>AF is associated with impaired cardiac sympathetic response to baroreceptor unloading compared with SR in CHF, possibly secondary to atrial fibrosis.</AbstractText>

Increased left atrial volume index is an independent predictor of raised serum natriuretic peptide in patients with suspected heart failure but normal left ventricular ejection fraction: Implication for diagnosis of diastolic heart failure.

Left atrial volume index (LAVI) is increasingly recognised as a relatively load-independent marker of left ventricular (LV) filling pressures. We assessed the capacity of LAVI to predict LV diastolic dysfunction in comparison with N-terminal pro B-type natriuretic peptide (NTproBNP) in patients with suspected heart failure and a normal ejection fraction (EF).</AbstractText>137 patients with suspected heart failure (HF), referred from the community for echocardiography, prospectively underwent Doppler echocardiography, LAVI and NTproBNP estimation. Raised LAVI and reduced LV systolic function were defined as &gt;26 ml/m2 and LV EF &lt;50% respectively.</AbstractText>Of 137 patients, 21 were excluded (2 with significant mitral valve disease and 19 with atrial fibrillation). Of the remaining 116 subjects, 92 showed normal LV systolic function. The univariate predictors of serum log NTproBNP were age (p &lt; 0.001), LA dimension (p = 0.001), LAVI (p &lt; 0.001), A wave (p = 0.001), E:A (p = 0.07) and septal wall thickness (p = 0.004). However on multivariate analysis, LAVI was found to be the most consistent and significant predictor of NTproBNP. The area under the curve of the receiver operating characteristic (ROC) curve for NTproBNP in detecting patients with LVEF &gt; or = 50% and LAVI &gt;26 ml/m2 was 0.81 (p &lt; 0.0001) and for patients with LAVI &gt; 26 ml/m2 with and without LVEF &gt; or = 50% was 0.82 (p &lt; 0.0001).</AbstractText>This data confirms that LAVI on resting echocardiography, specifically in patients with suspected HF and normal LV systolic function is a powerful independent predictor of LV diastolic dysfunction as predicted by serum NTproBNP. In a population with a high suspicion of diastolic heart failure, LAVI may significantly contribute to diagnostic precision.</AbstractText>

Critical mass hypothesis revisited: role of dynamical wave stability in spontaneous termination of cardiac fibrillation.

The tendency of atrial or ventricular fibrillation to terminate spontaneously in finite-sized tissue is known as the critical mass hypothesis. Previous studies have shown that dynamical instabilities play an important role in creating new wave breaks that maintain cardiac fibrillation, but its role in self-termination, in relation to tissue size and geometry, is not well understood. This study used computer simulations of two- and three-dimensional tissue models to investigate qualitatively how, in relation to tissue size and geometry, dynamical instability affects the spontaneous termination of cardiac fibrillation. The major findings are as follows: 1) Dynamical instability promotes wave breaks, maintaining fibrillation, but it also causes the waves to extinguish, facilitating spontaneous termination of fibrillation. The latter effect predominates as dynamical instability increases, so that fibrillation is more likely to self-terminate in a finite-sized tissue. 2) In two-dimensional tissue, the average duration of fibrillation increases exponentially as tissue area increases. In three-dimensional tissue, the average duration of fibrillation decreases initially as tissue thickness increases as a result of thickness-induced instability but then increases after a critical thickness is reached. Therefore, in addition to tissue mass and geometry, dynamical instability is an important factor influencing the maintenance of cardiac fibrillation.

Clinical and electrophysiologic profile of Brugada syndrome in Iranian patients.

Clinical and electrophysiologic characteristics of 20 patients (15 males; mean age, 42 +/- 9 years) with Brugada syndrome were studied. Electrocardiographic abnormalities (spontaneous in 6 and provoked in 14) were recognized in 5 symptomatic and 15 asymptomatic patients. Mean PR (188 +/- 18 vs. 184 +/- 24 ms) and QT (362 +/- 34 vs. 382 +/- 28 ms) intervals and ST-segment elevation (2.28 +/- 0.42 vs. 2.70 +/- 0.77 mm) were similar in both groups. The PR interval was slightly longer in males than females (191 +/- 21 vs.168 +/- 18 ms, p = 0.042), but ST-segment elevation (2.70 +/- 0.78 vs. 2.24 +/- 0.26 mm) was similar. The HV interval was longer in males than females (57 +/- 4 vs. 50 +/- 4 ms, p = 0.047). Ventricular arrhythmias were induced in 40% of asymptomatic patients. There was no significant difference in age, sex, PR interval, ST-segment elevation, or HV interval between inducible and non-inducible patients. A defibrillator was implanted in 8 patients. During 16 +/- 2 months of follow-up, one symptomatic patient had appropriate device therapy. None of the asymptomatic and non-inducible patients experienced a cardiac event. Electrophysiologic data have no role in predicting inducibility in programmed stimulation.

Combined minimally invasive pulmonary vein isolation, left atrial appendage excision and cardiac resynchronization therapy for heart failure: case report.

A 76-year-old male with ischemic cardiomyopathy presented with heart failure symptoms in the absence of angina. Several hospitalizations were required due to heart failure exacerbation and paroxysmal atrial fibrillation. Electrocardiography and tissue synchronization imaging confirmed ventricular dyssynchrony, requiring biventricular pacing. After a failed attempt of percutaneous placement of the left ventricular lead, a novel minimally invasive approach was indicated. It consisted of left ventricular epicardial lead placement, microwave pulmonary vein isolation, and left atrial appendage excision through bilateral minithoracotomies. The postoperative recovery was unremarkable, with reestablishment of the ventricular synchrony and regular rhythm.

De novo KCNQ1 mutation responsible for atrial fibrillation and short QT syndrome in utero.

We describe a genetic basis for atrial fibrillation and short QT syndrome in utero. Heterologous expression of the mutant channel was used to define the physiological consequences of the mutation.</AbstractText>A baby girl was born at 38 weeks after induction of delivery that was prompted by bradycardia and irregular rythm. ECG revealed atrial fibrillation with slow ventricular response and short QT interval. Genetic analysis identified a de novo missense mutation in the potassium channel KCNQ1 (V141M). To characterize the physiological consequences of the V141M mutation, Xenopus laevis oocytes were injected with cRNA encoding wild-type (wt) KCNQ1 or mutant V141M KCNQ1 subunits, with or without KCNE1.</AbstractText>Ionic currents were recorded using standard two-microelectrode voltage clamp techniques. In the absence of KCNE1, wtKCNQ1 and V141M KCNQ1 currents had similar biophysical properties. Coexpression of wtKCNQ1+KCNE1 subunits induced the typical slowly activating and voltage-dependent delayed rectifier K(+) current, I(Ks). In contrast, oocytes injected with cRNA encoding V141M KCNQ1+KCNE1 subunits exhibited an instantaneous and voltage-independent K(+)-selective current. Coexpression of V141M and wtKCNQ1 with KCNE1 induced a current with intermediate biophysical properties. Computer modeling showed that the mutation would shorten action potential duration of human ventricular myocytes and abolish pacemaker activity of the sinoatrial node.</AbstractText>The description of a novel, de novo gain of function mutation in KCNQ1, responsible for atrial fibrillation and short QT syndrome in utero indicates that some of these cases may have a genetic basis and confirms a previous hypothesis that gain of function mutations in KCNQ1 channels can shorten the duration of ventricular and atrial action potentials.</AbstractText>

[Dynamic ECG changes as a result of Brugada syndrome, an overlooked diagnosis?].

Brugada syndrome is a primary electrical disease involving a wide spectrum of phenotypes. The hallmark of Brugada syndrome is the ST elevation in leads V1 to V3. We present three cases of Brugada syndrome. The first patient was diagnosed via routine ECG and a programmed electric stimulation. The second patient was mistakenly diagnosed as having a right coronary occlusion. The last patient had been resuscitated before admittance and received an implantable cardioverter-defibrillator. Treatment of patients with Brugada syndrome is limited by the lack of reliable indicators of risk.

Extreme hyperkalemia.

Hyperkalemia is a potentially fatal condition and is defined by a serum potassium level (K+) of greater than 5.5 mmol/L. The associated prevalence of cardiac arrhythmia increases directly with the degree of hyperkalemia. The danger in the majority of hyperkalemia cases is cardiac dysrhythmia, and often ventricular fibrillation or asystole is the terminating event. Although there are many previous reports addressing this threatening problem and associated therapeutic maneuvers, there have not been many previous reports citing the fatal concentration of hyperkalemia irrespective of the causes. However, it is uniformly accepted that a K+ concentration greater than 10.0 mmol/L is fatal unless urgent treatment is instituted. This report describes a case of nonfatal hyperkalemia of 14 mmol/L with intact survival and complete recovery. Potassium homeostasis is revisited, and some explanations are proffered regarding the protective mechanism against hyperkalemia, including transcellular flux, renal tubular function, and endocrine responses.

The relationship between P wave dispersion and diastolic dysfunction.

We investigated the relationship between P wave dispersion, which is easily measured on the surface electrocardiogram and may be used in evaluating the risk of atrial fibrillation, and left ventricular diastolic function. There were 133 patients: 73 with diastolic dysfunction and 60 without. P wave dispersions were calculated by measuring minimum and maximum P wave duration values on the surface electrocardiogram. The relationships between P wave dispersion and the presence, cause, severity, and echocardiographic measurements of diastolic dysfunction were investigated. P wave dispersion was 53 +/- 9 ms in patients with diastolic dysfunction and 43 +/- 9 ms in the control group (P &lt; 0.01). When patients were grouped according to stage of diastolic dysfunction, P wave dispersion was 48 +/- 7 ms in stage 1, 54 +/- 8 ms in stage 2, and 58 +/- 9 ms in stage 3. As the severity of diastolic dysfunction increased, P wave dispersion increased but the difference did not reach statistical significance (P &lt; 0.05). When the cause of diastolic dysfunction was considered, P wave dispersion was 53 +/- 8 ms in patients with ischemic heart disease and 52 +/- 9 ms in patients with left ventricular hypertrophy (P &gt; 0.05). We conclude that P wave dispersion increases in diastolic dysfunction, but that this increase is not related to the severity or cause of diastolic dysfunction. When clinical and echocardiographic variables are taken into account, there is a weak but significant correlation only between P wave dispersion and left ventricular ejection fraction.

Arrhythmias after orthotopic heart transplantation.

Arrhythmias frequently occur after orthotopic heart transplantation (OHT).</AbstractText>The most common are ventricular premature complexes, atrial premature complexes, sinus or junctional bradycardia, atrial fibrillation, and atrial flutter, all of which have varying clinical significance depending on associated or causative conditions. Unique etiologic factors such as allograft rejection, transplant coronary artery disease, and altered anatomy and autonomic nervous system changes require that arrhythmias be treated differently after OHT compared with the general population.</AbstractText>The potentially severe ramifications of allograft rejection and coronary artery disease make treatment of these disorders in the setting of arrhythmias as important as treating the arrhythmias themselves. At the same time, autonomic denervation and altered anatomy after transplantation complicate drug and device therapies.</AbstractText>

Ablation of ventricular fibrillation and tachycardia.

Catheter ablation therapy for ventricular tachycardia has evolved over the past 20 years to become the first-line therapy. This development has been facilitated by technology that has allowed better anatomic and electrophysiologic correlations. A better understanding of radiofrequency (RF) ablation has led to safer and more effective treatments, allowing it to become a potent diagnostic and therapeutic tool in clinical cardiac electrophysiology. As more knowledge is gained about the mechanisms of arrhythmias through RF ablations, and better mapping technology and more effective methods for energy delivery become available, catheter ablation will become relevant for an increasing number of arrhythmias. This article addresses advances and applications of RF ablation to the treatment of ventricular arrhythmias in a variety of heart diseases.

Controversies in pacing: indications and programming.

This article reviews controversies in cardiac pacing in four areas: methods to prevent unnecessary right ventricular pacing and optimal ventricular pacing sites in the bradycardia population, pacing for prevention of atrial fibrillation (AF), a novel pacing technique for the treatment of heart failure, and pacing for the treatment of sleep apnea. Frequent right ventricular pacing has been reported to increase the incidence of AF and congestive heart failure. However, many patients with pacemakers for bradycardia have intrinsic atrioventricular conduction most of the time. Optimal programming of pacemakers and new algorithms designed to reduce unnecessary ventricular pacing are discussed. Pacing algorithms for prevention of AF have generally been shown to be ineffective. Atrial antitachycardia pacing has been shown to reduce the burden of atrial tachyarrhythmias in selected patients. Cardiac contractility modulation has recently been reported to be a promising new approach to the treatment of heart failure. Some pacing techniques may be effective in the treatment of sleep apnea but larger, long-term clinical trials are required to demonstrate a significant clinical benefit.

Cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) addresses abnormal left ventricular (LV) activation that produces detrimental effects on cardiac systolic and diastolic function. CRT improves symptoms and ventricular performance, promotes reverse remodeling, and decreases mortality and hospitalization in patients with congestive heart failure (CHF). Atrial-synchronized biventricular stimulation reverses many of the temporal delays in mechanical activation associated with LV dysfunction and conduction system disease. The therapy evolved from anecdotal application through surgical implantation of LV pacing leads to transvenous delivery of LV pacing leads for use with dedicated CRT devices. The controlled clinical trials included specific patient groups, and provided data leading to widely adopted indications for the therapy. Current indications exclude the use of CRT in patients with permanent atrial fibrillation, although small series suggest a benefit of the therapy in these patients. The role of cardiac imaging with echocardiography to detect cardiac dyssynchrony promises to improve patient selection by not only excluding likely nonresponders, but also extending the therapy to those with dyssynchrony in the absence of QRS prolongation. Expanded indications under evaluation include the role of CRT in patients with mildly symptomatic CHF, mild to moderate LV dysfunction, dyssynchrony in the absence of QRS prolongation, and dyssynchrony induced by right ventricular pacing.

Randomized double-blind trial of sotalol versus lignocaine in out-of-hospital refractory cardiac arrest due to ventricular tachyarrhythmia.

We aimed to compare the efficacy of sotalol versus lignocaine for the treatment of patients with out-of-hospital ventricular fibrillation refractory to &gt; or = 4 defibrillatory shocks.</AbstractText>The outcome of patients in ventricular fibrillation refractory to &gt; or = 4 defibrillatory shocks is poor. In a previous randomized trial, sotalol was superior to lignocaine for acute termination of ventricular tachycardia not causing loss of consciousness.</AbstractText>Patients of the Ambulance Service of New South Wales treated by paramedics with continued ventricular fibrillation despite standard resuscitation and &gt; or = 4 defibrillatory monophasic shocks were eligible. Drug doses were sotalol 100 mg or lignocaine 100 mg, given as i.v. boluses. A further 2 min of cardiopulmonary resuscitation was given and then defibrillation was repeated twice. If this failed, half the initial dose of the trial drug was repeated and a further &gt; or = 2 shocks were given.</AbstractText>Sixty patients were randomized to sotalol and 69 randomized to lignocaine. There was no significant difference between the two groups in the clinical characteristics of the patients or in the number of shocks received. Outcomes in the sotalol and lignocaine groups were survival to hospital admission in 7 (12%) and 16 (23%), respectively (P = 0.09), and survival to hospital discharge in 2 (3%) and 5 (7%), respectively (P = 0.33).</AbstractText>Sotalol is not superior to lignocaine for treatment of ventricular fibrillation refractory to multiple shocks. The overall outcome of this group of patients is poor regardless of the pharmacological intervention (lignocaine or sotalol).</AbstractText>

Atypical proarrhythmia with dofetilide: monomorphic VT and exercise-induced torsade de pointes.

Proarrhythmia with dofetilide has most typically taken the form of torsade de pointes (TdP) and generally occurs early with therapy, such that in-hospital initiation of dofetilide with 3 days of continuous electrocardiogram monitoring is recommended. This article reports two unusual variants of ventricular proarrhythmia with dofetilide: (1) nonsustained runs of monomorphic ventricular tachycardia shortly after taking the first dose of dofetilide, confirmed by rechallenge; and (2) TdP that followed the development of isolated ventricular premature beats during an exercise test in a patient with neither excessive QT prolongation on dofetilide nor any ectopy whatsoever during in-hospital telemetric monitoring but with significant QT interval prolongation after the postectopic pause. These cases demonstrate that clinicians must be alert to the appearance of proarrhythmia with dofetilide at times other than early during drug initiation if the electrophysiological milieu is altered during nonhospital activity and/or of a pattern other than TdP.

Arrhythmic storm responsive to quinidine in a patient with Brugada syndrome and vasovagal syncope.

A 37-year-old man with Brugada syndrome (BrS) and arrhythmic storm is described. One month after implantation of a cardioverter-defibrillator he presented with recurrent appropriate shocks for spontaneous ventricular fibrillation (VF). Because of this arrhythmic storm, quinidine therapy was initiated with total suppression of all spontaneous arrhythmias. He had remained free of arrhythmias for 22 months since quinidine initiation. Two episodes of VF occurred after the patient stopped taking the medication. The patient resumed quinidine and has been free of VF for the last 3 months. This response to quinidine in a patient with symptomatic BrS supports its role in the prophylaxis of arrhythmic events in BrS.

Bachmann's bundle: does it play a role in atrial fibrillation?

Cardiac anatomists have known the presence of a group of specialized fibers connecting the right and left atrium for years. However, only recently have clinical cardiologists come to recognize the potential importance of this specialized conduction system. Anatomical and microscopic studies have shown that the Bachmann's bundle (BB) represents a distinct structure similar to the atrio-ventricular node and the His-Purkinje conduction system but without any insulating tissue.</AbstractText>BB cells have specialized electrophysiological properties like supernormal excitability and faster longitudinal conduction that can facilitate more rapid impulse transmission compared to the normal atrial tissue. Experimental blockage of this pathway causes prolongation and widening of the P wave, which is associated with an increased incidence of atrial fibrillation. Atrial pacing is effective in reducing the incidence of atrial fibrillation by preventing bradycardia, synchronizing the atria, limiting anisotropy and reducing the dispersion of refractoriness. Various animal and human studies have shown pacing near the right atrial insertion of BB to have a beneficial effect in patients with interatrial conduction delay and atrial tachyarrhythmias. This mode of atrial septal pacing is convenient, safe, reliable, and clinically as effective as multisite pacing.</AbstractText>This article is an effort to define the special properties of BB and its possible role in prevention of atrial fibrillation by permanent pacemakers.</AbstractText>

Temporal relationship of implantable cardioverter defibrillator discharges and environmental physical activity.

Studies by our group have shown an inverse relationship between sudden death and cardiac rhythm disturbances and environmental levels of geomagnetic activity (GMA). The aim of this study was to use the precise data provided by automatic implantable cardioverter defibrillators (ICDs) regarding the onset of ventricular fibrillation and ventricular tachycardia to link these events to GMA level.</AbstractText>The study group included 25 patients (22 men; 22 with ischemic cardiomyopathy) aged 28-81 years in whom an ICD had been implanted between 1995 and 2004. Patients were referred to the cardiac intensive care unit after each event that induced one or more discharges. The number of events and the day on which they occurred were recorded. Data on GMA and other cosmophysical parameters were obtained from the U.S. National Geophysical and Space Service Centers and the Russian Academy of Sciences. GMA levels, graded from I (quiet) to IV (stormy) in the middle latitutes, were recorded for 1974-2003 (10,954 days) and for each day on which an ICD discharge occurred.</AbstractText>A total of 402 discharges were recorded on 137 days during the study period. Forty-six percent of the discharges took place on days of GMA I, compared with 38% - II, 13% - III, and 3% - IV. The daily distribution of GMA was as follows: level I - 35.2%, II - 37.3%, III - 21.86%, IV - 5.61%. Comparison of ICD discharge days and actual multiyear levels of GMA (in percent) yielded a ratio of 1.326 for GMA I, 1.076 - II, 0.459 - III, 0.390 - IV. There was a significant inverse correlation between GMA level and number of discharges (r =-0.97, P = 0.03) and days of treatment (r =-0.96, P = 0.039), and a significant difference between ICD discharges on days of GMA I and GMA II-IV (chi(2)= 5.05, P = 0.02).</AbstractText>The higher number of ICD discharges on days of lowest GMA may be explained by a possible antiarrhythmic effect of GMA. Environmental arrhythmogenic factors that act inversely to GMA may be activated at times of low GMA.</AbstractText>

Clinical and quality of life comparison of accelerometer, piezoelectric crystal, and blended sensors in DDDR-paced patients with sinus node dysfunction in the mode selection trial (MOST).

Permanent pacemakers are capable of increasing heart rate in response to physical activity by a variety of sensors including accelerometers, piezoelectric crystals, or blended sensors. The impact of these different physiologic sensors on cardiovascular events and quality of life is not known.</AbstractText>Of 2,010 patients randomized in the Mode Selection Trial, 1,245 patients were selected with the most commonly used pacemakers with these three sensors. Clinical characteristics and quality of life were compared between groups at baseline, 3 months, and then yearly.</AbstractText>There were 449 patients with an accelerometer sensor device, 682 with a piezoelectric sensor, and 114 with a blended sensor. The groups were similar in terms of age (mean 74 years), gender, and cardiac risk factors but differences existed in weight, heart rate, mitral regurgitation, revascularization history, and drug therapy. The median ventricular pacing frequency was 80% (25th, 75th percentiles 42, 97). After a median follow-up of 33.1 months, the risk of death, heart failure hospitalization, atrial fibrillation, and the combined endpoint of mortality and stroke was not significantly different between the sensor types, after adjustment for baseline differences. Quality of life analyses demonstrated that patients with blended sensors had significantly worse (P &lt; 0.01) physical function than did patients with the other two sensor systems. Moreover, patients receiving blended sensors had the poorest absolute scores, without reaching statistical significance, on 9 of 13 quality of life measures after adjusting for differences in the groups.</AbstractText>We found no significant differences among the three most utilized sensors in clinical endpoints. Those patients who received blended sensors had worse physical function quality of life scores. However, clinical selection of the most sophisticated sensor for the most ill patients cannot be excluded as an explanation of these results.</AbstractText>

[The progress of electrical treatment of arrhythmia].

Described here is the progress of the electrical treatment for arrhythmia during the past half a century. The mechanism, their expression and the principles of electrical treatment for bradycardia, tachycardia and fatal arrhythmia--ventricular fibrillation (VF) are introduced respectively. The current situation and future development of the pacemaker, RF ablation and implantable cardioversion defibrillator are also discussed in the paper.

Incidence and clinical relevance of slow ventricular tachycardia in implantable cardioverter-defibrillator recipients: an international multicenter prospective study.

This study aims to assess the incidence and clinical relevance of slow ventricular tachycardia (VT) and the effectiveness and/or deleterious effects of antitachycardia pacing in slow VT in implantable cardioverter-defibrillator recipients.</AbstractText>This multicenter prospective randomized study included 374 patients (326 men) without prior history of slow VT (&lt;148 bpm) implanted with a dual-chamber implantable cardioverter-defibrillator. Patients had a 3-zone detection configuration: a slow VT zone (101 to 148 bpm), a conventional VT zone (&gt;148 bpm), and a ventricular fibrillation zone. Patients were randomized to a treatment group (n=183) with therapy activated in the slow VT zone or a monitoring group (n=191) with no therapy in the slow VT zone. During follow-up (11 months), 449 slow VTs occurred in 114 patients (30.5% slow VT incidence); 181 VTs (54 patients) occurred in the monitoring group; 3 were readmitted to the hospital; and lightheadedness and palpitations occurred in 4 and 250 (60 patients) in the treatment group treated by antitachycardia pacing (89.8% success rate) and shock delivery (n=2). There were 10 crossovers from the monitoring to treatment group and 3 crossovers from the treatment to monitoring group (P=0.09). Quality of life scores were not different between groups.</AbstractText>Slow VT incidence (&lt;150 bpm) is high (30%) in implantable cardioverter-defibrillator recipients without prior history of slow VT, has limited clinical relevance, and is efficiently and safely terminated by antitachycardia pacing.</AbstractText>

Recurrent ST-segment elevations in a patient without significant coronary disease.

We report a case of recurrent ST-segment elevations totaling 7 times over 3 hours during subtotal gastrectomy and the early postoperative period in a patient with no history of coronary artery disease. Possible contributing factors include cold stimulus, epidural anesthesia, and inadequate depth of anesthesia. The first episode almost resulted in cardiac arrest and was treated with intravenous epinephrine. The second episode was associated with ventricular fibrillation, which was treated with defibrillation and intravenous verapamil. The third to the seventh episodes were successfully treated with intravenous nitrate. The electrocardiographic changes and postoperative coronary angiography were consistent with a clinical diagnosis of coronary artery spasm. This case suggests that coronary artery spasm is capable of occurring repeatedly in a cyclic pattern during perioperative periods.

Computer simulations of successful defibrillation in decoupled and non-uniform cardiac tissue.

The aim of the present study is to investigate the origin and effect of virtual electrode polarization in uniform, decoupled and non-uniform cardiac tissue during field stimulation.</AbstractText>A discrete bidomain model with active membrane behaviour was used to simulate normal cardiac tissue as well as cardiac tissue that is decoupled due to fibrosis and gap junction remodelling. Various uniform and non-uniform electric fields were applied to the external domain of uniform, decoupled and non-uniform resting cardiac tissue as well as cardiac tissue in which spiral waves were induced.</AbstractText>Field stimulation applied on non-uniform tissue results in more virtual electrodes compared with uniform tissue. The spiral waves were terminated in decoupled tissue, but not in uniform, homogeneous tissue. By gradually increasing local differences in intracellular conductivities, the amount and spread of virtual electrodes increased and the spiral waves were terminated.</AbstractText>Fast depolarization of the tissue after field stimulation may be explained by intracellular decoupling and spatial heterogeneity present in normal and pathological cardiac tissue. We demonstrated that termination of spiral waves by means of field stimulation can be achieved when the tissue is modelled as a non-uniform, anisotropic bidomain with active membrane behaviour.</AbstractText>

Effects of antiarrhythmic drug therapy on atrioventricular nodal function during atrial fibrillation in humans.

To assess the effects of metoprolol and amiodarone on atrial and ventricular activity during atrial fibrillation (AF) in post-surgical patients, and to develop and use a mathematical model of the atrioventricular (AV) node during AF that incorporates parameters describing the properties of the AV node to evaluate the physiological basis of the drug effects.</AbstractText>Ten post-surgical patients were evaluated where three received no medical therapy, three received metoprolol, three received amiodarone, and one received both metoprolol and amiodarone. The medications led to increases of 37-310 ms in the mean VV interval in treated patients, but much smaller changes in the mean AA intervals in the right and left atria. The mathematical model incorporating a random influence of the concealed conduction parameter was capable of reproducing the histograms of the VV intervals based on the input from the right atrium by systematically searching parameter space.</AbstractText>Changes in the ventricular rate are mainly due to the alteration in the AV nodal properties rather than changes in the atrial rhythm. The medications can display differential effects on the physiological properties of the AV node, and therefore the mathematical model may help to identify novel pharmacological targets.</AbstractText>

Mechanisms for the maintenance of ventricular fibrillation: the nonuniform dispersion of refractoriness, restitution properties, or anatomic heterogeneities?

The relative importance of nonuniform dispersion of refractoriness, steep restitution slopes, and anatomic heterogeneities in causing conduction block during ventricular fibrillation (VF) remains unknown.</AbstractText>In six open-chest pigs, ventricular refractoriness and restitution curves were estimated from activation recovery intervals (ARIs) calculated from 504 (21 x 24) unipolar electrode recordings 2 mm apart in a plaque sutured to the left ventricular (LV) free wall. A steady-state restitution protocol was performed twice at each of two pacing sites: the LV base and near the left anterior descending artery. VF was electrically induced four times and the incidence of conduction block at each electrode during the first 20 seconds was determined by an automated algorithm. The gradient of the ARI was calculated at each electrode to estimate the spatial dispersion of refractoriness. An exponential curve was fit to the restitution plots of ARIs versus the corresponding diastolic intervals (DIs) for all pacing cycle lengths at each electrode. The locations of epicardial blood vessels were noted after the study. Spatial patterns of conduction block were significantly correlated between the four VF episodes in the same animal (r = 0.66 +/- 0.07, P &lt; 0.05). At the shortest pacing cycle length, the spatial distribution of ARIs, ARI gradients, and restitution slopes was not random but formed clusters of similar values. However, none of these variables was significantly correlated with the incidence of conduction block, even though ARI gradients &gt;2 msec/mm were present between many clusters and approximately 90% of restitution slopes were &gt;1. Instead, conduction block frequently appeared to cluster along epicardial vessels.</AbstractText>Neither the dispersion of refractoriness nor action potential duration restitution determined during rapid pacing by itself is the major determinant of the location of conduction block during early VF in normal pigs. It may be that these factors interact synergistically with each other as well as with other factors, including anatomic heterogeneities such as those caused by blood vessels, which may be particularly important for the formation of conduction block and maintenance of VF.</AbstractText>

Enhanced coagulation activation by in vitro lipopolysaccharide challenge in patients with ventricular fibrillation complicating acute myocardial infarction.

Indicators of coagulation and inflammation are elevated in patients with coronary heart disease. A role of coagulation activation in ventricular fibrillation during acute myocardial infarction has not been described.</AbstractText>Whole blood samples of 21 patients with a history of acute myocardial infarction complicated by ventricular fibrillation and whole blood samples of 18 patients without ventricular fibrillation were incubated with lipopolysaccharide (LPS). In both groups, the in vitro blood coagulation time was measured with the ReoRox, a viscometric whole blood coagulometer. CD62P expression on platelets, tissue-factor binding on monocytes, and platelet-monocyte aggregates were measured with flow cytometry. Without LPS, no difference in the coagulation times were observed in both patient groups. After incubation with LPS, patients with a history of ventricular fibrillation showed a significantly decreased coagulation time compared to patients without ventricular fibrillation. The decrease of coagulation time after incubation with LPS also differed significantly in both groups. Expression of CD62P on platelets was significantly higher in patients with a history of ventricular fibrillation after incubation with LPS. Although in each patient group incubation with LPS induced a significantly increased amount of tissue factor on monocytes and a significantly increased the number of platelet-monocyte aggregates, the two groups did not differ significantly concerning tissue factor binding on monocytes and the amount of platelet-monocyte aggregates.</AbstractText>After in vitro LPS challenge, patients with a history of ventricular fibrillation during myocardial infarction show an enhanced coagulation activation, which may partly be due to an enhanced platelet activation.</AbstractText>

Comparison of induced and spontaneous atrial tachyarrhythmias in patients with a history of spontaneous atrial tachyarrhythmias.

This retrospective study investigated whether induced episodes could be used to predict the morphology of future spontaneous atrial episodes.</AbstractText>Eighty-two patients (64 +/- 12 years; 77% male; CAD in 60%; left ventricular ejection fraction 45 +/- 16%) with a history of atrial tachycardia or atrial fibrillation (AT/AF) were implanted with a dual-chamber implantable cardioverter defibrillator (ICD) and followed for 6 months. A total of 224 episodes of induced and spontaneous AT/AF were classified into type I, II, and III according to the method of Israel et al. and then compared based on average cycle length (CL) and atrial amplitude. Episodes were also grouped as "pace-terminable" or "nonpace-terminable" based on the CL definition of Gillis et al.</AbstractText>The analysis of 121 induced episodes (from 80 patients) and 103 spontaneous episodes (from 43 patients) showed that within each arrhythmia type, there were no significant differences in CL or mean amplitude between induced and spontaneous episodes. Additional analysis of patients that had both induced and spontaneous episodes (n = 41) showed 78% had at least one spontaneous episode that matched the induced episode. Fifty-seven percent of spontaneous episodes were considered to be pace-terminable based on CL.</AbstractText>Our data suggest that there is no significant difference between induced and spontaneous episodes of AT/AF of the same type. The majority of patients had at least one spontaneous episode of the same type as the induced episode, showing that induced atrial arrhythmias may be useful in predicting the morphology of future spontaneous episodes and in identifying patients potentially benefiting from atrial antitachycardia pacing.</AbstractText>

Multicenter, prospective, randomized safety and efficacy study of a new atrial-based managed ventricular pacing mode (MVP) in dual chamber ICDs.

Ventricular desynchronization caused by right ventricular pacing may impair ventricular function and increase risk of heart failure (CHF), atrial fibrillation (AF), and death. Conventional DDD/R mode often results in high cumulative percentage ventricular pacing (Cum%VP). We hypothesized that a new managed ventricular pacing mode (MVP) would safely provide AAI/R pacing with ventricular monitoring and DDD/R during AV block (AVB) and reduce Cum%VP compared to DDD/R.</AbstractText>MVP RAMware was downloaded in 181 patients with Marquis DR ICDs. Patients were initially randomized to either MVP or DDD/R for 1 month, then crossed over to the opposite mode for 1 month. ICD diagnostics were analyzed for cumulative percentage atrial pacing (Cum%AP), Cum%VP, and duration of DDD/R pacing for spontaneous AVB.</AbstractText>Baseline characteristics included age 66 +/- 12 years, EF 36 +/- 14%, and NYHA Class II-III 36%. Baseline PR interval was 190 +/- 53 msec and programmed AV intervals (DDD/R) were 216 +/- 50 (paced)/189 +/- 53 (sensed) msec. Mean Cum%VP was significantly lower in MVP versus DDD/R (4.1 +/- 16.3 vs 73.8 +/- 32.5, P &lt; 0.0001). The median absolute and relative reductions in Cum%VP during MVP were 85.0 and 99.9, respectively. Mean Cum%AP was not different between MVP versus DDD/R (48.7 +/- 38.5 vs 47.3 +/- 38.4, P = 0.83). During MVP overall time spent in AAI/R was 89.6% (intrinsic conduction), DDD/R 6.7% (intermittent AVB), and DDI/R 3.7% (AF). No adverse events were attributed to MVP.</AbstractText>MVP safely achieves functional atrial pacing by limiting ventricular pacing to periods of intermittent AVB and AF in ICD patients, significantly reducing Cum%VP compared to DDD/R. MVP is a universal pacing mode that adapts to AVB and AF, providing both atrial pacing and ventricular pacing support when needed.</AbstractText>

Dose response curves for microwave ablation in the cardioplegia-arrested porcine heart.

Microwave ablation has been used clinically for the surgical treatment of atrial fibrillation, particularly during valve procedures. However, dose- response curves have not been established for this surgical environment. The purpose of this study was to examine dosimetry curves for the Flex 4 and Flex 10 microwave devices in an acute cardioplegia-arrested porcine model.</AbstractText>Twelve domestic pigs (40-45 kg) were acutely subjected to Flex 4 (n = 6) and Flex 10 (n = 6) ablations. On a cardioplegically arrested heart maintained at 10-15(o)C, six endocardial atrial and seven epicardial ventricular lesions were created in each animal. Ablations were performed for 15 s, 30 s, 45 s, 60 s, 90 s, 120 s, and 150 s (65 W, 2.45 GHz). The tissue was stained with 2,3,5-triphenyl-tetrazolium chloride and lesions were sectioned at 5 mm intervals. Lesion depth and width were determined from digital photomicrographs of each lesion (resolution +/- .03 mm).</AbstractText>Average atrial thickness was 2.88 +/- .4 mm (range 1.0 to 8.0 mm). 94% of ablated atrial sections created by the FLEX 4 (n = 16) and the FLEX 10 (n = 16) were transmural at 45 seconds. 100% of atrial sections were transmural at 90 seconds with the FLEX 10 (n = 14) and at 60 seconds with the Flex 4 device (n = 15). Lesion width and depth increased with duration of application.</AbstractText>Both devices were capable of producing transmural lesions on the cardioplegically arrested heart at 65 W. These curves will allow surgeons to ensure transmural ablation by tailoring energy delivery to the specific atrial geometry.</AbstractText>

Phase singularities and filaments: simplifying complexity in computational models of ventricular fibrillation.

In the whole heart, millions of cardiac cells are involved in ventricular fibrillation (VF). Experimental studies indicate that VF is sustained by re-entrant activity, and that each re-entrant wave rotates around a filament of phase singularity. Filaments act as organising centres, and offer a way to simplify and quantify the complex spatio-temporal behaviour observed in VF. Where a filament touches the surface of fibrillating myocardium re-entrant activity can be observed, however the behaviour of filaments within bulk ventricular myocardium is difficult to observe directly using present experimental techniques. Large scale computational simulations of VF in three-dimensional (3D) tissue offer a tool to investigate the properties and behaviour of filaments, and the aim of this paper is to review recent advances in this area as well as to compare recent computational studies of fibrillation in whole ventricle geometries.

Entrainment of the natural pacemakers of the heart precedes atrial fibrillation.

A new measure of heart rate variability is proposed to investigate the interaction of the sino-atrial (SA) and atrio-ventricular (AV) pacemakers. Using electrocardiogram (ECG) fiduciary markers corresponding to the depolarization time of the SA and AV pacemakers, the variability of SA and AV depolarization rate is jointly analyzed by spectral analysis. The result of this joint analysis provides evidence of a distinct pattern of interaction between the SA and AV nodes prior to the onset of paroxysmal atrial fibrillation (PAF): frequency entrainment between the primary and secondary pacemakers of the heart, occurring at the respiratory frequency. We propose a measure of this entrainment as a diagnostic indicator for PAF, and compare it to standard diagnostic measures. The entrainment measure is found to have greater diagnostic power than five other common ECG-derived measures.

Antiarrhythmic effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia/reperfusion injury in rats.

The present study was designed to determine the antiarrhythmic effect of caffeic acid phenethyl ester (CAPE), an active component of propolis, which exhibits antioxidant properties, in rats subjected to myocardial ischemia and ischemia-reperfusion (I/R) injury.</AbstractText>Rats were subjected to 30 min coronary artery occlusion for evaluating the effect of CAPE on the myocardial ischemia injury. While in the myocardial I/R injury study, the coronary artery was ligated for a 5-min period of ischemia followed by a 30-min period of reperfusion. Animals were pretreated with or without CAPE before coronary artery ligation and the severity of myocardial ischemia- and I/R-induced arrhythmias and mortality were compared.</AbstractText>Pretreatment of CAPE (0.1 and 1 microg/kg) not only reduced both the incidence and duration of ventricular tachycardia (VT) and ventricular fibrillation (VF) but also decreased the mortality during the myocardial ischemia and I/R injury period.</AbstractText>Our results suggest that CAPE is a potent antiarrhythmic agent with cardioprotective effects in myocardial ischemia and I/R injury rats.</AbstractText>

Prevalence and clinical significance of left atrial remodeling in competitive athletes.

In the present study we assessed the distribution and clinical significance of left atrial (LA) size in the context of athlete's heart and the differential diagnosis from structural heart disease, as well as the proclivity to supraventricular arrhythmias.</AbstractText>The prevalence, clinical significance, and long-term arrhythmic consequences of LA enlargement in competitive athletes are unresolved.</AbstractText>We assessed LA dimension and the prevalence of supraventricular tachyarrhythmias in 1,777 competitive athletes (71% of whom were males), free of structural cardiovascular disease, that were participating in 38 different sports.</AbstractText>The LA dimension was 23 to 50 mm (mean, 37 +/- 4 mm) in men and 20 to 46 mm (mean, 32 +/- 4 mm) in women and was enlarged (i.e., transverse dimension &gt; or = 40 mm) in 347 athletes (20%), including 38 (2%) with marked dilation (&gt; or = 45 mm). Of the 1,777 athletes, only 14 (0.8%) had documented, symptomatic episodes of either paroxysmal atrial fibrillation (n = 5; 0.3%) or supraventricular tachycardia (n = 9; 0.5%), which together occurred in a similar proportion in athletes with (0.9%) or without (0.8%; p = NS) LA enlargement. Multivariate regression analysis showed LA enlargement in athletes was largely explained by left ventricular cavity enlargement (R2 = 0.53) and participation in dynamic sports (such as cycling, rowing/canoeing) but minimally by body size.</AbstractText>In a large population of highly trained athletes, enlarged LA dimension &gt; or = 40 mm was relatively common (20%), with the upper limits of 45 mm in women and 50 mm in men distinguishing physiologic cardiac remodeling ("athlete's heart") from pathologic cardiac conditions. Atrial fibrillation and other supraventricular tachyarrhythmias proved to be uncommon (prevalence &lt; 1%) and similar to that in the general population, despite the frequency of LA enlargement. Left atrial remodeling in competitive athletes may be regarded as a physiologic adaptation to exercise conditioning, largely without adverse clinical consequences.</AbstractText>

The dubious value of echocardiographic and plasma ANP measurements in predicting outcome of cardioversion in patients with persistent atrial fibrillation.

Atrial fibrillation (AF) is a common arrhythmia with important therapeutic and prognostic implications. An attempt to restore sinus rhythm is considered in most patients with AF. The aim of this study was to assess the value of echocardiographic examination and plasma atrial natriuretic peptide (ANP) evaluation in predicting the outcome of cardioversion and maintenance of sinus rhythm in patients with persistent AF.</AbstractText>Eighty-one consecutive patients, aged 62+/-9 years, with AF of duration 4.7 months were subjected to an echocardiography examination and ANP assessment before cardioversion. The patients were predominantly hypertensive men with moderately enlarged left atrium and ejection fraction of left ventricle of about 50%. All patients were in controlled AF and had normalized blood pressure. In order to predict the outcome of cardioversion, and maintenance of sinus rhythm over a 1 month period, a multivariate logistic regression method was performed using the following variables: left atrial and left ventricular dimensions, left ventricular ejection fraction and plasma ANP levels.</AbstractText>Sixty-nine out of the 81 patients were successfully converted to sinus rhythm. At 1 month 57 patients remained in sinus rhythm. There were no statistical differences between sinus rhythm and AF group in baseline ANP levels (59.4 vs 64.2 pg/ml, consecutively), clinical and echocardiographic characteristics. In logistic regression analysis neither baseline echocardiographic variable nor ANP level, predicts successful cardioversion over a 1-month period of observation.</AbstractText>Echocardiographic data and ANP level should not be included as an important variable when considering patients for cardioversion.</AbstractText>

Somatosensory and brainstem auditory evoked potentials in cardiac arrest patients treated with hypothermia.

To evaluate the prognostic value of short-latency median nerve somatosensory evoked potentials and brainstem auditory evoked potentials in outcome prediction for comatose cardiac arrest patients treated with hypothermia.</AbstractText>Prospective, randomized, controlled trial of mild hypothermia after out-of-hospital cardiac arrest; a substudy of the European Hypothermia After Cardiac Arrest study.</AbstractText>Intensive care unit of a tertiary referral hospital (Helsinki University Central Hospital).</AbstractText>Sixty consecutive patients (aged 18-75 yrs) resuscitated from out-of-hospital ventricular fibrillation and comatose at 24 hrs after cardiac arrest; all patients were randomly assigned either to therapeutic hypothermia of 33 degrees C or normothermia.</AbstractText>All patients received standard intensive care for at least 2 days. Patients randomized to hypothermia were cooled with an external cooling device for 24 hrs and then allowed to rewarm slowly for 12 hrs. In the normothermia group, the core temperature was kept below 38 degrees C with antipyretics and by physical means. The clinical outcome was assessed 6 months after cardiac arrest.</AbstractText>Somatosensory evoked potentials and brainstem auditory evoked potentials were recorded 24-28 hrs after cardiac arrest. All wave latencies were significantly prolonged in the hypothermia group. Bilaterally absent N20 waves predicted permanent coma with a specificity of 100% in both treatment groups. Brainstem auditory evoked potential recordings did not correlate with the outcome in either treatment group.</AbstractText>The prognostic ability of median nerve short-latency somatosensory evoked potentials does not seem to be affected by therapeutic hypothermia. Brainstem auditory evoked potentials had no additional value in outcome prediction.</AbstractText>

Effect of transthoracic shocks on left ventricular function.

Although defibrillating shocks are thought to depress ventricular function transiently, the independent effects of high strength shocks (without the metabolic sequelae of pre-shock fibrillation) have not been assessed systematically in humans. Therefore, we delivered three consecutive synchronized monophasic transthoracic shocks (200, 200 and 360 J) at 60s intervals during sinus rhythm and evaluated the effect on left ventricular chamber size and function as determined by transesophageal echocardiography in 11 patients (mean age 67+/-8 years, 9M/2F) with depressed left ventricular function (left ventricular ejection fraction: 14-37%). The shocks did not alter hemodynamics consistently. On average, the shocks did not alter stroke volume, cardiac output, left ventricular ejection fraction or regional wall thickening (all p&gt;0.05 versus baseline). This effect was highly variable and 36% of patients experienced a &gt;25% reduction in cardiac output by the final shock. There was a tendency for regional wall thickening to worsen in the best baseline sextant with an offsetting significant increase in thickening in the worst baseline sextant (p=0.05). Thus, repetitive defibrillation strength transthoracic shocks do not impair left ventricular function consistently in patients with cardiomyopathy. However, the effect is widely variable and potentially important depression of left ventricular function does occur in some patients.

Survival of a neurologically intact patient with subarachnoid hemorrhage and cardiopulmonary arrest.

Subarachnold hemorrhage (SAH) is a relatively common cause of cardiopulmonary arrest (CPA). Long-term survival with SAH and CPA is rare, and the vast majority of those who survive have moderate to severe neurologic disability. To our knowledge, there are no prior reports of patients with SAH who experience CPA and survive without neurologic deficit. We describe a patient with SAH who experienced CPA shortly after hospital admission and survived without neurologic sequelae (Cerebral Performance Category 1). Prompt defibrillation of SAH-induced ventricular fibrillation and timely neurologic intervention are essential for good neurologic outcome.

B-type natriuretic peptide as a biomarker beyond heart failure: speculations and opportunities.

Cardiac secretion of B-type natriuretic peptide (BNP) Increases with the progression of heart failure (HF), and plasma measurement of BNP has emerged recently as a useful, cost-effective biomarker for the diagnosis and prognosis of HF. The diagnostic utility of BNP is complemented by its therapeutic use in decompensated HF. Although clinical use of BNP as a biomarker in HF is Increasing, the specificity of BNP for HF is not robust, suggesting that other mechanisms beyond simple ventricular stretch stimulate BNP release. Several studies have shown that BNP levels Increase in other cardiovascular disease states including ischemia, arrhythmias, fibrosis, cardiac hypertrophy, and coronary endothelial dysfunction. Furthermore, 2 important studies revealed recently that moderate elevations In BNP level, well below the HF range, have prognostic value for future cardiovascular events. Specifically, BNP levels greater than 20 pg/mL were associated with significantly Increased risk of HF and atrial fibrillation. These observations increase speculation that elevated BNP levels represent a final common pathway for many cardiovascular pathologic states and that BNP can be used as a biomarker for non-HF mechanisms, preclinical disease, and other pathologic states of myocardial disease.

Cytotoxic actions of palytoxin on aortic smooth muscle cells in culture.

Palytoxin (PTX), isolated from a zoanthid of the genus Palythoa, is the most potent marine toxin known. Intoxication by PTX leads to vasoconstriction, hemorrhage, ataxia, muscle weakness, ventricular fibrillation, pulmonary hypertension, ischemia and death. In this study, clonal A7r5 rat aortic smooth muscle cells were used to study the mechanism of PTX-mediated cytotoxicity. A7r5 cells exposed to PTX for &gt; or = 15 min exhibited surface granularities, vacuoles and rounding. These alterations culminated in a loss of viability as indicated by marked increases in the release of lactate dehydrogenase. Electrophysiological recording from A7r5 cells disclosed a profound membrane depolarization and an increase in conductance to Na+ and K+. PTX-mediated cytotoxicity could not be reversed by washout or by the addition of 10 microM verapamil but was antagonized by 100 microM ouabain or by removal of extracellular Na+ or Ca2+. In light of the involvement of vascular smooth muscle in PTX poisoning, A7r5 cells could serve as a useful model to test specific drugs for treatment of PTX intoxication.

Machine and operator performance analysis of automated external defibrillator utilization.

The availability of an automated external defibrillator (AED) can improve the outcome of patients with out-of-hospital cardiac arrest (OHCA). On June 1, 2000, Taipei City became the first city in Taiwan to equip emergency medical services personnel with AEDs. This study was conducted to assess the performance of the AED machine in detecting ventricular fibrillation (VF) and ventricular tachycardia (VT) in the population, and to assess operator performance in its use.</AbstractText>AED use in OHCA patients was assessed over a 1-year period. Electrocardiography and voice records retrieved from AED data cards were analyzed. A shockable rhythm was defined as either VF or VT. AED machine performance was assessed based on the correct identification of these rhythms. Operator performance was evaluated according to American Heart Association guidelines.</AbstractText>A total of 978 AED rhythm analyses were obtained for 653 OHCA patients. The sensitivity and specificity for detecting shockable rhythms by the AED machine were 90.0% (95% confidence interval [CI], 85.3% to 93.3%) and 100% (95% CI, 99.5% to 100%), respectively. Sensitivity for coarse VF, fine VF, rapid VT, and slow VT was 97.5%, 74.2%, 63.6% and 60.0%, respectively. An AED was deployed in 18 non-OHCA patients and in 119 patients after they had been moved into the ambulance. Non-compliance with standard procedures occurred during AED use in 162 patients, including interference of movement by cardiopulmonary resuscitation (CPR) in progress in 69, untimely machine turn-off in 49, leads fell off or disconnected in 33, failure of shock delivery after charge in 28, and interference of movement other than CPR in 22.</AbstractText>This study found that the AED machine has high specificity and high sensitivity in detecting VF and VT, especially coarse VF. Efforts are needed to improve the timing of AED deployment and emergency medical technician compliance with standard procedures.</AbstractText>

Elimination of spiral chaos by pulse entrainment in the Aliev-Panfilov model.

Pulse entrainment between two excitatory media is studied in the Aliev-Panfilov model. We show that a spiral chaos in the continuous excitatory medium can be eliminated by a grid network using the pulse entrainment. This mechanism may be applied to the cardiac system, where the ventricular fibrillation is interpreted as the spiral chaos and the Purkinje fibers act as the grid network.

Dynamics of conduction blocks in a model of paced cardiac tissue.

We study numerically the dynamics of conduction blocks using a detailed electrophysiological model. We find that this dynamics depends critically on the size of the paced region. Small pacing regions lead to stationary conduction blocks while larger pacing regions can lead to conduction blocks that travel periodically towards the pacing region. We show that this size-dependence dynamics can lead to a novel arrhythmogenic mechanism. Furthermore, we show that the essential phenomena can be captured in a much simpler coupled-map model.

Selected controversies in cardiopulmonary resuscitation.

Cardiopulmonary resuscitation (CPR) is performed frequently by paramedics, emergency department personnel, and inpatient physicians. Unfortunately, after more than 40 years of practice and study, there are still many controversies and unresolved treatment issues. This article focuses on four current controversies in CPR: (1) the role of end-tidal CO2 (ETCO2) detection, (2) the use of bicarbonate, (3) whether epinephrine is the optimal alpha agonist, and (4) whether amiodarone should replace lidocaine as the initial antiarrhythmic of choice in the treatment of ventricular fibrillation.

Myosin heavy chain composition and the economy of contraction in healthy and diseased human myocardium.

Changes in myosin heavy chain (MHC) isoform expression and protein composition occur during cardiac disease and it has been suggested that even a minor shift in MHC composition may exert a considerable effect on myocardial energetics and performance. Here an overview is provided of the cellular basis of the energy utilisation in cardiac tissue and novel data are presented concerning the economy of myocardial contraction in diseased atrial and ventricular human myocardium. ATP utilisation and force development were measured at various Ca(2+) concentrations during isometric contraction in chemically skinned atrial trabeculae from patients in sinus rhythm (SR) or with chronic atrial fibrillation (AF) and in ventricular muscle strips from non-failing donor or end-stage failing hearts. Contractile protein composition was analysed by one-dimensional gel electrophoresis. Atrial fibrillation was accompanied by a significant shift from the fast alpha-MHC isoform to the slow beta-MHC isoform, whereas both donor and failing ventricular tissue contained almost exclusively the beta-MHC isoform. Simultaneous measurements of force and ATP utilisation indicated that economy of contraction is preserved in atrial fibrillation and in end-stage human heart failure.

Assessment of potential cardiotoxic side effects of mitoxantrone in patients with multiple sclerosis.

Previous studies showed that mitoxantrone can reduce disability progression in patients with multiple sclerosis (MS). There is, however, concern that it may cause irreversible cardiomyopathy with reduced left ventricular (LV) ejection fraction (EF) and congestive heart failure. The aim of this prospective study was to investigate cardiac side effects of mitoxantrone by repetitive cardiac monitoring in MS patients. The treatment protocol called for ten courses of a combined mitoxantrone (10 mg/m(2) body surface) and methylprednisolone therapy. Before each course, a transthoracic echocardiogram was performed to determine the LV end-diastolic diameter, the end-systolic diameter and the fractional shortening; the LV-EF was calculated. Seventy-three patients participated (32 males; age 48 +/- 12 years, range 20-75 years; 25 with primary progressive, 47 with secondary progressive and 1 with relapsing-remitting MS) who received at least four courses of mitoxantrone. Three of the 73 patients were excluded during the study (2 patients discontinued therapy; 1 patient with a previous history of ischemic heart disease developed atrial fibrillation after the second course of mitoxantrone). The mean cumulative dose of mitoxantrone was 114.0 +/- 33.8 mg. The mean follow-up time was 23.4 months (range 10-57 months). So far, there has been no significant change in any of the determined parameters (end-diastolic diameter, end-systolic diameter, fractional shortening, EF) over time during all follow-up investigations. Mitoxantrone did not cause signs of congestive heart failure in any of the patients. Further cardiac monitoring is, however, needed to determine the safety of mitoxantrone after longer follow-up times and at higher cumulative doses.

Echocardiographic ejection fraction in patients with acute heart failure: correlations with hemodynamic, clinical, and neurohormonal measures and short-term outcome.

Although echocardiographic ejection fraction (EF) is frequently used for the estimation of left ventricular contractility in patients with acute heart failure, its exact role and correlations with clinical, hemodynamic, and neurohormonal variables of cardiac contractility is not known.</AbstractText>Patients (343) with acute heart failure, enrolled into two prospective placebo-controlled hemodynamic studies of tezosentan, and in whom EF was available at baseline, were included. Outcome was evaluated in a subset of 94 patients who were enrolled in the placebo arms of the studies.</AbstractText>Higher echocardiographic EF was correlated with older age, increased incidence of hypertension and atrial fibrillation, and female gender. We observed weak correlation between EF and cardiac output or cardiac power and no correlation with wedge pressure, and the change in hemodynamic variables over time. Higher EF was correlated with more baseline leukocytosis and higher plasma levels of endothelin-1 and blood urea nitrogen, while lower EF was related to higher baseline B-type natriuretic peptide (BNP). We observed no overall correlations between EF and outcome.</AbstractText>In patients with acute heart failure, echocardiographic EF is weakly correlated with hemodynamic measures of left ventricular contractility and outcome; hence, it should be interpreted cautiously when evaluating patients admitted due to acute heart failure.</AbstractText>

Brady-tachy syndrome: rapid atrial pacing efficacy in preventing atrial fibrillation recurrence assessed by reliable electrograms: the prefib pilot study.

Recent studies have tested different atrial pacing rates, modes, and sites for preventing atrial fibrillation (AF) recurrence. Present generation pacemakers offer reliable electrograms (EGMs) storage for optimizing the arrhythmia diagnosis. Based on these EGMs, the study objective was to assess the rate of AF recurrence at two different pacing rates.</AbstractText>Thirty patients suffering exclusively from symptomatic brady-tachy syndrome (BTS) resistant to &gt; or =2 drugs, were implanted with a DDDR pacemaker. After a 5-days observation period, the DDD pacing rate was randomly programmed at 60 bpm (-15 bpm hysteresis) or at 80 bpm for 12 weeks. The two sequences were crossed over at the end of this fixed period or when earlier symptomatic AF recurred. Antiarrhythmics were maintained. Stored EGMs of &gt; or =4 s duration identified all AF recurrence.</AbstractText>Thirty patients (17 males, 77.2 +/- 8.1 years old) were included. One patient withdrew prematurely for severe heart failure associated with AF recurrence and rapid ventricular response. For the remainder of the 29 patients, fast atrial pacing neither provoked symptoms nor haemodynamic change. AF recurred in 16 patients paced at 60 (-15) bpm (mean time: 29 days; range 1-61) and in 9 patients paced at 80 bpm (mean time: 55 days; range 5-83) (P &lt; 0.05). AF recurrence was asymptomatic in 50% of patients.</AbstractText>These results confirm that rapid atrial pacing is 1) significantly effective for preventing AF recurrence in symptomatic BTS patients, and 2) haemodynamically well tolerated.</AbstractText>

Rate stabilization by right ventricular apex or His bundle pacing in patients with atrial fibrillation.

In patients with atrial fibrillation right ventricular pacing can block antegrade conduction at pacing intervals longer than the shortest spontaneous R-R interval, causing the stabilization of ventricular rhythm. In this study the effects of pacing at two sites were compared in order to evaluate the role of conduction times in determining the stabilization of ventricular rhythm.</AbstractText>In eight patients with permanent atrial fibrillation, the ventricular rate was recorded before and during pacing at the right ventricular apex and the His bundle with different cycle lengths.</AbstractText>In all patients, we obtained a reduction in spontaneous QRS complexes with respect to those anticipated at pacing rates slightly above the spontaneous mean rate, and the ventricular rhythm stabilized at pacing intervals longer than the spontaneous shortest R-R intervals. Between pacing sites we did not observe any difference in the reduction in spontaneous beats and the cycle stabilizing the rhythm. Moreover, simulation of the interaction between antegrade and retrograde impulses in a computer model confirmed that results obtained by pacing at the His bundle cannot be readily explained as a consequence of conduction delays.</AbstractText>This study suggests that the lag introduced by the His-Purkinje conduction cannot explain, as proposed, the stabilization of ventricular rhythm observed in patients with atrial fibrillation and right ventricular pacing.</AbstractText>

Surgical management of Ebstein's anomaly in the adult.

Ebstein's anomaly is a rare cardiac malformation that affects the tricuspid valve, right ventricle, and right atrioventricular junction. These anatomical and functional abnormalities cause important tricuspid regurgitation that results in right atrial and right ventricular dilatation and atrial and ventricular arrhythmias. Diagnosis is made by echocardiography. Operation includes tricuspid valve repair or replacement, closure of any interatrial communications, and appropriate antiarrhythmia procedures. Repair of Ebstein's anomaly eliminates right-to-left intracardiac shunting, improves exercise tolerance and functional class, and reduces supraventricular arrhythmias. In addition, quality of life and longevity are improved.

Mechanism of sudden cardiac death in pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy.

Pigs with viable chronically dysfunctional myocardium and ischemic cardiomyopathy are at high risk of sudden cardiac death (SCD). We sought to identify the arrhythmic mechanism of SCD, the relation to changes in left ventricular (LV) function, and inducibility of malignant arrhythmias before SCD. Juvenile pigs (n = 72) were instrumented with chronic stenoses on proximal left anterior descending and circumflex arteries. Survival was only 29% 3 mo after instrumentation, and all deaths were sudden and without prodromal symptoms of heart failure. Triphenyltetrazolium chloride staining demonstrated necrosis in only nine animals averaging 2.3 +/- 0.9% of the LV, with no difference between SCD animals and survivors. Implantable loop recorders (n = 13) documented both ventricular fibrillation (n = 6) and bradyasystole (n = 2) as the arrhythmic mechanism of death. Although regional and global function were depressed [anteroseptal wall thickening 1.8 +/- 0.2 vs. 4.2 +/- 0.2 mm in Sham animals (P &lt; 0.001); fractional shortening 21 +/- 2 vs. 31 +/- 1% in Sham animals (P &lt; 0.01)], there were no differences between SCD animals and survivors. LV mass increased in animals with ischemic cardiomyopathy and was greater in animals with SCD (4.0 +/- 0.2 vs. 3.1 +/- 0.1 g/kg in survivors; P &lt; 0.001). Serial programmed ventricular stimulation failed to induce any sustained arrhythmias. We conclude that pigs with viable dysfunctional myocardium and globally reduced LV function have a high rate of SCD with a spectrum of arrhythmias similar to patients with ischemic cardiomyopathy. The risk is independent of necrosis but appears to increase with LV hypertrophy. Like patients with ischemic cardiomyopathy, programmed stimulation is insensitive to predict SCD when viable dysfunctional myocardium is the pathological substrate.

Randomized comparison of anterolateral versus anteroposterior electrode position for biphasic external cardioversion of atrial fibrillation.

In biphasic external cardioversion (CV) of atrial fibrillation (AF), the influence of different electrode positions on efficacy and incidence of early recurrent atrial fibrillation is not known. This study compared anteroposterior (AP) vs anterolateral (AL) electrode positioning.</AbstractText>Consecutive patients referred for CV of persistent AF were randomized either to an AP or an AL electrode position. Biphasic external CV was performed with standardized electrode positions and rising energy delivery.</AbstractText>Both groups (N = 123, mean age 66 years, 71% male, 83% with structural cardiovascular disease or hypertension) did not differ concerning age, sex, body mass index, chronic antiarrhythmic therapy, duration of AF, left ventricular ejection fraction, and left atrial diameter. Cumulative success rates were comparable (AP 94.9% vs AL 95.2%, P = ns). First-shock efficacy did not differ (AP 78.3% vs AL 74.6%, P = ns). Early recurrent atrial fibrillation (AF relapse &lt; 1 minute after successful CV) occurred in 8.1% (AP 11.6% vs AL 4.8%, P = ns). Mean number of shocks was 1.3 per patient with the AP configuration and 1.4 per patient with the AL configuration (P = ns). Mean cumulative energy delivery was also comparable (AP 171 WS vs AL 198 WS, P = ns).</AbstractText>Both electrode positions are similar in biphasic external CV of AF with regard to acute success and early recurrent atrial fibrillation. Also, the number of shocks needed and energy delivery are comparable with both electrode configurations.</AbstractText>

Effects of [5-(2-methoxy-5-fluorophenyl)furan-2-ylcarbonyl]guanidine (KR-32560), a novel sodium/hydrogen exchanger-1 inhibitor, on myocardial infarct size and ventricular arrhythmias in a rat model of ischemia/reperfusion heart injury.

The cardioprotective effects of the novel sodium/hydrogen exchanger-1 (NHE-1) inhibitor KR-32560 {[5-(2-methoxy-5-fluorophenyl)furan-2-ylcarbonyl]guanidine} were studied in an anesthetized rat model of 30-min ischemia / 2.5-h reperfusion heart injury. KR-32560 (0.01 - 1 microM) dose-dependently inhibited NHE-1-mediated rabbit platelet swelling induced by intracellular acidification. KR-32560 at 0.1 and 1.0 mg/kg (i.v. bolus, given 10 min before ischemia) reduced infarct size from 65.9% (control) to 49.7% and 32.7%, respectively, while reducing the extension of myocardial injury (mm(3)/g of left heart weight) from 405.1 (control) to 302.9 and 185.4, respectively (all P&lt;0.05 vs control). KR-32560 dose-dependently reduced the total number of ventricular premature beats (VPBs) during ischemia from 510.2 (control) to 353.8 and 134.2 beats (all P&lt;0.05, n = 6), while reducing ventricular tachycardia (VT) incidence from 49.3 (control) to 26.8 and 4.3 and VT duration from 249.2 s (control) to 150.5 and 26.7 s (all P&lt;0.05, n = 6). KR-32560 dose-dependently reduced ventricular fibrillation (VF) incidence from 19.0 (control) to 9.2 and 1.2 and VF duration from 88.0 s to 34.5 and 2.8 s (all P&lt;0.05, n = 6). KR-32560 also exerted similar effects on reperfusion arrhythmias, except for VPBs. These results indicate that KR-32560 may exert significant cardioprotective effects in ischemia/reperfusion heart injury.

Induction of mild hypothermia with infusion of cold (4 degrees C) fluid during ongoing experimental CPR.

Therapeutic hypothermia after resuscitation has been shown to improve the outcome regarding neurological state and to reduce mortality. The earlier hypothermia therapy is induced probably the better. We studied the induction of hypothermia with a large volume of intravenous ice-cold fluid after cardiac arrest during ongoing cardiopulmonary resuscitation (CPR).</AbstractText>Twenty anaesthetised piglets were subjected to 8 min of ventricular fibrillation, followed by CPR. They were randomized into two groups. The hypothermic group was given an infusion of 4 degrees C acetated Ringer's solution 30 ml/kg at an infusion rate of 1.33 ml/kg/min, starting after 1 min of CPR. The control group received the same infusion at room temperature. All pigs received a bolus dose of vasopressin after 3 min of CPR. After 9 min, defibrillatory shocks were applied to achieve restoration of spontaneous circulation (ROSC). Core temperature and haemodynamic variables were measured at baseline and repeatedly until 180 min after ROSC. Cortical cerebral blood flow was measured, using Laser-Doppler flowmetry.</AbstractText>All pigs had ROSC, except one animal in the hypothermic group. Only one animal in the hypothermic group died during the observation period. The calculated mean temperature reduction was 1.6+/-0.35 degrees C (S.D.) in the hypothermic group and 1.1+/-0.37 degrees C in the control group (p=0.009). There was no difference in cortical cerebral blood flow and haemodynamic variables.</AbstractText>Inducing hypothermia with a cold infusion seems to be an effective method that can be started even during ongoing CPR. This method might warrant consideration for induction of early therapeutic hypothermia in cardiac arrest victims.</AbstractText>

Factors influencing mortality in atrial fibrillation. Post hoc analysis of an observational study in outpatients.

Whether patients with atrial fibrillation (AF) have an increased mortality compared with the general population is controversially assessed.</AbstractText>The mortality of 409 outpatients with AF (36% female, mean age 62 years, 39% paroxysmal AF, 27% lone AF), who were included in a prospective observational study, was compared with the mortality of the general population.</AbstractText>The mortality was 4%/year and constant during the 10 years of follow-up. Age (p&lt;0.0001), heart failure (p=0.0013) and echocardiographically detected reduced left ventricular systolic function (p=0.0353) were independent predictors. The mortality of AF patients was 1.4-fold higher than in the general population, of female 1.5 and of male 1.3. Patients with permanent AF had a 1.5-fold higher and patients with heart failure a 1.7-fold higher mortality than the general population. Patients with lone AF did not differ in the mortality from the general population. The mortality of AF patients was not influenced by the duration of atrial fibrillation.</AbstractText>The prognosis of AF patients is dependent on the cardiovascular co-morbidity, especially the presence or absence of heart failure.</AbstractText>

Use of amiodarone in emergency.

Amiodarone is one of the most common anti-arrhythmic drugs used in the Emergency Department. Recent guidelines on cardiac arrest with shockable rhythm [refractory ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT)] recommend amiodarone as anti-arrhythmic of first choice. Amiodarone is also first choice drug in the treatment of various ventricular and supra-ventricular tachyarrhythmias. This paper deals with the main therapeutical indications of amiodarone in emergency medicine: dosage, side effects, contraindications and pharmacological interactions are reviewed. Amiodarone is effective for control of hemodynamically stable VT, polymorphic VT and wide-complex tachycardia of uncertain origin. It is also helpful for ventricular rate control of rapid atrial arrhythmias in patients with severely impaired left ventricular (LV) function, when digitalis has been ineffective, and is an adjunct to electrical cardioversion. The major side effects of amiodarone are hypotension, bradycardia and peripheral phlebitis. Major contraindications to the intravenous (i.v.) injection of amiodarone are bradycardia, senoatrial block, severe disturbs of conduction, second or third degree atrio-ventricular blocks. Other contraindications are hypotension, severe respiratory failure, hepatocellular failure and hyperthyroidism. Pharmacological interactions are reported with HMG-CoA reductase inhibitors, class I antiarrhythmic agents and other drugs which contribute to prolong QT interval, digoxin, oral anticoagulants and general anaesthesia.

Neuroprotective and cardioprotective actions of an association of pyruvate, vitamin E and fatty acids.

Oxidative stress may involve overproduction of hydrogen peroxide which can generate highly cytotoxic hydroxyl radicals in the presence of ferrous ions. This work demonstrates that TCAT (Tricomponent Antioxidant Therapy), an association of pyruvate, vitamin E and fatty acids, provides neuronal and cardiac protection in oxidative stress, ex vivo. Mouse P19 neuron cultures were exposed for 30 min to low millimolar H2O2 concentrations in the absence or presence of Fe2+. Concentrations 1X (10 mmol/L pyruvate, 0.1 U/mL vitamin E and 0.1% fatty acids) and 3X of TCAT, respectively, prevented neuronal death caused by these treatments. Analysis of the contribution of TCAT components to neuroprotection showed that vitamin E and fatty acids enhanced pyruvate action whereas they displayed no neuroprotection by themselves. In contrast, vitamin E and fatty acids were as potent antioxidants as pyruvate in an in vitro cell-free assay, indicating that TCAT protection is modulated by the existence of the cellular membrane barriers. Isolated rat hearts were perfused under electrolysis or subjected to regional ischemia-reperfusion. TCAT 1X prevented the electrolysis-induced decrease in left ventricular pressure, heart rate and coronary flow. At 0.25X concentration, TCAT abolished the incidence of irreversible ventricular fibrillation in ischemia-reperfusion. The results indicate that TCAT could have a broad therapeutic utility in neurological and cardiac injuries associated with oxidative stress. The protective action of TCAT can surpass that of its components, revealing a benefit of the association.

Effects of KB-R9032, a new Na+/H+ exchange inhibitor, on canine coronary occlusion/reperfusion-induced ventricular arrhythmias.

We investigated the effects of KB-R9032 (N-(4-isopropyl-2,2-dimethyl-3-oxo-3,4-dihydro-2H-benzo[1,4]oxazine-6-carbonyl) guanidine methanesulfonate), a new Na(+)/H(+) exchange inhibitor, on a coronary artery occlusion/reperfusion-induced arrhythmia model in pentobarbital anesthetized dogs. KB-R9032 reduced the number of ventricular premature contractions seen during the coronary occlusion, while it did not alter the heart rate, mean blood pressure, or electrocardiographic parameters (PR, QRS, or QTc interval). KB-R9032 also decreased the incidence of fatal ventricular fibrillation during coronary artery occlusion and/or after reperfusion. These antiarrhythmic effects were observed not only in the pre-ischemic administration group, but also in the group given KB-R9032 at the 15th min of the 30-min occlusion. These findings support the view that Na(+)/H(+) exchanger may play an important role in inducing coronary ischemia/reperfusion arrhythmias. This suggests that the use of Na(+)/H(+) exchange inhibitors, such as KB-R9032, may be an effective clinical approach to suppress sudden cardiac death due to acute myocardial ischemia/reperfusion such as during coronary bypass surgery, cardiac valve surgery, or percutaneous transluminal coronary angioplasty.

Pretreatment with an adenosine A1 receptor agonist and lidocaine: a possible alternative to myocardial ischemic preconditioning.

The heart possesses an extraordinary ability to remember short episodes of sublethal ischemia and reperfusion (angina), which protects the myocardium and coronary vasculature from a subsequent lethal insult, a phenomenon known as ischemic preconditioning. A therapeutic goal for more than 2 decades has been to develop a pharmacologic mimetic comparable with ischemic preconditioning. Our aim was to investigate the preconditioning effect of a new combinatorial therapy targeting adenosine A1 receptors and voltage-dependent sodium fast channels in the in vivo rat model of regional ischemia.</AbstractText>Ischemia-reperfusion was achieved by placing a reversible tie around the left coronary artery in anesthetized and ventilated Sprague-Dawley rats (n = 37). Rats were randomly assigned to 1 of 5 groups: (1) saline control (n = 13); (2) ischemic preconditioning (n = 6); (3) lidocaine only (608 microg . kg -1 . min -1 , n = 5); (4) adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CCPA; 5 microg/kg, n = 7); and (5) CCPA plus lidocaine (n = 6). Ischemic preconditioning was achieved by using 3 cycles of ischemia and reperfusion lasting 3 minutes each. Lidocaine was infused continuously 5 minutes before and throughout 30 minutes of ischemia and ceased at reperfusion. A bolus of CCPA was infused 5 minutes before ligation along with a constant infusion of lidocaine (as above). All animals were reperfused for 120 minutes for infarct size measurement.</AbstractText>Fifty-four percent of saline control rats, 17% of ischemic preconditioning-treated rats, and 29% of CCPA-treated rats died during ischemia from ventricular fibrillation. Infarct size of saline control animals was 61% +/- 5%. Pretreating with CCPA and lidocaine infusion resulted in no deaths, no severe arrhythmias, and significant infarct size reduction compared with that seen in saline control animals (P &lt; .05). Remarkably, infarct size reduction in CCPA plus lidocaine-treated rats (12% +/- 4%) was equivalent to that achieved with ischemic preconditioning (11% +/- 3%), whereas infarct size in rats undergoing CCPA-only and lidocaine-only treatments was 42% +/- 7% and 60% +/- 6%, respectively. Although CCPA plus lidocaine treatment reduced heart rate, mean arterial pressure, and systolic pressure during ischemia, no correlation was found between these variables and infarct size reduction.</AbstractText>We conclude that activating adenosine A1 receptor subtype with CCPA and concomitantly modulating sodium fast channels with lidocaine was comparable with ischemic preconditioning and might offer a new therapeutic window to minimize myocardial damage during surgical ischemia and reperfusion.</AbstractText>

Right axillary incision: a cosmetically superior approach to repair a wide range of congenital cardiac defects.

We sought to evaluate the safety of a right axillary incision, a cosmetically superior approach than anterolateral thoracotomy, to repair various congenital heart defects.</AbstractText>All the patients who were approached with this incision between March 2001 and October 2004 were included in the study. There were 80 patients (median age, 4 years) with atrial septal defect closure (38 patients), repair of partial abnormal pulmonary venous return (14 patients), partial atrioventricular canal (16 patients), and perimembranous ventricular septal defect (12 patients). The surgical technique involved peripheral and central cannulation for institution of cardiopulmonary bypass. Electrically induced ventricular fibrillation was used for defects located in front of the atrioventricular valves, and cardioplegic arrest was used for those located at the level or behind these valves.</AbstractText>The repair was possible without need for conversion to another approach. One patient sustained a transient neurologic deficit. The patients were all in excellent condition after a mean follow-up of 14 months. The cardiac defect was repaired with no residual defect in 75 patients and with trivial residual defect in 5 patients (3 with mitral valve regurgitation, 1 with atrial septal defect, and 1 with ventricular septal defect). The incision healed properly in all, and the thorax showed no deformity.</AbstractText>The right axillary incision provides a quality of repair for various congenital defects similar to that obtained by using standard surgical approaches. Because it lies more laterally and is hidden by the resting arm, it provides superior cosmetic results compared with conventional incisions, including the anterolateral thoracotomy. Finally, the incision is unlikely to interfere with subsequent development of the breast.</AbstractText>

Supraventricular tachycardia in children.

Several different mechanisms are responsible for paroxysmal supraventricular tachycardia in children. Different forms of tachycardia occur at different age. Atrio-ventricular reentry tachycardia results from the presence of congenital atrio-ventricular bypass tracts and is frequently encountered at all ages. Infants may present with ectopic atrial tachycardia or atrial flutter. Atrio-ventricular node reentry tachycardia becomes more frequent in adolescence. Atrial scarring resulting from open heart surgery predisposes to complex intra-atrial reentry. Certain forms of congenital and acquired heart disease are associated with specific types of arrhythmia. Many children with paroxysmal supraventricular tachycardia do not require any therapy. The decision to proceed with treatment should be based on the frequency and severity of symptoms and on the effect of arrhythmia on the quality of life. Infants require medical treatment because of the difficulty to recognize symptoms of tachycardia and a risk of heart failure. Patients with Wolff-Parkinson-White syndrome as well as those with significant heart disease are at risk of sudden death. Syncope in children with paroxysmal tachycardia may indicate a severe fall in cardiac output from extremely rapid heart rate. Patients with potentially life-threatening arrhythmia should not participate in competitive physical activities. Treatment options have undergone significant evolution over the past decade. Indications for the use of specific antiarrhythmic medications have been refined. Contemporary catheter ablation procedures employ different forms of energy allowing for safe and effective procedures. Catheter ablation is the treatment of choice for symptomatic paroxysmal tachycardia in school children and in some infants who failed medical treatment. Surgery is the preferred treatment in few selected cases. The goal of this review is to present the state of the art approach to the diagnosis and management of paroxysmal supraventricular tachycardia in infants, children and adolescents.

Clinical characteristics and treatment of short QT syndrome.<Pagination><StartPage>611</StartPage><EndPage>617</EndPage><MedlinePgn>611-7</MedlinePgn></Pagination><Abstract><AbstractText>Short QT syndrome is a new inherited disorder associated with familial atrial fibrillation and/or sudden death or syncope. To date, three different mutations in genes encoding cardiac ion channels (KCNH2, KCNQ1 and KCNJ2) have been identified as causing short QT syndrome. All mutations lead to a gain in function of the affected current (IK(r), IK(s )and IK(1)). The syndrome is characterized in the few patients identified so far by a shortened QT interval of less than 300-325 ms after correction for heart rate at rates below 80 beats per minute. However, no boundary or limit for the QT interval can yet be determined, as more knowledge about this disease is still restricted to a small patient population. Furthermore, the QT interval lacks adaptation to heart rate. The majority of patients exhibit shortened atrial and ventricular effective refractory periods and inducibility of ventricular fibrillation. Death already occurs in newborns, so the short QT syndrome may also account for deaths classified as sudden infant death syndrome. The therapy of choice in families with a history of sudden death or syncope seems to be the implantable cardioverter-defibrillator. Whether patients without a family history of sudden death or symptoms need a defibrillator cannot yet be answered, and requires further investigation. Pharmacologic treatment has only been investigated in patients with a mutation in KCNH2 (HERG), and it could be demonstrated that the mutant currents may be insufficiently suppressed by drugs that are targeted to block the specific current (e.g., sotalol or ibutilide) in patients with a mutation in the IK(r-)coding gene KCNH2 (HERG). Interestingly, in this specific patient population, quinidine proved to be efficient in prolonging the QT interval and normalizing the effective refractory periods. Implantable cardioverter-defibrillator therapy is associated with an increased risk of inappropriate therapies for T-wave oversensing, although this risk can be resolved by reprogramming implantable cardioverter-defibrillator detection algorithms.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wolpert</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1st Department of Medicine-Cardiology, University Hospital Mannheim, Faculty of Clinical Medicine of the Ruprecht-Karls-University Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. christian.wolpert@med.ma.uni-heidelberg.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schimpf</LastName><ForeName>Rainer</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Veltmann</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Giustetto</LastName><ForeName>Carla</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Gaita</LastName><ForeName>Fiorenzo</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Borggrefe</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Rev Cardiovasc Ther</MedlineTA><NlmUniqueID>101182328</NlmUniqueID><ISSNLinking>1477-9072</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>17</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>8</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>8</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>8</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16076272</ArticleId><ArticleId IdType="doi">10.1586/14779072.3.4.611</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16076053</PMID><DateCompleted><Year>2005</Year><Month>08</Month><Day>18</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0201-7563</ISSN><JournalIssue CitedMedium="Print"><Issue>3</Issue><PubDate><Year>2005</Year><Season>May-Jun</Season></PubDate></JournalIssue><Title>Anesteziologiia i reanimatologiia</Title><ISOAbbreviation>Anesteziol Reanimatol</ISOAbbreviation></Journal>[Cardioversion and central hemodynamics in patients with arrhythmic and genuine cardiogenic shock].

Short QT syndrome is a new inherited disorder associated with familial atrial fibrillation and/or sudden death or syncope. To date, three different mutations in genes encoding cardiac ion channels (KCNH2, KCNQ1 and KCNJ2) have been identified as causing short QT syndrome. All mutations lead to a gain in function of the affected current (IK(r), IK(s )and IK(1)). The syndrome is characterized in the few patients identified so far by a shortened QT interval of less than 300-325 ms after correction for heart rate at rates below 80 beats per minute. However, no boundary or limit for the QT interval can yet be determined, as more knowledge about this disease is still restricted to a small patient population. Furthermore, the QT interval lacks adaptation to heart rate. The majority of patients exhibit shortened atrial and ventricular effective refractory periods and inducibility of ventricular fibrillation. Death already occurs in newborns, so the short QT syndrome may also account for deaths classified as sudden infant death syndrome. The therapy of choice in families with a history of sudden death or syncope seems to be the implantable cardioverter-defibrillator. Whether patients without a family history of sudden death or symptoms need a defibrillator cannot yet be answered, and requires further investigation. Pharmacologic treatment has only been investigated in patients with a mutation in KCNH2 (HERG), and it could be demonstrated that the mutant currents may be insufficiently suppressed by drugs that are targeted to block the specific current (e.g., sotalol or ibutilide) in patients with a mutation in the IK(r-)coding gene KCNH2 (HERG). Interestingly, in this specific patient population, quinidine proved to be efficient in prolonging the QT interval and normalizing the effective refractory periods. Implantable cardioverter-defibrillator therapy is associated with an increased risk of inappropriate therapies for T-wave oversensing, although this risk can be resolved by reprogramming implantable cardioverter-defibrillator detection algorithms.</Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Wolpert</LastName><ForeName>Christian</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>1st Department of Medicine-Cardiology, University Hospital Mannheim, Faculty of Clinical Medicine of the Ruprecht-Karls-University Heidelberg, Theodor-Kutzer-Ufer 1-3, 68167 Mannheim, Germany. christian.wolpert@med.ma.uni-heidelberg.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schimpf</LastName><ForeName>Rainer</ForeName><Initials>R</Initials></Author><Author ValidYN="Y"><LastName>Veltmann</LastName><ForeName>Christian</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Giustetto</LastName><ForeName>Carla</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Gaita</LastName><ForeName>Fiorenzo</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Borggrefe</LastName><ForeName>Martin</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Expert Rev Cardiovasc Ther</MedlineTA><NlmUniqueID>101182328</NlmUniqueID><ISSNLinking>1477-9072</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D001145" MajorTopicYN="N">Arrhythmias, Cardiac</DescriptorName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004562" MajorTopicYN="N">Electrocardiography</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>17</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>8</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>8</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>8</Month><Day>4</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16076272</ArticleId><ArticleId IdType="doi">10.1586/14779072.3.4.611</ArticleId></ArticleIdList></PubmedData></PubmedArticle><PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16076053</PMID><DateCompleted><Year>2005</Year><Month>08</Month><Day>18</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0201-7563</ISSN><JournalIssue CitedMedium="Print"><Issue>3</Issue><PubDate><Year>2005</Year><Season>May-Jun</Season></PubDate></JournalIssue><Title>Anesteziologiia i reanimatologiia</Title><ISOAbbreviation>Anesteziol Reanimatol</ISOAbbreviation></Journal><ArticleTitle>[Cardioversion and central hemodynamics in patients with arrhythmic and genuine cardiogenic shock].</ArticleTitle><Pagination><StartPage>64</StartPage><EndPage>67</EndPage><MedlinePgn>64-7</MedlinePgn></Pagination><Abstract>Arrhythmic shock (AS) results primarily from many types of tachyarrhythmias: atrial fibrillation and flutter, supraventricular tachyarrhythmias, ventricular paroxysmal tachycardias. AS is distinguished from the stable course of the above arrhythmias by pronounced changes in central hemodynamics (CH) and by rapid and frequently negative manifestations. The status of CH is an important criterion when whether electrical cardioversion is performed is decided. CH was studied in 306 patients with genuine cardiogenic shock and in 32 patients with AS. In case of effective cardioversion, central hemodynamics in patients with AS underwent rapid changes: first of all, stroke volume and cardiac index increased and end systolic volume decreased. In case of effective of antishock measures, CH in patients with cardiogenic shock normalized only within 3-4 weeks of their stay at an intensive care unit, but ejection fraction also remained decreased at their discharge from hospital.

[Sudden cardiac death: state of the art].

Sudden cardiac death (SCD) is an integral term for several heart diseases among which SCD caused by ischemic heart disease (IHD) designated as sudden coronary death (SCD) ranks first. SCD associated with alcoholic cardiomyopathy ranks second. Risk factors and pathologic manifestations of SCD correspond to those of IHD, atherosclerosis, myocardial infarction. Cardiac arrest takes place because of fibrillation of ventricular myocardium. Factor inducing fibrillation is an advanced irreversable myocardial ischemia complicated with reperfusion. The latter promotes elimination of arrythmogenic substances from the ishemic zone leading to electric unstability of the myocardium and fatal arrythmia. Possibility of idiopathic ventricular fibrillation and its mechanisms is discussed.

Intrathoracic pressure regulator during continuous-chest-compression advanced cardiac resuscitation improves vital organ perfusion pressures in a porcine model of cardiac arrest.

A novel device, the intrathoracic pressure regulator (ITPR), combines an inspiratory impedance threshold device (ITD) with a vacuum source for the generation of controlled -10 mm Hg vacuum in the trachea during cardiopulmonary resuscitation (CPR) while allowing positive pressure ventilation. Compared with standard (STD) CPR, ITPR-CPR will enhance venous return, systemic arterial pressure, and vital organ perfusion in both porcine models of ventricular fibrillation and hypovolemic cardiac arrest.</AbstractText>In protocol 1, 20 pigs (weight, 30+/-0.5 kg) were randomized to STD-CPR or ITPR-CPR. After 8 minutes of untreated ventricular fibrillation, CPR was performed for 6 minutes at 100 compressions per minute and positive pressure ventilation (100% O2) with a compression-to-ventilation ratio of 15:2. In protocol 2, 6 animals were bled 50% of their blood volume. After 4 minutes of untreated ventricular fibrillation, interventions were performed for 2 minutes with STD-CPR and 2 minutes of ITPR-CPR. This sequence was repeated. In protocol 3, 6 animals after 8 minutes of untreated VF were treated with ITPR-CPR for 15 minutes, and arterial and venous blood gases were collected at baseline and minutes 5, 10, and 15 of CPR. A newer, leak-proof ITPR device was used. Aortic, right atrial, endotracheal pressure, intracranial pressure, and end-tidal CO2 values were measured (mm Hg); common carotid arterial flow also was measured (mL/min). Coronary perfusion pressure (diastolic; aortic minus right atrial pressure) and cerebral perfusion pressure (mean arterial minus mean intracranial pressure) were calculated. Unpaired Student t test and Friedman's repeated-measures ANOVA of ranks were used in protocols 1 and 3. A 2-tailed Wilcoxon signed-rank test was used for analysis in protocol 2. Fischer's exact test was used for survival. Significance was set at P&lt;0.05. Vital organ perfusion pressures and end-tidal CO2 were significantly improved with ITPR-CPR in both protocols. In protocol 1, 1-hour survival was 100% with ITPR-CPR and 10% with STD-CPR (P=0.001). Arterial blood pH was significantly lower and Paco2 was significantly higher with ITPR-CPR in protocol 1. Arterial oxygen saturation was 100% throughout the study in both protocols. Paco2 and Pao2 remained stable, but metabolic acidosis progressed, as expected, throughout the 15 minutes of CPR in protocol 3.</AbstractText>Compared with STD-CPR, use of ITPR-CPR improved hemodynamics and short-term survival rates after cardiac arrest.</AbstractText>

The signal-averaged P-wave duration is longer in hypertensive patients with history of paroxysmal atrial fibrillation as compared to those without.

Onset of atrial fibrillation in hypertensive patients is usually associated with a high occurrence of cardiovascular complications. Therefore, it is important to assess non-invasively the risk of developing paroxysmal atrial fibrillation (PAF) in hypertensive patients during sinus rhythm. This study was undertaken to determine if hypertensive patients with history of PAF could be identified while in sinus rhythm by measurement of signal-averaged ECG P-wave duration.</AbstractText>Signal-averaged electrocardiography (SAECG) P-wave recording was performed in 44 hypertensive patients (30 men and 14 women; mean age 60+/-11 years, group A) who had a history of paroxysmal AF and in 50 hypertensive patients without history of AF (33 men and 17 women; mean age 57+/-12, group B). All patients were also evaluated by using echocardiography to measure left ventricular ejection fraction (LVEF) and left atrial diameter (LAD).</AbstractText>SAECG P-wave duration was found to be significantly higher in group A than in group B (146+/-14 ms vs. 128+/-11 ms, p&lt;0.001). Left atrial diameter was not significantly different (40.1+/-3.4 mm vs. 39.3+/-3.0 mm, p&gt;0.05), whereas LVEF was significantly lower in group A than group B (63+/-5% vs. 67+/-4%, p=0.03). There was a correlation between SAECG P-wave duration and age (r=0.32, p&lt;0.05). In univariate analysis, SAECG P-wave duration and LVEF were significant predictors of PAF, but only SAECG P-wave duration remained a significant independent predictor of PAF in multivariate analysis.</AbstractText>The results of this study indicate that hypertensive patients with history of PAF can be detected while in sinus rhythm by signal-averaged ECG P-wave duration.</AbstractText>

Rate versus rhythm control in patients with atrial fibrillation: what the trials really say.

Despite new insights into the pathophysiological triggers of atrial fibrillation (AF) and the development of novel ablative techniques and antiarrhythmic drugs, the management of this chronic rhythm disturbance remains problematic. At present, there are two fundamental interventional choices: restoration and maintenance of normal sinus rhythm (NSR) or control of the ventricular rate. While there are compelling theoretical benefits in restoring and maintaining NSR, until recently there has been little evidence supporting the comparative advantages of either strategy. During the past few years, five randomised trials investigating the two treatment strategies have been completed: PIAF (Pharmacological Intervention in Atrial Fibrillation), STAF (Strategies of Treatment of Atrial Fibrillation), RACE (RAte Control versus Electrical conversion), AFFIRM (Atrial Fibrillation Follow-up of Rhythm Management) and HOT-CAFE (How to Treat Chronic Atrial Fibrillation). Results from these studies indicate that a strategy of rate control in AF patients can be at least as effective as efforts to control rhythm with respect to several specific outcomes. These trials have also revealed the necessity of continuing antithrombotic treatment even when long-term sinus rhythm is obtained. However, these trials had different patient selection criteria, endpoints and therapeutic interventions, limiting the applicability of their findings to all AF populations. This article looks beyond the primary results from these important studies, using recent substudy analyses to draw new conclusions and to generate hypotheses that will require prospective evaluation in adequately powered trials. One substudy suggested, for instance, that failure of rhythm control to show superiority may be a result of the toxicity of current antiarrhythmic drugs. New class III compounds with novel mechanisms are now in varying stages of clinical development. These drugs appear to block multiple membrane ion channels, with predominant effects on the atria and low proarrhythmic potential. It is anticipated that these agents will be safer than, and at least as effective as, currently available drugs, thereby reducing AF-related morbidity and mortality. Until more effective treatments are available, physicians should use the evidence generated from the major studies to guide decision making based upon the characteristics and symptomatic presentation of individual patients.

Do discharge codes underestimate hospitalisation due to heart failure? Validation study of hospital discharge coding for heart failure.

Discharge codes are frequently used to describe hospital activity related to heart failure (HF).</AbstractText>To determine whether discharge codes for HF underestimated or overestimated hospital activity related to HF.</AbstractText>Patients with atrial fibrillation (AF), who commonly have HF, were identified and their case notes reviewed to identify cases of HF missed by discharge codes.</AbstractText>Patients admitted between November 1997 and January 1998 with either HF or AF. Identification of HF and AF by ICD10 hospital discharge codes. Identification of additional cases of AF from a central hospital-wide ECG database.</AbstractText>We identified 330 cases with an ICD 10 code for HF, of which 43 (13%) were deemed to be miscoded, 32 patients (10%) were classified as possible, 39 (12%) as probable and 216 (65%) as definite HF. Results were similar whether or not HF was the primary discharge diagnosis. We identified 452 patients with AF, of whom 45 (10%) were classified as probable and 193 (43%) as definite HF. 129 (54%) of these cases had no diagnostic discharge code for HF. ICD 10 discharge codes for HF were correct in 77% of cases but identified only 66% of patients with probable or definite HF in this analysis. Screening of other diagnoses would have identified further cases of HF.</AbstractText>Hospital discharge codes substantially underestimate hospital events related to HF in the UK.</AbstractText>

Microvolt T-wave alternans: a review of techniques, interpretation, utility, clinical studies, and future perspectives.

Microvolt T-wave alternans (TWA) testing involves measuring variation in the morphology of the T-wave on an every other beat basis. The magnitude of the variation observed is typically on the order of a few microvolts. Thus in order to detect microvolt TWA, specialized recording and signal processing methods must be employed for reliable measurement. Additionally, microvolt TWA is not generally present at rest even in patients at risk of ventricular tachyarrhythmias and therefore exercise stress, pharmacologic stress, or atrial pacing must be utilized in order to elevate the heart rate. A positive MTWA test is one in which sustained TWA is present with an onset heart rate &lt; or = 110 bpm. With current instrumentation, microvolt TWA represents an inexpensive, convenient non-invasive testing modality. Microvolt TWA has been evaluated prospectively in a variety of patient populations as a means of predicting occurrence of ventricular tachyarrhythmic events and its association with the genesis of ventricular arrhythmias has been demonstrated. Future role of microvolt TWA testing in noninvasive risk stratification is awaiting results of ongoing clinical trials. In this article, we tried to review the techniques, interpretation, indications, clinical studies, and future perspectives of microvolt TWA.