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Surgical closure of combined symptomatic patent foramen ovale and atrial septum aneurysm for prevention of recurrent cerebral emboli.

Patients with patent foramen ovale (PFO) have an undefined but certainly considerable risk of repeated cerebral ischemia due to paradoxical embolism. Especially, if a cerebrovascular event has already occurred and the combination with an atrial septum aneurysm (ASA) is present this risk increases tremendously. The aim of this study was to demonstrate that surgical closure of PFO in combination with an ASA is safe and useful in preventing recurrent strokes.</AbstractText>Ten patients with previous cerebral ischemia, proven by CT or MRI, and PFO in combination with an ASA were prospectively scheduled for surgical closure. Patients with extracardiac sources of embolic disease were excluded from this study. However, one patient suffered from a hypercoagulability syndrome.</AbstractText>All patients (mean age 35.5 +/- 19.1 years) underwent direct suture of the PFO and plication of the ASA with the aid of cardiopulmonary bypass and cardioplegic arrest (n = 3) or ventricular fibrillation (n = 7). Mean operation time was 123.1 +/- 20.2 minutes; mean bypass time was 34.5 +/- 9.9 minutes. There was no mortality or significant postoperative morbidity. Mean hospital stay was 5.1 +/- 1.5 days. During a follow-up of &gt;4 years, no recurrent stroke or transient ischemic attack occurred and no patient received anticoagulation therapy.</AbstractText>Our data suggest that surgical closure of PFO in combination with ASA in patients with previous stroke is safe and efficacious to prevent recurrent strokes and avoids lifelong anticoagulation.</AbstractText>

Closure of atrial septal defect in the adult. Cardiac remodeling is an early event.

Study aimed to describe the extent and the temporal profile of cardiac remodeling after atrial septal defect closure in the adult.</AbstractText>Prospective and longitudinal echocardiographic assessment of right and left heart size before and after (1 day-1 week/1/4/12 months) surgical or catheter-based atrial septal closure in 39 adults (age 54+/-15 years).</AbstractText>Right ventricular and atrial sizes were markedly reduced, left ventricular size increased and left atrial size remained unchanged after closure. Older age and a history of atrial fibrillation reduced the potential to normalize right and left atrial size after closure. The greater part of the changes occurred very early, in the 1st day/1st week. From then on the speed of change gradually diminished and after 4 months no important changes were observed. The mode of closure did not influence the degree or the pace of the remodeling.</AbstractText>Cardiac remodeling after atrial septal closure in the adult is a common and early event that seems by and large completed within the first half year after closure. The ventricles seem to have a higher capacity of remodeling than the atria in this setting. The mode of closure does not seem to significantly impact remodeling.</AbstractText>

Multiple appropriate and spurious defibrillator shocks in a patient with right ventricular cardiomyopathy.

An implantable cardioverter defibrillator (ICD) has been implanted in a 69-year-old patient with arrhythmogenic right ventricular cardiomyopathy (ARVC) for treatment of syncopal ventricular tachycardia (VT). Two types of ICD-related emergencies complicated the clinical course within 15 months. The first arrhythmic event occurred 3 months after ICD implantation as electrical storm with repetitive fast VT, resulting in 87 consecutive shocks at maximal output. Intravenous administration of amiodarone and reprogramming of the device were the measures to control VT. A year later, the patient experienced a cluster of 97 inappropriate shocks. Lead insulation failure produced electrical noise on the ventricular sensing channel and was misidentified as ventricular fibrillation (VF). The depleted ICD and the dual-coil lead were explanted and replaced by a new system. Multiple ICD shocks constitute a medical emergency in ICD patients, which requires immediate device interrogation for differentiation of appropriate and spurious discharges.

Spironolactone and its main metabolite canrenoic acid block hKv1.5, Kv4.3 and Kv7.1 + minK channels.

Both spironolactone (SP) and its main metabolite, canrenoic acid (CA), prolong cardiac action potential duration and decrease the Kv11.1 (HERG) current. We examined the effects of SP and CA on cardiac hKv1.5, Kv4.3 and Kv7.1+minK channels that generate the human I(Kur), I(to1) and I(Ks), which contribute to the control of human cardiac action potential duration.hKv1.5 currents were recorded in stably transfected mouse fibroblasts and Kv4.3 and Kv7.1 + minK in transiently transfected Chinese hamster ovary cells using the whole-cell patch clamp. SP (1 microM) and CA (1 nM) inhibited hKv1.5 currents by 23.2 +/- 3.2 and 18.9 +/- 2.7%, respectively, shifted the midpoint of the activation curve to more negative potentials and delayed the time course of tail deactivation.SP (1 microM) and CA (1 nM) inhibited the total charge crossing the membrane through Kv4.3 channels at +50 mV by 27.1 +/- 6.4 and 27.4 +/- 5.7%, respectively, and accelerated the time course of current decay. CA, but not SP, shifted the inactivation curve to more hyperpolarised potentials (V(h)-37.0 +/- 1.8 vs -40.8 +/- 1.6 mV, n = 10, P &lt; 0.05).SP (10 microM) and CA (1 nM) also inhibited Kv7.1 + minK currents by 38.6 +/- 2.3 and 22.1 +/- 1.4%, respectively, without modifying the voltage dependence of channel activation. SP, but not CA, slowed the time course of tail current decay.CA (1 nM) inhibited the I(Kur) (29.2 +/- 5.5%) and the I(to1) (16.1 +/- 3.9%) recorded in mouse ventricular myocytes and the I(K) (21.8 +/- 6.9%) recorded in guinea-pig ventricular myocytes.A mathematical model of human atrial action potentials demonstrated that K(+) blocking effects of CA resulted in a lengthening of action potential duration, both in normal and atrial fibrillation simulated conditions. The results demonstrated that both SP and CA directly block hKv1.5, Kv4.3 and Kv7.1 + minK channels, CA being more potent for these effects. Since peak free plasma concentrations of CA ranged between 3 and 16 nM, these results indicated that blockade of these human cardiac K(+) channels can be observed after administration of therapeutic doses of SP. Blockade of these cardiac K(+) currents, together with the antagonism of the aldosterone proarrhythmic effects produced by SP, might be highly desirable for the treatment of supraventricular arrhythmias.

Electrophysiological and haemodynamic effects of endothelin ETA and ETB receptors in normal and ischaemic working rabbit hearts.

The aims of this study were to determine if endothelin-1 (ET-1) under normal and ischaemic conditions exhibits a direct arrhythmogenic effect that is independent of its ability to cause coronary vasoconstriction, and to determine the contribution of the ET(A) and ET(B) receptor subtype. ET(A/B) (with ET-1) and ET(A) (ET-1 in the presence of BQ-788) receptor activation resulted in a significant reduction in both epi- and endocardial monophasic action potential duration (MAPD(90)). ET(A) receptor activation reduced both epi- and endocardial effective refractory period (ERP). This MAPD(90) and ERP shortening were associated with a reduction in coronary flow, myocardial contractility and induction of ventricular fibrillation (VF) during ERP measurement. The ET(B) agonist sarafotoxin (S6c) had no marked, or concentration-dependent, effect on MAPD(90), ERP, myocardial contractility or induction of arrhythmias. Neither ET-1 nor S6c, given prior to coronary artery occlusion, significantly changed the ischaemia-induced dispersion of MAPD(90), ERP or the % incidence of VF. In conclusion, neither ET(A) nor ET(B) receptor stimulation has a direct arrhythmogenic effect in isolated rabbit hearts under normal or ischaemic conditions. The ET-1-induced arrhythmogenic effect observed in nonischaemic hearts is likely to be the result of the associated coronary vasoconstriction caused by ET(A) receptor stimulation resulting in myocardial ischaemia.

The frequency and pattern of cardiotoxicity observed with capecitabine used in conjunction with oxaliplatin in patients treated for advanced colorectal cancer (CRC).

We examined the cardiotoxicity in 153 patients treated with capecitabine and oxaliplatin in two prospective trials for advanced colorectal cancer. Ten patients (6.5%) developed cardiac events. One patient (0.7%) had sudden death, one patient developed cardiac failure with raised troponin I while another developed ventricular tachycardia (VT). The remaining seven patients (4.6%) experienced angina and three of the seven patients had raised troponin I, one of which developed ventricular fibrillation. Eight events occurred within cycle 1 (median cycle 1 day 10). Four patients with angina and one patient with VT recovered on stopping capecitabine, four patients required additional medical management and the remaining patient died suddenly at home. Patients with ischaemic heart disease appeared to be at increased risk. Physicians and patients need to be aware of these complications, so that prompt discontinuation of treatment and appropriate interventions may be instituted.

Surgical intervention for advanced valvular heart disease in 227 cases.

Although the results of surgical treatment in cardiac valve disease continue to improve, the postoperative mortality rate and the rate of complications in patients with advanced valvular heart disease (AVHD) are still very high. We did this retrospective study to summarize the surgical experience of heart valve replacement for patients with AVHD and discuss effective ways to improve the surgical outcome.</AbstractText>From January 1994 to October 2003, surgical procedures of heart valve replacement were performed on 227 (136 men and 91 women) patients with AVHD in our Department of Cardiothoracic Surgery. The clinical data of all patients were collected and analysed. Patients' age ranged from 10 years to 77 years. In preoperative cardiac function grading, 157 cases were NYHA III and 70 cases NYHA IV. Fifty-one patients had had cardiac operations. The ultrasonic cardiac graphs showed that 145 patients suffered from moderate or severe pulmonary hypertension and 73 had combined giant left ventricle. Mitral valve replacement was performed in 32 cases, aortic valve replacement in 90, tricuspid valve replacement in 1, combined mitral and aortic replacement in 103 and combined mitral and tricuspid replacement in 1. Nineteen patients also received surgical corrections for other minor abnormalities during the operations. A logistic model was established to evaluate the influence of perioperative factors on the mortality rate.</AbstractText>The operative mortality rate was 13.2% (30/227). The main causes of death included multiple organ dysfunction syndrome (MODS), low cardiac output syndrome and ventricular fibrillation. From the results of the binary noncounterpart multivariate logistic regression, the following statistically significant factors were found to influence the operative mortality rate: redo operation, age &gt;/= 55 years, preoperative NYHA cardiac function grading, extracorporeal circulation time &gt;/= 120 minutes and postoperative usage of GIK (glucose, insulin and potassium) solution. All factors were risk ones except postoperative application of GIK. The Hosmer-Lemeshow goodness of fit coefficient of this model was 0.976.</AbstractText>The risk factors associated with postoperative mortality rate in the patients with AVHD were redo operation, age &gt;/= 55 years, preoperative NYHA cardiac function grading and extracorporeal circulation time &gt;/= 120 minutes. Postoperative usage of GIK acted as a kind of metabolic therapy and will improve the recovery for patients with AVHD. Active perioperative management and care will play a very important role in reducing the operative risk and improving the short term outcome of surgical treatment for the patients with AVHD.</AbstractText>

Long-term clinical outcome in patients with severe left ventricular dysfunction and an implantable cardioverter-defibrillator after ventricular tachyarrhythmias.

Left ventricular ejection fraction (LVEF) is accepted as an important prognostic marker in patients (pts) with implantable cardioverter-defibrillators (ICD). The impact of this therapeutic approach in the survival of pts with life-threatening arrhythmias and severe left ventricular dysfunction remains a matter of discussion.</AbstractText>To evaluate the long-term clinical implications of severe left ventricular dysfunction in pts with an ICD implanted for secondary prevention of sudden cardiac death (SD).</AbstractText>Out of 70 pts undergoing ICD implantation in our institution over four consecutive years, we studied 24 pts with LVEF &lt;35% and a post-ICD follow-up of &gt;12 months (87.5% male; age 62.79 years). The index arrhythmia was ventricular tachycardia in 19 cases and SD with ventricular fibrillation in 5 cases. The underlying disease was ischemic cardiomyopathy (n=19), dilated cardiomyopathy (n=4) and hypertensive heart disease (n=1). Mean LVEF at the time of implant was 25 +/- 7% (between 11% and 34%; NYHA class II/III in 83.3%). A du chamber system was implanted in 5 cases, and an ICD plus cardiac resynchronization pacing in 2 cases. There was no perioperative mortality. At the time of discharge, 71.2% of the pts were taking amiodarone and 66.7 % beta-blockers. During a 38 +/- 16-month follow-up (4 appointments/year), we analyzed the following parameters: rehospitalization for cardiovascular cause, appropriate ICD shocks, inappropriate detections/therapy, nonfatal major arrhythmic events (arrhythmic storm, therapeutic exhaustion, recurrent ventricular tachycardia), cardiac mortality, SD and total mortality.</AbstractText>Forty-five readmissions (1.9 +/- 2.3/pt) occurred in 14 pts (58%), 24.4% due to congestive heart failure. Appropriate ICD shocks (without hospitalization) occurred in 62.5% of the pts, 16.6% had inappropriate therapy (50% because of increased heart rate due to atrial fibrillation) and 37.5% suffered nonfatal major arrhythmic events. Death due to SD was 4.2%, cardiac mortality 12.5% and total mortality 25%.</AbstractText>Severe left ventricular dysfunction is common in ICD pts. During long-term follow-up, the majority of these pts receive appropriate ICD shocks, which emphasizes the importance of SD prevention in this population. The frequent documentation of supraventricular arrhythmias (causing inappropriate ICD therapy) and nonfatal major arrhythmic events also reflects the presence of a worse arrhythmic substrate in this subgroup. Despite the poor initial prognosis associated with ventricular tachyarrhythmias in pts with severe left ventricular dysfunction, ICD therapy may contribute to a better long-term clinical outcome.</AbstractText>

Deployment of left ventricular lead from the ipsilateral side of central vein obstruction.

Cardiac resynchronisation therapy improves symptoms and reduces mortality in patients with chronic heart failure. In patients with previously implanted devices, particularly automatic defibrillators, central venous stenoses provide a challenge to upgrading to resynchronisation devices. We present a patient with central venous obstruction secondary to previously implanted defibrillator leads, in whom we achieved coronary sinus pacing through the ipsilateral internal jugular vein.

Benign outcome in a long-term follow-up of patients with hypertrophic cardiomyopathy in Brazil.

Selected patients with hypertrophic cardiomyopathy (HCM) have 3% to 4% annual mortality as compared to only 0.5% to 1.5% in nonselected patients. Our aim was to evaluate survival and prognostic factors in HCM in patients in a tertiary care center.</AbstractText>From 1980 to 1997, 214 patients were prospectively studied, with a mean follow-up of 7 years (range 1-25 years); there were 102 male and 112 female patients, aged 37 +/- 16 years (range 3-76 years). All patients had 12-lead electrocardiogram, 24-hour Holter monitor, and surface echocardiography. Univariate analysis was performed for known adverse factors such as young age, family history, syncope, functional class, atrial fibrillation, ventricular hypertrophy, left ventricular outflow tract obstruction, and nonsustained ventricular tachycardia.</AbstractText>There were 22 deaths (10%), 15 directly related to HCM (sudden in 11). The cumulative survival rates were 94.5% at 5 years, 91% at 10 years, and 87.9% at 15 years. The annual mortality rate was 1%. Only New York Heart Association functional class III/IV and maximal ventricular wall thickness &gt;30 mm were associated with HCM-related cardiac death.</AbstractText>We concluded that even a referred population of HCM patients may have a relatively benign outcome. Prognosis is related to advanced functional class and degree of left ventricular hypertrophy.</AbstractText>

The presence of contractile reserve has no predictive value for the evolution of left ventricular function following atrio-ventricular node ablation in patients with permanent atrial fibrillation.

Transcatheter ablation of the atrio-ventricular (AV) node followed by ventricular pacing has been shown to improve symptoms and quality of life (QOL) of patients with permanent atrial fibrillation (AF). In a considerable number of patients, cardiac function deteriorates after AV node ablation. We aimed to determine whether the absence of contractile reserve assessed by low dose dobutamine stress echocardiography (LDDSE) could identify those patients whose left ventricular (LV) function deteriorates after AV node ablation.</AbstractText>All 25 patients studied had permanent AF for at least 12 months. LVEF was determined 6 days and 3 months after AV node ablation by radionuclide ventriculography (RNV), at a paced rate of 80 beats/min. Deterioration in cardiac function was defined as a decrease in LVEF&gt;5%. LDSE was performed in all patients before and after ablation. The presence of contractile reserve was defined as an improvement in regional function of &gt;or=1 grade at low dose dobutamine in at least 4 segments. QOL measurements were taken using Minnesota, NHBP and MPWB questionnaires.</AbstractText>LVEF showed no improvement in the overall group (52.8+/-11.1% vs. 51.8+/-9.8%, p=NS). QOL showed significant improvement in all questionnaires (Minnesota: 4.1+/-2.1 vs. 2.5+/-2, p=0.001; NHBP: 54.8+/-43.3 vs. 34.2+/-34.3, p=0.002; MPWB: 22.2+/-4.6 vs. 19.4+/-6.2, p=0.03). There was no significant difference in change of LVEF between patients with and without contractile reserve (-0.4+/-8.7 vs. 1.6+/-11.3, p=NS). However, patients with a preserved LVEF at baseline showed more frequently a reduced LVEF after AV node ablation (62.2+/-10.4% vs. 47.5+/-7.6%, p=0.001).</AbstractText>(1) The absence of contractile reserve does not predict deterioration of cardiac function after AV node ablation. (2) AV node ablation results in a significant improvement in QOL, which is not necessarily associated with improvement of LVEF. (3) Higher baseline LVEF predicts deterioration of cardiac function. These data suggest that although AV node ablation is an excellent way of controlling symptoms, it should be avoided in patients with normal LV function.</AbstractText>

Clinical predictors of cardiac events in patients with isolated syncope and negative electrophysiologic study.

Patients with syncope or near syncope of unknown etiology represent a great challenge to cardiologists. An initial symptomatic episode triggers a series of diagnostic analysis which remain unsatisfactory when negative. More invasive tools such as electrophysiologic testing yield only partial answers to risk stratification while the complementary implantable holter diagnostics are not usually considered until a recurrent episode is documented.</AbstractText>This study targets predictors of significant cardiac rhythmic events in patients with a reported episode of syncope or near syncope presenting with negative diagnostics and electrophysiologic study results (EPS). A significant cardiac rhythmic event was defined as a combined end-point of (1) symptomatic AV block; (2) symptomatic conduction abnormalities requiring pacemaker therapy; (3) symptomatic sustained ventricular arrhythmia; and (4) sudden death.</AbstractText>All patients undergoing EPS after a first episode of syncope or presyncope between January 1997 and December 2001 were included for analysis. The study population consisted of 329 pts (42.6% women), 21 to 96 years old (mean 70+/-15 years) referred for an EP study for syncope or near syncope.</AbstractText>Of the 329 patients who underwent EPS, 305 (92.7%) had follow-up data. The population, mean age 70 (+/- 15 years) and composed of 42% women, presented with hypertension (51.5%), diabetes mellitus (14.4%), hypercholesterolemia (30%), tobacco use (35%), a familial history of coronary heart disease (22%), history of stroke (4%), history of MI (12%), history of atrial fibrillation (10%), structural heart disease (17.4%), left ventricular ejection fraction 61 (+/- 11%) and ECG abnormalities (37%). These anomalies included right (RBBB) or left (LBBB) bundle branch blocks, left anterior fascicular block (LAFB), left posterior fascicular block (LPFB), bifascicular block (RBBB+LAFB) and traces of myocardial infarction. The mean follow-up was 31+/-20 months with 5% of patients recording significant cardiac rhythmic events (15/305): AV block requiring pacemaker therapy in 7 patients, sinus dysfunction in 4, sudden death in 3 and ventricular tachycardia in 1. Univariate analysis reveals structural heart disease, ECG abnormalities and LVEF associated with the risk of significant cardiac rhythmic events defined by the combined end-point. Multivariate analysis using a Cox model found that the only independent predictor of events was an ECG abnormality. The long-term risk of significant event in the subset with ECG abnormalities is of 10.6% (12/113). If unexplained syncope recurrence was included in the combined end-point, ECG abnormality and LVEF were both determinants with a 13.3% (15/113) risk of a arrhythmic events analysis in the subset of patients presenting with ECG abnormalities and Cox model found ECG abnormality as the only independent predictor of event.</AbstractText>This study demonstrated that an ECG abnormality is the only predictive variable associated with a significant arrhythmic event in patients with a lone episode of syncope or near syncope and a negative EPS.</AbstractText>

Left ventricular pacing through the anterior interventricular vein in a patient with mechanical tricuspid, aortic and mitral valves.

Transvenous endocardial pacemaker implantation is contraindicated in patients after mechanical tricuspid valve replacement. A 76-year-old woman who suffered from bradyarrhythmia was implanted with a left ventricular pacing lead through a transvenous coronary vein after aortic, mitral, and tricuspid valve replacements. There were no complications and the stimulation thresholds were stable. The use of coronary vein leads provides a minimally invasive approach, safety, and effective stimulation for patients with a mechanical tricuspid valve.

Atrioventricular valve procedures with repeat fontan operations: influence of valve pathology, ventricular function, and arrhythmias on outcome.

The purpose of this study is to analyze atrioventricular valve procedures when performed in association with repeat Fontan operations and to determine the influence of atrioventricular valvar pathology, ventricular function, and arrhythmias on outcome.</AbstractText>Between December 1994 and August 2004, 80 patients had repeat Fontan operations that included arrhythmia surgery (78 of 80), venous pathway revision (78 of 80), atrioventricular valve repair-replacement (15 of 80), and other associated procedures. Mean ages were the following: at operation, 20.3 +/- 8.4 years; at prior Fontan, 7.1 +/- 5.8 years. Atrioventricular valve procedures were performed on 8 functionally mitral and 7 functionally tricuspid valves. The average cross-clamp and cardiopulmonary bypass times were 61.9 +/- 42.8 minutes and 218 +/- 82 minutes, respectively.</AbstractText>Ventricular dysfunction (8% vs 54%, p &lt; 0.0001), valvar dysfunction (13% vs 25%, p &lt; 0.05), and atrial arrhythmias (18% vs 86%, p &lt; 0.0001) increased during the preceding 12.0 +/- 4.7 years before the most recent Fontan operation. Multivariate analysis for death, orthotopic cardiac transplantation (OCT), or renal dialysis showed severe ventricular dysfunction, age greater than 25 years, right or ambiguous functional ventricle, and ischemic time greater than 100 minutes to be highly significant. Notably, cardiac index, elevated end diastolic pressure, and atrial fibrillation were not predictors of outcome. Mitral valve repairs were inconsistent due to probable technical misjudgments; most tricuspid valves could not be repaired. Operative and late mortality were 1.2% and 5.0%, respectively. Emergent and late OCT were 1.2% and 3.7%, respectively.</AbstractText>Risk factors for poor outcome are severe ventricular dysfunction, right or ambiguous single ventricle, age greater than 25 years, and ischemic time greater than 100 minutes. Mitral valves are potentially more amenable to repair than are tricuspid valves. Prosthetic valve replacement should be considered when valve repair is questionable.</AbstractText>

Patients, mean age 70 years, with automatic implantable cardioverter-defibrillators treated with dual-chamber rate responsive pacing (DDDR-70) have a higher mortality than patients with backup ventricular pacing (VVI-40) at 3.7-year follow-up.

One study showed in 506 patients with automatic implantable cardioverter-defibrillators (AICDs) that the mortality at 1-year follow-up was 6.5% with ventricular backup pacing at 40/minute (VVI-40) versus 10.1% in patients with dual-chamber rate responsive pacing at 70/minute (DDDR-70).</AbstractText>We performed a retrospective study to determine all-cause mortality in all patients at a university hospital who had AICDs without indications for antibradycardia pacing. Of 535 patients, mean age 70 +/- 12 years, 271 patients had backup ventricular pacing with a VVI-40, and 264 patients had dual-chamber rate responsive pacing with a DDDR-70.</AbstractText>At 3.7-year mean follow-up, all-cause mortality was 19% (50 of 264 patients) in patients with DDDR-70 pacing versus 11% (29 of 271 patients) with VVI-40 pacing (p &lt; .01).</AbstractText>Because of the increased mortality, increased cost, and complexity for dual-chamber rate responsive pacing in patients with AICDs, concomitant DDDR pacing at a rate of 70/minute in patients without an indication for antibradycardia pacing is not warranted.</AbstractText>

[Analysis of the frequency of cardiac arrhythmias and conduction disturbances from a health-care perspective].

Over the last few years, our understanding of the mechanisms underlying cardiac arrhythmias has increased substantially. However, few data on their prevalence exist. Our objectives were to analyze the prevalence of cardiac arrhythmias and conduction disturbances in cardiology clinic outpatients and to determine the number of patients with a class-I or -IIa recommendation for electrophysiological studies (EPS).</AbstractText>We investigated cardiac arrhythmias and conduction disturbances in 2045 patients and determined their prevalence in those seen for the first time. Specific conditions investigated included supraventricular and ventricular arrhythmias, ischemic disease with an ejection fraction (EF) &lt;30%, second-degree or higher atrioventricular (AV) block, intraventricular block, and sick sinus syndrome.</AbstractText>In total, 798 (39%) of all patients and 153 of the 704 (22%) seen for the first time presented with 1 or more of the specified conditions. Their distribution in all patients was: atrial fibrillation, 524 (26%); atrial flutter, 34 (2%); narrow-QRS tachycardia, 58 (3%); ventricular arrhythmias or EF&lt;30% due to ischemic disease or both, 46 (2%); AV block or sinus dysfunction, 68 (3%); intraventricular block, 157 (8%); and other conditions, 4 (0.2%). Some 7% (143/2045) of all patients and 3.5% (25/704) of those seen for the first time had an indication for EPS.</AbstractText>a) Almost 40% of all patients seen in a cardiology outpatient clinic and 1 in 4 of those seen for the first time presented with a cardiac arrhythmia or conduction disturbance; and b) more than 3% of patients seen for the first time had an indication for EPS.</AbstractText>

Ischemic enterocolitis examined by colonoscopy and selective angiography.

To study the value of colonoscopy and selective angiography in diagnosing ischemic enterocolitis.</AbstractText>Among the 16 cases under study, 10 cases had hypertension and a history of coronary artery disease (one was hospitalized for sub-ventricular-wall infarction). The blood pressure of 10 of the 16 cases ranged from 13.9-23.8 to 13.3-14.6 kPa (170-180/100-110 mmHg). Two cases had chronic auricular fibrillation, and in four cases, a cardiogram showed left-front branch conduction block. Sixteen patients were examined by colonoscopy. Among them, 14 cases had a long course of angiocardiac disease, and were further examined by selective mesenteric inferior angiography.</AbstractText>The colonoscopy revealed local mucous hyperemia edema and blood on contact. Lesions were found in the sigmoid colon in four cases, in the descending colon in eight cases and in splenic flexure in four cases, which suggests that the lesion always appeared in the left part of colon. There were different degrees of inflammatory cell infiltration, submucous bleeding, edema, fibro-embolism and hemosiderosis by biopsy in the 16 patients whose membranes affect part of the enteral wall. Of the 14 patients examined by mesenteric inferior angiography, 3 cases showed mesenteric amphraxis inferior and formation of collateral circulation. There were different degrees of stenosis in the other 11 subjects' mesenteric inferior cavities which grew slim and their branches were stenotic, so the radiographic image was not complete and the ends of some branches even cannot be seen.</AbstractText>The colonoscopy and the selective mesenteric inferior angiography are both helpful in the diagnosis of ischemic enterocolitis.</AbstractText>

Myocardial perfusion/metabolism mismatch and ventricular arrhythmias in the chronic post infarction state.

Ventricular arrhythmias have been shown to originate in the myocardial peri-infarct region due to irregular heterotopic conduction. Hypoperfused but viable myocardium is often localised in those areas and may be involved in the pathogenesis of arrhythmias. We tested the hypothesis that these myocardial perfusion/metabolism mismatches (MM) are significantly associated with ventricular arrhythmias in the chronic post infarction state.</AbstractText><AbstractText Label="PATIENTS, METHODS" NlmCategory="METHODS">47 post infarction patients were included in the study. 33 suffered from ventricular arrhythmia whereas 14 did not. All patients underwent (99m)Tc tetrofosmin SPECT and (18)F-FDG PET. A region-of-interest(ROI)-analysis was used to assess viable myocardium based on predefined MM-criteria. Univariate analyses as well as a logistic regression model for the multivariate analysis were carried out.</AbstractText>94% of the arrhythmic patients displayed at least one MM-segment as compared to 64% of the non-arrhythmic patients. MM-segments and arrhythmia showed a statistically significant relation (p = 0.018). The logistic regression model predicted the occurrence or absence of arrhythmia in 85% of all cases. Multivariate analysis gave consistent results, after adjusting for symptomatic chronic heart failure (CHF), aneurysms and age.</AbstractText>Our results support the hypothesis that hypoperfused but viable myocardium represents an arrhythmogenic substrate and is a relevant risk factor for developing ventricular arrhythmias following myocardial infarction. Therefore, the detection of MM-segments allows the identification of patients with a higher risk for future cardiac events.</AbstractText>

Tempol reduces reperfusion-induced arrhythmias in anaesthetized rats.

The generation of reactive oxygen species (ROS) contributes to reperfusion-induced arrhythmias. In the present study, the antiarrhythmic effects of tempol and tiron, two membrane-permeable radical scavengers, on reperfusion-induced arrhythmias in rats in vivo were investigated. The anaesthetized rats were subjected to 5 min of left descending coronary artery (LAD) occlusion followed by 30 min of reperfusion. All rats pretreated with saline developed ventricular tachycardia (VT) and ventricular fibrillation (VF) at the onset of reperfusion, and most of the rats died from irreversible VF at the end of reperfusion. However, pretreatment with tempol (30 or 100 mg kg(-1)) 5 min before reperfusion reduced mortality, arrhythmia score and the incidence and duration of VT and VF. In the rats pretreated with high dose of tempol (100 mg kg(-1)), no VF happened and all rats were alive at the end of the experiment. The arrhythmia score was also significantly decreased compared with that of rats pretreated with saline (0.80 +/- 0.4 versus 5.6 +/- 0.4, P &lt; 0.01). Tiron also provided nearly complete protection against reperfusion-induced arrhythmias when given 2 min before reperfusion. On the other hand, intravenous administration of tempol induced decreases in mean arterial pressure (MAP), heart rate (HR) and pressure rate index (PRI), a relative indicator of myocardial oxygen consumption. In order to determine whether the antiarrhythmic effects of tempol were secondary to the reduction of myocardial oxygen consumption, continuous electrical stimulation of the aortic depressor nerve (3 V, 10 ms and 10 Hz) was carried out in a group of rats to induce decreases in MAP, HR and PRI similar to those in the high dose of Tempol group. However, these rats did not show significant changes in the severity of reperfusion-induced arrhythmias. We conclude that both tempol and tiron significantly reduce reperfusion-induced arrhythmias in rats, and this protective action is independent of hemodynamic effects.

A review of carvedilol arrhythmia data in clinical trials.

beta-Blockers are currently being evaluated more intensively to define their role in clinical use as antiarrhythmic agents. beta-Adrenergic blockade has been studied in relation to atrial fibrillation, ventricular arrhythmias, and sudden death; however, it is apparent from a number of studies that not all beta-blockers are equally effective. Randomized clinical trial data, both in heart failure and post-myocardial infarction (MI) patients, have shown differences in mortality benefits in addition to a variable effect on arrhythmias and sudden death. Carvedilol, a third-generation beta-blocker with proven clinical benefit in the management of heart failure and post-MI patients, has properties that may make it an effective antiarrhythmic agent. This paper reviews the current clinical arrhythmia data available for carvedilol from large-scale clinical trials and small studies. The trial evidence demonstrates that carvedilol therapy can be an effective adjunctive rate-control therapy in patients with atrial fibrillation, prevent mortality in patients with heart failure or post-MI with left ventricular dysfunction, with or without atrial fibrillation, and reduce its onset and the incidence of ventricular arrhythmia and sudden death.

Antiadrenergic therapy in the control of atrial fibrillation.

Atrial fibrillation (AF) in heart failure develops commonly in older individuals and its prevalence increases as heart failure severity progresses. Because of deteriorating hemodynamics, patients with heart failure are at increased risk for developing AF and, conversely, AF in heart failure patients is associated with adverse hemodynamic changes. AF is believed to increase the mortality risk in heart failure, which may be minimized by treatment that includes the control of ventricular rate, prevention of thrombotic events, and conversion to normal sinus rhythm. Clinical guidelines recommend amiodarone or dofetilide in heart failure patients, but these drugs have certain drawbacks, such as an increased risk for bradyarrhythmias with amiodarone and proarrhythmic reaction with dofetilide. Some but not all clinical trials have suggested that rate control should be the primary therapeutic goal in high-risk heart failure patients with AF and, if unsuccessful, followed by rhythm control. The former is effectively achieved with rate-lowering beta-blockers alone or in combination with digoxin. Recent studies evaluating the effects of combination carvedilol/digoxin therapy demonstrate synergistic effects between the two drugs. This combination therapy decreased heart failure symptoms, effectively reduced ventricular rate, and improved ventricular function to a greater extent compared with that produced by either drug alone. Although digoxin alone is an effective heart failure treatment, its use as a single rate-control therapy is often ineffective in heart failure patients with AF associated with rapid ventricular response. Carvedilol is effective, alone or in combination, with digoxin in such heart failure patients with AF, and has been shown to reduce mortality risk in patients with chronic heart failure during prolonged therapy.

Beta-Adrenergic blockers as antiarrhythmic and antifibrillatory compounds: an overview.

Beta-Adrenergic blockers have a wide spectrum of action for controlling cardiac arrhythmias that is larger than initially thought. Data from the past several decades indicate that, as an antiarrhythmic class, beta-blockers remain among the very few pharmacologic agents that reduce the incidence of sudden cardiac death, prolong survival, and ameliorate symptoms caused by arrhythmias in patients with cardiac disease. As a class of compounds, beta-blockers have a fundamental pharmacologic property that attenuates the effects of competitive adrenergic receptors. However, the net clinical effects of the different beta-receptor blockers may vary quantitatively because of variations in associated intrinsic sympathomimetic agonism and in their intrinsic potency for binding to beta-receptors. These individual compounds also differ in their selectivity for beta(1)- and beta(2)-receptors. Metoprolol is a beta(1)-selective blocker, whereas carvedilol is a nonselective beta(1)- and beta(2)-blocker, an antioxidant, and has a propensity to inhibit alpha(1)-receptors and endothelin. Evolving data from controlled and uncontrolled clinical trials suggest that there are clinically significant differences among this class of drugs. Recent evidence also suggests that the antiarrhythmic actions of certain beta-receptor blockers such as carvedilol and metoprolol extend beyond the ventricular tissue to encompass atrial cells and help maintain sinus rhythm in patients with atrial fibrillation, especially in combination with potent antifibrillatory agents such as amiodarone. This introduction provides a current perspective on these newer developments in the understanding of the antiarrhythmic and antifibrillatory actions of beta-blockers.

Carvedilol mitigates adverse effects of epinephrine during cardiopulmonary resuscitation.

Earlier studies have implicated the adverse effects of beta- and alpha(1)-adrenergic receptors during cardiopulmonary resuscitation (CPR). Because carvedilol is both a nonselective beta- and alpha1-selective adrenergic receptor-blocking agent, we hypothesized that pretreatment with carvedilol would convert the actions of epinephrine to that of a selective alpha2-agonist.</AbstractText>Ventricular fibrillation (VF) was induced in Sprague-Dawley rats weighing approximately 500 g. Animals were randomized to 4 groups of 5 animals each: (1) placebo pretreatment and epinephrine treatment, (2) carvedilol pretreatment and placebo treatment, (3) carvedilol pretreatment and epinephrine treatment, and (4) placebo pretreatment and placebo treatment. Carvedilol (50 microg/kg) was injected as a bolus into the right atrium 15 minutes before VF was induced. VF was untreated for 8 minutes, after which CPR (chest compression and mechanical ventilation) was begun. Epinephrine (30 microg/kg) was injected into the right atrium 2 minutes after the start of CPR. Electrical defibrillation was attempted after 14 minutes of VF.</AbstractText>All but 2 animals were successfully resuscitated. Approximately equivalent increases in coronary perfusion pressure from 23 +/- 1 mm Hg to 30 +/- 3 mm Hg were observed after the injection of epinephrine independently of carvedilol pretreatment. Carvedilol pretreatment followed by epinephrine treatment reduced early postresuscitation ventricular ectopy (116 +/- 147 vs 834 +/- 380, P &lt; .01) and minimized increases in arterial blood lactate at 5 minutes after resuscitation (10.9 +/- 2.1 mmol/L vs 17.4 +/- 3.5 mmol/L, P &lt; .01). The postresuscitation cardiac index measured 4 hours later was increased (307 +/- 43 mL x min(-1) x kg(-1) vs 210 +/- 6 mL x min(-1) x kg(-1), P &lt; .05). Left ventricular diastolic pressures were decreased (6 +/- 1 vs 14 +/- 1 mm Hg, P &lt; .05). Animals pretreated with carvedilol survived longer (71 +/- 1 vs 45 +/- 22 hours, P &lt; .05) and with less postresuscitation neurologic deficit.</AbstractText>After beta- and alpha1-adrenergic blockade with carvedilol before inducing cardiac arrest, epinephrine administered during CPR yielded better postresuscitation myocardial and neurologic functions and significantly increased postresuscitation survival.</AbstractText>

High-sensitivity C-reactive protein is predictive of successful cardioversion for atrial fibrillation and maintenance of sinus rhythm after conversion.

Cardioversion for atrial fibrillation (AF) is the most effective treatment for the restoration of sinus rhythm (SR). Recently, an elevated level of hs-CRP has been shown to be associated with AF burden, suggesting that inflammation increases the propensity for persistence of AF. We examined whether the level of high-sensitivity C-reactive protein (hs-CRP) was predictive of the outcome of cardioversion for AF.</AbstractText>One hundred and six patients with a history of symptomatic AF lasting &gt; or =1 day (age 63+/-14 years, mean+/-S.D.) underwent cardioversion. Echocardiography and hs-CRP assay were performed immediately prior to cardioversion. SR was restored in 84 patients (79%). By using selected cutoff values, multiple discriminant analysis revealed significant associations between successful cardioversion and a shorter duration of AF (AF duration&lt; or =36 days, odds ratio (OR), 0.98; 95% confidence interval (CI), 0.97-0.99), smaller left atrial diameter (left atrial diameter&lt; or =40 mm, OR 0.82, 95% CI 0.71-0.94), better-preserved left ventricular ejection fraction (left ventricular ejection fraction&gt; or =60%, OR 0.92, 95% CI 0.86-0.99), and lower hs-CRP level (hs-CRP&lt; or =0.12 mg/dL, OR 0.33, 95% CI 0.21-0.51). During a follow-up period of 140+/-144 days, AF recurred in 64 patients (76%). By using a cutoff value of hs-CRP&gt; or =0.06 mg/dL, Cox proportional-hazards regression model found that only hs-CRP level was an independent predictor of AF recurrence (OR 5.30, 95% CI 2.46-11.5) after adjustment for coexisting cardiovascular risks. When patients were divided by the hs-CRP level of 0.06 mg/dL, percentage of maintenance of SR below and above the cutoff was 53% and 4%, respectively (log-rank test, p&lt;0.0001).</AbstractText>hs-CRP level determined prior to cardioversion represents an independent predictor of both successful cardioversion for AF and the maintenance of SR after conversion.</AbstractText>

Providing automated external defibrillators to urban police officers in addition to a fire department rapid defibrillation program is not effective.

The aim of this study was to determine if providing automated external defibrillators (AEDs) to urban police officers would increase the proportion of patients with out-of-hospital cardiac arrest (OOH-CA) who were discharged alive from the hospital.</AbstractText>This prospective, controlled study was conducted in a city with about 332,000 persons. The EMS system included paramedic ambulances and fire department based first responders equipped with defibrillators, but police officers did not respond routinely to medical emergencies. Between March 1997 and February 1999, all OOH-CAs in four police districts were identified and followed until death or hospital discharge. All 35 police cars in one police district were provided with AEDs, and all police officers in that district were trained in CPR and the use of AEDs. Police and fire first response units were dispatched simultaneously in district 3 (intervention group). Fire first response was dispatched without police in districts 2, 4, and 5 (control group).</AbstractText>A total of 645 OOH-CAs occurred over the 2 years. Sixty-two were outside of the study area. Two did not have accurate address information to determine the police district. Of the remaining cases, 154 (27%) occurred in the intervention district and 427 (73%) were in the control area. Survival to hospital discharge was similar; it was 11/154 (7.1%) in the intervention and 16/427 (3.8%) in the control districts (odds ratio=1.98; 95% CI 0.90--4.36). Survival to hospital discharge for witnessed OOH-CA events occurring prior to EMS arrival and found to be in ventricular fibrillation or ventricular tachycardia was 4/27 (15%) in the intervention area and 9/73 (12%) in the control area (odds ratio=1.2; 95% CI 0.4-4.4).</AbstractText>Equipping police cars with AEDs in an urban area where the fire department-based first response system also carries defibrillators did not improve the hospital discharge survival rate for victims of OOH-CA.</AbstractText>

Are transthoracic echocardiographic parameters associated with atrial fibrillation recurrence or stroke? Results from the Atrial Fibrillation Follow-Up Investigation of Rhythm Management (AFFIRM) study.

The purpose of this study was to evaluate the associations of transthoracic echocardiographic parameters with recurrent atrial fibrillation (AF) and/or stroke.</AbstractText>The Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study, an evaluation of elderly patients with AF at risk for stroke, provided an opportunity to evaluate the implications of echocardiographic parameters in patients with AF.</AbstractText>Transthoracic echocardiographic measures of mitral regurgitation (MR), left atrial (LA) diameter, and left ventricular (LV) function were evaluated in the AFFIRM rate- and rhythm-control patients who had sinus rhythm resume and had these data available. Risk for recurrent AF or stroke was evaluated with respect to transthoracic echocardiographic measures.</AbstractText>Of 2,474 patients studied, 457 had &gt; or =2(+)/4(+) MR, and 726 had a LA diameter &gt;4.5 cm. The LV ejection fraction was abnormal in 543 patients. The cumulative probabilities of at least one AF recurrence/stroke were 46%/1% after 1 year and 84%/5% by the end of the trial (&gt; 5 years), respectively. Multivariate analysis showed that randomization to the rhythm-control arm (hazard ratio [HR] = 0.64; p &lt; 0.0001) and a qualifying episode of AF being the first known episode (HR = 0.70; p &lt; 0.0001) were associated with decreased risk. Duration of qualifying AF episode &gt;48 h (HR = 1.55; p &lt; 0.0001) and LA diameter (p = 0.008) were associated with an increased risk of recurrent AF. Recurrent AF was more likely with larger LA diameters (HR = 1.21, 1.16, and 1.32 for mild, moderate, and severe enlargement, respectively). No transthoracic echocardiographic measures were associated with risk of stroke.</AbstractText>In the AFFIRM study, large transthoracic echocardiographic LA diameters were associated with recurrent AF, but no measured echocardiographic parameter was associated with stroke.</AbstractText>

Phosphorylated heat shock protein 27 is involved in enhanced heart tolerance to ischemia in short-term type 1 diabetic rats.

To examine the tolerance of type 1 diabetic hearts to ischemia and reperfusion injury. Myocardial contents of 27-kDa and 70-kDa heat shock proteins (hsp) as well as phosphorylated hsp27 were also determined.</AbstractText>Hearts from hyperglycemic rats 3 weeks after streptozocin injection and age-matched normal rats were subjected to ischemia and reperfusion in vitro. Cardiac function and electrocardiogram were recorded throughout experiments. Myocardial heat shock proteins were detected with Western blot.</AbstractText>Despite depressed systolic function at the baseline, diabetic hearts exhibited considerable enhancement in post-ischemic heart function, manifested by an increase in the maximal rate of left ventricular pressure rise and fall (post-ischemic dp/dtmax and dp/dtmin were 560+/-117 and -313+/-68 mmHg/s in control, n=7, 1249+/-57 and -1204+/-36 mmHg/s in diabetes, n=10, P&lt;0.01). Reperfusion ventricular fibrillation in the diabetic group were attenuated compared with controls (1.5+/-0.3 vs 7.2+/-2.1 min in control, P&lt;0.01). The increased heart resistance to ischemia in diabetes was associated with hyperglycemia and accompanied by enhanced expression of myocardial phosphorylated hsp27 with normal aortic vessel relaxation. Cardioprotection was abrogated by metabolic correction with insulin and accompanied by phospho-hsp27 reduction.</AbstractText>Heart resistance to ischemia is increased in type 1 diabetes, and hyperglycemia may present a mild yet stressful stimulus leading to upregulation of endogenous stress protein, which may play a potential role in cardioprotection and compensate for detrimental effects of hyperglycemia in diabetes.</AbstractText>

Volumetric cine CMR to quantify atrial structure and function in patients with atrial dysrhythmias.

To implement a cardiac magnetic resonance (CMR)-based protocol to define atrial structure and function in individuals with paroxysmal atrial fibrillation (PAF), heritable cardiac conduction and myocardial disease with atrial dysrhtyhmias (HCCMD), and healthy controls.</AbstractText>Fifteen controls, 20 PAF, and 12 HCCMD subjects underwent CMR examination including: multislice short-axis cine, multislice horizontal long-axis cine, and gadolinium-enhanced coronal plane magnetic resonance angiography (MRA) for pulmonary vein analysis. We also assessed for ventricular myopathy with delayed myocardial enhancement (DME) acquisitions.</AbstractText>Right and left ventricular measurements did not differ among the three groups. Seven heritable atrial dysrhythmia subjects and no control or PAF subjects demonstrated midmyocardial fibrosis of the basal interventricular septum by DME. Left atrial (LA) volume at the onset of atrial systole and minimal LA volume were significantly higher in PAF subjects compared to controls (p &lt; 0.05 for both), LA percent emptying was significantly lower in PAF subjects (p &lt; 0.01), and RA percent emptying was significantly lower in PAF subjects compared to controls (p &lt; 0.01), though these differences were not significant when controlling for heart rate, age and gender. There was no significant difference in right atrial (RA) volumes among study groups. Atrial volumes and function did not differ significantly between heritable atrial dysrhtyhmia subjects and controls. PAF subjects had greater frequency of a right middle pulmonary vein (RMPV) than controls (6/20 vs. 3/15) that did not reach statistical significance.</AbstractText>CMR can quantify atrial structure and function in patients with PAF compared to controls. This protocol could not detect abnormalities in atrial function in early affected patients with heritable cardiomyopathy and atrial premature beats.</AbstractText>

Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators: a randomized controlled trial.

Clinical studies of omega-3 polyunsaturated fatty acids (PUFAs) have shown a reduction in sudden cardiac death, suggesting that omega-3 PUFAs may have antiarrhythmic effects.</AbstractText>To determine whether omega-3 PUFAs have beneficial antiarrhythmic effects in patients with a history of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF).</AbstractText>Randomized, double-blind, placebo-controlled trial performed at 6 US medical centers with enrollment from February 1999 until January 2003.</AbstractText>Two hundred patients with an implantable cardioverter defibrillator (ICD) and a recent episode of sustained VT or VF.</AbstractText>Patients were randomly assigned to receive fish oil, 1.8 g/d, 72% omega-3 PUFAs, or placebo and were followed up for a median of 718 days (range, 20-828 days).</AbstractText>Time to first episode of ICD treatment for VT/VF, changes in red blood cell concentrations of omega-3 PUFAs, frequency of recurrent VT/VF events, and predetermined subgroup analyses.</AbstractText>Patients randomized to receive fish oil had an increase in the mean percentage of omega-3 PUFAs in red blood cell membranes from 4.7% to 8.3% (P&lt;.001), with no change observed in patients receiving placebo. At 6, 12, and 24 months, 46% (SE, 5%), 51% (5%), and 65% (5%) of patients randomized to receive fish oil had ICD therapy for VT/VF compared with 36% (5%), 41% (5%), and 59% (5%) for patients randomized to receive placebo (P = .19). In the subset of 133 patients whose qualifying arrhythmia was VT, 61% (SE, 6%), 66% (6%), and 79% (6%) of patients in the fish oil group had VT/VF at 6, 12, and 24 months compared with 37% (6%), 43% (6%), and 65% (6%) of patients in the control group (P = .007). Recurrent VT/VF events were more common in patients randomized to receive fish oil (P&lt;.001).</AbstractText>Among patients with a recent episode of sustained ventricular arrhythmia and an ICD, fish oil supplementation does not reduce the risk of VT/VF and may be proarrhythmic in some patients.</AbstractText>

Hypothermia improves defibrillation success and resuscitation outcomes from ventricular fibrillation.

Induced hypothermia is recommended to improve neurological outcomes in unconscious survivors of out-of-hospital ventricular fibrillation (VF) cardiac arrest. Patients resuscitated from a VF arrest are at risk of refibrillation, but there are few data on the effects of already existing hypothermia on defibrillation and resuscitation.</AbstractText>Thirty-two swine (mean+/-SE weight, 23.0+/-0.6 kg) were divided into 4 groups: normothermia (n=8), mild hypothermia (35 degrees C) (n=8), moderate hypothermia (33 degrees C) (n=8), and severe hypothermia (30 degrees C) (n=8). Hypothermia was induced by surrounding the animal with ice, and VF was electrically induced. After 8 minutes of unsupported VF (no CPR), the swine were defibrillated (biphasic waveform) with successive shocks as needed and underwent CPR until resumption of spontaneous circulation or no response (&gt; or =10 minutes). First-shock defibrillation success was higher in the moderate hypothermia group (6 of 8 hypothermia versus 1 of 8 normothermia; P=0.04). The number of shocks needed for late defibrillation (&gt; or =1 minute after initial shock) was less in all 3 hypothermia groups compared with normothermia (all P&lt;0.05). None of the 8 animals in the normothermia group achieved resumption of spontaneous circulation compared with 3 of 8 mild hypothermia (P=NS), 7 of 8 moderate hypothermia (P=0.001), and 5 of 8 severe hypothermia (P=0.03) animals. Coronary perfusion pressure during CPR was not different between the groups.</AbstractText>When VF was induced in the setting of moderate or severe hypothermia, resuscitative measures were facilitated with significantly improved defibrillation success and resuscitation outcome. The beneficial effect of hypothermia was not due to alteration of coronary perfusion pressure, which suggests that changes in the mechanical, metabolic, or electrophysiological properties of the myocardium may be responsible.</AbstractText>

Thoracic spinal cord stimulation reduces the risk of ischemic ventricular arrhythmias in a postinfarction heart failure canine model.

Thoracic spinal cord stimulation (SCS) is a promising therapy in treating refractory angina. This study was designed to investigate SCS with regard to the risk of arrhythmias during myocardial ischemia and its cardiac electrophysiological effects.</AbstractText>We studied 22 dogs with healed anterior myocardial infarction (MI) and superimposed heart failure (HF) induced by rapid ventricular pacing. SCS was applied at the dorsal T1-T2 segments of the spinal cord (at 50 Hz, 0.2 ms) for 15 minutes. Transient (2-minute) myocardial ischemia was induced on 2 separate occasions (no SCS and SCS) to provoke ventricular arrhythmias (ventricular tachycardia/ventricular fibrillation; VT/VF). Ischemic episodes were separated by 90 minutes, and dogs were randomly assigned to receive SCS or no SCS before the first or second ischemic episode. SCS reduced the occurrence of VT/VF from 59% to 23% when SCS was applied during transient myocardial ischemia (odds ratio, 0.36; 95% confidence interval, 0.1626 to 0.5646; P=0.0009). SCS also decreased sinus rate by 7.5+/-14 bpm (P=0.048), increased the PR interval by 11.1+/-14.7 ms (P=0.009), and reduced systolic blood pressure by 9.8+/-13.6 mm Hg (P=0.02).</AbstractText>Thoracic SCS appears to protect against ischemic VT/VF in a canine model of healed MI and HF. SCS reduced sinus rate and systolic blood pressure, changes consistent with the previously known antisympathetic effect of SCS, which may have contributed to the antiarrhythmic benefits.</AbstractText>

Doppler estimation of left ventricular filling pressures in patients with mitral valve disease.

Conventional Doppler measurements have limitations in the prediction of left atrial pressure (LAP) in patients with mitral valve disease (MVD), given the confounding effect of valve area, left ventricular (LV) relaxation, and stiffness. However, the time interval between the onset of early diastolic mitral inflow velocity (E) and annular early diastolic velocity (Ea) by tissue Doppler imaging (TDI), T(E-Ea), which is well related to the time constant of LV relaxation (tau) in canine and clinical studies, is not subject to these variables. We therefore undertook this study to test its usefulness in a patient population.</AbstractText>Two-dimensional Doppler and TDI echocardiography were performed simultaneously with right-heart catheterization in 51 consecutive patients (mean+/-SD age, 64+/-11 years) with MVD: 35 with moderately severe to severe mitral regurgitation (MR) and 16 with moderate to severe mitral stenosis (MS). Among several Doppler measurements, only the mitral E/A ratio, isovolumetric relaxation time (IVRT), and pulmonary venous Ar duration had significant relations with mean pulmonary capillary wedge pressure (PCWP). The ratio of IVRT to T(E-Ea) (for MR, r=-0.92; for MS, r=-0.88; both P&lt;0.001) and the ratio of IVRT to tau (for MR, r=-0.74; for MS, r=-0.85; both P&lt;0.001) had the best correlations with PCWP. In 54 repeat studies, including those performed after MV repair or replacement, these ratios tracked well the changes in PCWP and readily identified changes in mean PCWP by &gt; or =5 mm Hg. A similar correlation was noted in 13 patients with atrial fibrillation (r=-0.92, P&lt;0.01) and in a prospective group of 14 patients with MR (r=-0.93, P&lt;0.001).</AbstractText>The ratio of IVRT to T(E-Ea) or to tau can be readily applied for estimating mean PCWP in patients with MVD and can track changes in PCWP after valve surgery.</AbstractText>

Very high survival among patients defibrillated at an early stage after in-hospital ventricular fibrillation on wards with and without monitoring facilities.

The association between the interval between collapse and defibrillation and outcome is well described in out of hospital cardiac arrest but not as well in in-hospital cardiac arrest. We report the outcome among patients who suffered an in-hospital cardiac arrest and were found in ventricular fibrillation (VF) with the emphasis on the delay to defibrillation.</AbstractText>In patients who suffered an in-hospital cardiac arrest at Sahlgrenska University Hospital in G&#xf6;teborg between 1994 and 2002 there were 1.570 calls for the rescue team of which 71% had suffered a cardiac arrest. Among cardiac arrests 47% took place on monitored wards. The proportion of patients found in VF was 59% on wards with monitoring facilities and 45% on wards without (p&lt;0.0001). Approximately 90% of these patients were defibrillated &lt;or=3 min after collapse on monitored wards compared with 54% on non-monitored wards (p&lt;0.0001). Among all patients, there was a strong relationship between the interval between collapse to the first defibrillation and survival to discharge from hospital (p&lt;0.0001): 66% were discharged alive if defibrillated &lt;or=3 min compared with 20% if defibrillated &gt;12 min. On monitored wards, the survival was 63% if defibrillated &lt;or=3 min compared with 60% if defibrillated &gt;3 min after collapse (NS). The corresponding values for non-monitored wards were 72% and 35%, respectively (p=0.0003). Cerebral function among survivors at discharge appeared to be good among the majority of patients both in monitored and non monitored wards.</AbstractText>If patients with in hospital VF were defibrillated early in both monitored and non monitored wards survival to hospital discharge was high. This highlights the importance of being prepared for the rapid defibrillation on wards without monitoring facilities.</AbstractText>

Supraventricular tachycardia with a baseline ECG pattern of Brugada syndrome.

The typical arrhythmias found in patients with the Brugada syndrome is either ventricular fibrillation or polymorphic ventricular tachycardia. We report the case of a patient who presented with supraventricular tachycardia accompanied by ECG features of the Brugada syndrome (BrS) during both tachyarrhythmia and sinus rhythm. This case lends support to the recently reported association between supraventricular tachyarrhythmia and BrS and the hypothesis that the arrhythmogenic substrate in BrS is not limited to the ventricular level.

Cross-ventricular pacemaker-mediated tachycardia by myopotential induction during biventricular pacing.

Patients in permanent atrial fibrillation treated for heart failure and ventricular asynchrony can be implanted with conventional dual chamber pacemakers (DDD) pacemakers used in the biventricular mode. The left ventricular lead is connected to the atrial channel.</AbstractText>We report the case of a patient who developed ventriculo-ventricular pacemaker-mediated tachycardia (PMT) induced by myopotential sensing in the atrial channel, inhibiting left ventricular pacing.</AbstractText>In the absence of specifically designed pacemakers, the use of DDD pacemakers in the biventricular mode requires certain precautions, such as anti-PMT mode activation, disabling automatic sensitivity, and lengthening the postventricular atrial refractory period (PVARP), or mode switch to DVIR.</AbstractText>

Cerebral oxygenation during defibrillator threshold testing of implantable cardioverter defibrillators.

The induction of ventricular fibrillation (VF) during defibrillator threshold testing of implantable cardioverter defibrillators (ICD) provokes global cerebral hypoperfusion and impaired oxygen delivery. Limited data are available on the neurophysiological effects of defibrillator threshold testing. Near infrared spectroscopy (NIRS) can noninvasively measure changes in specific chromophores, which reflect cerebral oxygenation at the intravascular and mitochondrial levels. We performed a prospective trial using NIRS to analyze cerebral cortical oxygenation during defibrillator threshold testing.</AbstractText>Eleven patients (men = 9; age = 64 +/- 11 years: LVEF = 44 +/- 11%) underwent subpectoral ICD implantation and defibrillator threshold testing under general anesthesia. A NIRO 300 spectrometer was used to measure the absolute changes in the concentrations of oxyhemoglobin, de-oxyhemoglobin, and cytochrome c oxidase copper moiety during each procedure. The mean arterial blood pressure was monitored simultaneously.</AbstractText>The mean number of defibrillator threshold tests was two (range 2-6). Twenty-six episodes of VF (duration 13.1 +/- 9.7 seconds; cycle length 230.2 +/- 20.8 ms) and two episodes of VT (duration 15 +/- 2.8 seconds; cycle length 320 +/- 11.3 ms) were induced. Each episode of VF and VT resulted in a decrease in the mean arterial blood pressure to 23.9 +/- 7.5 mmHg (p &lt; or = 0.05) and oxyhemoglobin (-4.2 +/- 1.7 micromol/L; p &lt; or = 0.05) and an increase in de-oxyhemoglobin (2.7 +/- 1.4 micromol/L). There was no change in the cytochrome c oxidase copper moiety redox status (0.09 +/- 0. 30 micromol/L).</AbstractText>Our results suggest that impaired oxygen delivery during induced VF and VT does not affect oxygen availability at the cellular intra-mitochondrial level.</AbstractText>

Detection of the defibrillation threshold using the upper limit of vulnerability following defibrillator implantation.

This study was designed to test defibrillation threshold (DFT) with the least number of fibrillation inductions using upper limit of vulnerability (ULV) and to describe the most practical set of ICD during DFT following implantation.</AbstractText>Although the correlation between ULV and DFT has been well described, there has been no uniform DFT testing protocol taking the advantage of ULV after defibrillator (ICD) implantation.</AbstractText>A total of 26 patients undergoing a new ICD implantation had a DFT induced with scanned T wave shock. The hypothesis that ventricular fibrillation (VF) could be defibrillated with 5 J higher than the highest T wave shock needed to induce VF or with 10 J if the T wave shock needed to induce VF was less than 5 J, was tested and 20 patients fulfilled these criteria. The methodology is improved by detecting peak T wave with 12-lead ECG, applying biphasic T wave shock and scanning the T wave shock in a wider window.</AbstractText>Five patients in the first group (n = 15) and one patient in the second group (n = 11) did not fulfill the above hypothesis. The common features of six patients who did not fulfill the hypothesis were that T wave shock needed to induce VF was either under 5 J (5 patients) or high (1 patient).</AbstractText>This study revealed the importance of methodology in studies regarding ULV and DFT. Following ICD implantation, we propose the first biphasic T wave detected by 12-lead ECG and rescue shock set at 10 and 15 J, respectively. If any of the scanned T wave (40 ms before and 40 ms after the peak T wave with decrements and increments of 20 ms) shocks could not induce VF, then the T wave and the first rescue shock should be set at 5 and 10 J, respectively. If the induction of VF has been unsuccessful with T wave shock at 5 J, then a safe defibrillation with 10 J should be expected in majority.</AbstractText>

The prevention of sudden cardiac death: the role of the automated external defibrillator.

Sudden death is usually the result of hemodynamically destabilizing ventricular tachycardia or ventricular fibrillation. Because the only definitive treatment for ventricular tachycardia/ventricular fibrillation is a direct current shock, and because that defibrillating shock must be given very quickly to be effective, the American Heart Association's "chain of survival" approach to persons with a cardiac arrest emphasizes early access to care, early cardiopulmonary resuscitation, early cardiac defibrillation and early advanced life support. The link in this chain of survival that has been changing most dramatically over the past decade is that of early defibrillation. The automated external defibrillator enables life-saving defibrillation therapy to be provided to the cardiac arrest victim by nontraditional responders, such as the general public. The present review evaluates the current role of the automated external defibrillator in the ongoing struggle to prevent sudden cardiac death.

Differential functional effects of two 5-HT4 receptor isoforms in adult cardiomyocytes.

Serotonin 5-HT4 receptors are present in human atrial myocytes and have been proposed to contribute to the generation of atrial fibrillation. However, 5-HT4 receptors have so far been only found in human and pig atria and are absent from the heart of small laboratory animals, such as rat, guinea pig, rabbit and frog, which limits the experimental settings for studying their functional properties. In this study, we developed an adenovirus expression system to examine the properties of two human 5-HT4 receptor splice variants, h5-HT4(b) and h5-HT4(d), expressed in adult cardiomyocytes devoid of native 5-HT4 receptors. When expressed in the HL-1 murine cell line of atrial origin, both receptors caused specific binding of the 5-HT4 selective antagonist GR113808 and activated adenylyl cyclase in the presence of serotonin (5-HT, 1 microM). When expressed in freshly isolated adult rat ventricular cardiomyocytes, a stimulation of the L-type Ca2+ current (ICa,L) by 5-HT (100 nM) was revealed. Both effects were blocked by GR113808. In HL-1 cells, the h5-HT4(d) receptor was found to be more efficiently coupled to adenylyl cyclase than the h5-HT4(b). Pertussis toxin treatment (250 ng/ml for 5 h) potentiated the stimulatory effect of 5-HT on ICa,L in rat myocytes expressing the h5-HT4(b) but not the h5-HT4(d) receptor, indicating a likely coupling of the (b) isoform to both Gs and Gi/o proteins. Adenoviral expression of h5-HT4 receptor isoforms in adult cardiac myocytes provides a valuable means for the exploration of the receptor signaling cascades in normal and pathological situations.

Consequences of atrial electrical remodeling for the anti-arrhythmic action of class IC and class III drugs.

Atrial fibrillation (AF) induces electrical and ionic remodeling of the atria. We investigated whether AF-induced remodeling alters the electrophysiological and anti-fibrillatory effects of class I (flecainide) and class III (d-sotalol, ibutilide) anti-arrhythmic drugs.</AbstractText>In 9 goats, the effects of flecainide (6 mg/kg) and d-sotalol (6 mg/kg) on atrial electrophysiology were measured both before and after 48 h of electrically induced AF. During a 1-h infusion period the atrial effective refractory period (AERP) and conduction velocity (CV) were measured both during slow and rapid pacing (interval 400 and 200 ms). In 8 other goats, the rate-dependent effects of ibutilide (0.12 mg/kg) on AERP were determined.</AbstractText>The effects of flecainide on atrial conduction and refractoriness were not altered after 48 h of AF. At a dose of 6 mg/kg flecainide reduced the CV200 by 19+/-5% in normal atria and by 21+/-9% after 48 h of AF (p=0.20). The AERP200 was prolonged by 10+/-6% and 8+/-7%, respectively (p=0.40). In contrast, the effect of d-sotalol on atrial refractoriness was markedly diminished. During control d-sotalol prolonged the AERP400 by 17+/-6% compared to only 6+/-5% after 2 days of AF (p&lt;0.01). Also ibutilide lost much of its class III effect on the AERP by electrical remodeling (from 15 to 5%; p&lt;0.05). The loss of class III action was less pronounced at rapid heart rates.</AbstractText>AF-induced atrial electrical remodeling in the goat did not modulate the action of flecainide on atrial conduction and refractoriness. In contrast, the class III effects of d-sotalol and ibutilide on the atria were strongly reduced after 2 days of AF. The prolongation of QT-duration was not affected.</AbstractText>

[Immediate cardioversion of atrial fibrillation and atrial flutter lasting less than 90 days by ibutilide versus propafenone: a multicenter study].

To compare the efficacy and safety of ibutilide versus propafenone in immediate cardioversion of atrial fibrillation (AF) and atrial flutter (AFL) lasted less than 90 days.</AbstractText>212 consecutive patients suffering from AF or AFL all lasting less than 90 days that were diagnosed and treated in 5 medical centers were randomly assigned into two groups: ibutilide group (n = 107, including 75 AF cases and 32 AFL cases, receiving intravenous injection of ibutilide 1mg over 10 minutes) and propafenone group as control group (n = 105, including 76 AF cases and 29 AFL cases, receiving intravenous injection of propafenone 70 mg over 10 minutes). If AF/AFL still persisted 10 minutes after treatment, the above dose was repeated. The conversion rate within 1.5 hours and adverse effects within 4 hours were observed.</AbstractText>(1) The conversion rate on AFL of the ibutilide group was 78.1%, significantly higher than that of the propafenone group (48.3%, P &lt; 0.01), while no significant difference was observed in the conversion rate on AF (54.7% vs. 39.5%, P &gt; 0.05) and the mean conversion time (P &gt; 0.05). However the overall conversion rate on AFL and AF of the ibutilide group was 61.7%, significantly higher than that of the propafenone group (41.9%, P &lt; 0.05). (2) The conversion rate on AF/AFL lasting less than 48 h was 65.9% in the ibutilide group, not significantly different from that of the propafenone group (55.7%), the conversion rate on AF/AFL lasting 3 approximately 30 d in the ibutilide group was 66.7%, significantly higher than that of the propafenone group (26.3%, P &lt; 0.05), and the conversion rate on AF/AFL lasting 31 - 88 d was 50%, significantly higher than that of the propafenone group (0, P &lt; 0.01). (3) There was no difference in the times needed for conversion between these 2 groups. (4) The most severe adverse effect in the ibutilide group was short run of ventricular tachycardia occurring in 5 cases among which 4 cases recovered simultaneously and one case recovered after accepting a bolus dose of 100 mg lidocaine. The most severe adverse effects in propafenone group were RR interval longer than 1.5 s (4 cases) and transient hypotension. An acute coronary event was also seen in propafenone group, however, unrelated to the experimental drug.</AbstractText>Intravenous administration of ibutilide in cardioversion of AF and AFL is safe and effective.</AbstractText>

Electrocardiographic changes and myocarditis in trichinellosis: a retrospective study of 154 patients.

The frequencies of electrocardiographic (ECG) abnormalities and myocarditis were determined, retrospectively, among 154 cases of trichinellosis [101 males and 53 females, with a mean (S.D.) age of 35.60 (14.64) years] who were hospitalized at the University Hospital for Infectious Diseases in Zagreb, Croatia, over a 5-year period. Eighty-seven (56%) of the patients, most of them in the invasive phase of infection with Trichinella spiralis, were found to have abnormalities when examined by 12-lead, resting electrocardiography. The ECG disorder most frequently observed was a non-specific ventricular repolarization disturbance (with ST-T wave changes), followed by bundle-branch conduction disturbances, and sinus tachycardia. The other ECG disorders recorded, during various phases of the infection, were sinus bradycardia, right bundle-branch block, supraventricular and ventricular extrasystoles, low-voltage QRS complexes in standard limb leads, first-degree atrio-ventricular block, and atrial fibrillation. Eighteen (12%) of the patients were identified as cases of myocarditis (13 in the invasive phase and five in the convalescent) and two (1.3%) as cases of myopericarditis. One patient developed acute myocardial infarction 28 days after the onset of disease and died soon thereafter; an autopsy revealed multiple necroses and fibroses of the myocardium and thrombus of a coronary artery. Although ECG abnormalities appear to be a common feature of trichinellosis, especially during the invasive phase of the disease, they are rarely associated with a poor prognosis. A transient, non-specific, ventricular-repolarization disturbance is the abnormality most commonly observed.

Therapy implications of transthoracic echocardiography in acute ischemic stroke patients.

Stroke is the third leading cause of death in most Western countries. Cardioembolism might be responsible for 15% to 20% of ischemic strokes. Although atrial fibrillation can be diagnosed by electrocardiography, the remaining causes of cardioembolic stroke are diagnosed by echocardiography. Recent recommendations on the management of acute ischemic stroke fail to consider echocardiography as an essential test in all patients.</AbstractText>We conducted a prospective observational study, performing transthoracic echocardiography on all patients admitted in our hospital with ischemic stroke, in sinus rhythm, from January 7, 2002, to October 16, 2003. Findings compatible with heart diseases that would indicate anticoagulation as beneficial were identified.</AbstractText>Of the 853 patients admitted with ischemic stroke, transthoracic echocardiography was performed on 846 (99.2%). Of the 435 patients with ischemic stroke, in sinus rhythm, 37.2% had findings indicating anticoagulation as beneficial: dilated cardiopathy (19.1%), previous anterior wall myocardial infarction (6.2%), left ventricular systolic dysfunction with an ejection fraction &lt;35% (3.7%), mitral valve stenosis with enlarged left atria (1.6%), intracardiac masses (0.5%), valvular prosthesis (0.2%), and &gt;1 abnormality (5.5%).</AbstractText>In our study, transthoracic echocardiography had therapy implications in 37.2% of ischemic stroke patients in sinus rhythm. Transthoracic echocardiography should be considered an essential test in all ischemic stroke patients in sinus rhythm.</AbstractText>

Atrial fibrillation in KCNE1-null mice.

Although atrial fibrillation is the most common serious cardiac arrhythmia, the fundamental molecular pathways remain undefined. Mutations in KCNQ1, one component of a sympathetically activated cardiac potassium channel complex, cause familial atrial fibrillation, although the mechanisms in vivo are unknown. We show here that mice with deletion of the KCNQ1 protein partner KCNE1 have spontaneous episodes of atrial fibrillation despite normal atrial size and structure. Isoproterenol abolishes these abnormalities, but vagomimetic interventions have no effect. Whereas loss of KCNE1 function prolongs ventricular action potentials in humans, KCNE1-/- mice displayed unexpectedly shortened atrial action potentials, and multiple potential mechanisms were identified: (1) K+ currents (total and those sensitive to the KCNQ1 blocker chromanol 293B) were significantly increased in atrial cells from KCNE1-/- mice compared with controls, and (2) when CHO cells expressing KCNQ1 and KCNE1 were pulsed very rapidly (at rates comparable to the normal mouse heart and to human atrial fibrillation), the sigmoidicity of IKs activation prevented current accumulation, whereas cells expressing KCNQ1 alone displayed marked current accumulation at these very rapid rates. Thus, KCNE1 deletion in mice unexpectedly leads to increased outward current in atrial myocytes, shortens atrial action potentials, and enhances susceptibility to atrial fibrillation.

Role of repolarization restitution in the development of coarse and fine atrial fibrillation in the isolated canine right atria.

Although the role of action potential duration restitution (APD-R) in the initiation and maintenance of ventricular fibrillation (VF) has been the subject of numerous investigations, its role in the generation of atrial fibrillation (AF) is less well studied. The cellular and ionic basis for coarse versus fine AF is not well delineated.</AbstractText>We measured APD-R during acetylcholine-mediated AF as well as during pacing (standard and dynamic protocols) in crista teriminalis, pectinate muscle, superior vena cava, and appendage of isolated canine arterially perfused right atria (n = 15). Transmembrane action potential (TAP), pseudo-ECG, and isometric tension development were simultaneously recorded. Acetylcholine flattened APD-R measured by both standard and dynamic protocols, but promoted induction of AF. AF was initially coarse, converting to fine within 3-15 minutes of AF. Coarse, but not fine AF was associated with dramatic fluctuations in tension development, reflecting wide variations in intracellular calcium activity ([Ca(2+)](i)). During coarse AF, APD-R data displayed a cloud-like distribution pattern, with a wide range of maximum APD-R slope (from 1.21 to 0.35). A maximum APD-R slope &gt;1 was observed only in crista terminalis (3/10). The APD-R relationship was relatively linear and flat during fine AF. Reduction of [Ca(2+)](i) was associated with fine AF whereas augmentation of [Ca(2+)](i) with coarse AF.</AbstractText>Our data indicate that while APD-R may have a limited role in the maintenance of coarse AF, it is unlikely to contribute to the maintenance of fine AF and that [Ca(2+)](i) dynamics determine the degree to which AF is coarse or fine.</AbstractText>

Atrial response to ventricular antitachycardia pacing discriminates mechanism of 1:1 atrioventricular tachycardia.

Inappropriate shocks from implantable cardioverter defibrillators (ICD) remain a significant clinical problem despite device discrimination algorithms. The atrial response to antitachycardia pacing (ATP) may determine the mechanism of 1:1 A:V tachycardia.</AbstractText>For this study we refer to sinus tachycardia, atrial tachycardia (AT), atrial fibrillation, and flutter as atrial tachycardia (AT), and all other tachycardia as "non-AT." Three atrial response patterns during the burst of ATP were determined. The atrial cycle length (ACL) may be unchanged (type 1) indicating AT. The ACL may show variation during ATP (type 2) indicating variable VA block and does not discriminate between an AT and a non-AT mechanism, in which case a default diagnosis of non-AT is made. The ACL may accelerate to the ATP cycle length (type 3) indicating entrainment. A VAAV response at the end of ATP was considered diagnostic of AT (type 3A) whereas a VAV or VVA response was considered a non-AT mechanism (type 3B). This algorithm was applied to ICD tracings from 68 episodes of spontaneous 1:1 A:V tachycardia that had 136 sequences of ATP administered. The rhythm "truth" was determined by consensus of two experienced clinicians.</AbstractText>The algorithm correctly identified AT with a sensitivity of 71.9% (95% CI: 67.1-73.6), and specificity of 95% (83.5-99.1). The PPV was 97.2% (90.9-99.5), and NPV 58.5% (51.4-61.0). Kappa was 0.57 (0.43-0.62). If used clinically the algorithm would have aborted 53.3% (8/15) of inappropriate shocks delivered into an AT-mechanism tachycardia and would not have withheld a shock for any episode of VT.</AbstractText>Analysis of atrial response patterns during and after ventricular ATP can successfully discriminate tachycardia mechanism and may reduce inappropriate ICD shocks.</AbstractText>

Outcomes after ventricular fibrillation out-of-hospital cardiac arrest: expanding the chain of survival.

Coronary heart disease is the most common cause of death in the United States, with ventricular fibrillation (VF) the most common initial rhythm when cardiac disease causes arrest. Survival after VF out-of-hospital cardiac arrest (OHCA) depends on a sequence of events called the chain of survival, which Includes rapid access to emergency medical services, cardiopulmonary resuscitation, defibrillation, and advanced care. Because of widespread implementation of defibrillation programs, more patients survive VF OHCAs, making subsequent care of these patients important. Early hospitalization must focus on potential neurologic injury and therapy targeted at the underlying cardiac disease and antiarrhythmic therapy for long-term secondary prevention of sudden death. Attention to certain cohorts who are at high risk despite their underlying disease, such as women and elderly patients, is necessary. These cohorts may have the greatest response to short-term and long-term therapies for cardiac rehabilitation. With these approaches, long-term survival and quality of life after VF OHCA are favorable. Broadening the focus of the chain of survival to include in-hospital and long-term care will further improve favorable outcomes achieved in an early defibrillation program.

[Brugada syndrome].

Brugada syndrome is believed to be responsible for 4 to 12% of all sudden deaths and for 20% of deaths in patients with structurally normal hearts. As a distinct clinical entity with a high risk of sudden cardiac death it was first described in 1992. The syndrome characterized by ST segment elevation in right precoardial leads V1 to V3 unrelated to ischemia and by electrolyte disturbance without obvious structural heart disease. The clinical findings are based on ECG and syncope or sudden death. The arrhythmia leading to sudden death is a rapid polymorphic ventricular tachycardia. The electrocardiographic signature of the syndrome is dynamic and often concealed, but can be unmasked by potent sodium channel blockers such as flecainde, ajmaline. The Brugada syndrome is a familial disease displaying an autosomal dominant mode of transmission with incomplete penetration and with incidence ranging between 5 and 66 per 10,000. The syndrome has been linked to mutations in SCNA5, the gene encoding for the a subunit of the sodium channel. Implantation of an automatic cardiverter-defibrillator is the only currently proven effective therapy.

Optimized perioperative biventricular pacing in setting of right heart failure.

A 78-year-old female with prior atrioventricular junctional ablation for paroxysmal atrial fibrillation and implantation of DDDR pacemaker underwent repair of severe tricuspid insufficiency. Effects of biventricular pacing were tested with temporary wires at the conclusion of cardiopulmonary bypass.</AbstractText>An ultrasonic flow probe was placed on the ascending aorta for real time cardiac output measurements. Atrioventricular delay optimization was performed and biventricular pacing was initiated while right-left ventricular delays were varied.</AbstractText>There was no advantage of biventricular pacing (optimum right-left ventricular delay of +80 ms) compared with existing DDD.</AbstractText>This study confirms the physiological effects of right-left ventricular delay on cardiac output after cardiopulmonary bypass.</AbstractText>

Cardiac resynchronisation therapy versus dual site right ventricular pacing in a patient with permanent pacemaker and congestive heart failure.

A 46-year-old male patient who had long-term right ventricular (RV) pacing for symptomatic complete heart block, initially by an epicardial, later with an endocardial pacing lead at the RV apex, developed congestive heart failure (CHF) and chronic atrial fibrillation 7 years following the pacemaker implantation and was medically treated. During follow-up, his pacemaker was upgraded to a cardiac resynchronisation therapy (CRT) device, because of uncontrolled CHF symptoms, New York Heart Association (NYHA) functional class IV, while on drugs. The patient's symptomatic status improved to NYHA functional class II with CRT. After 17 months of CRT, the battery became depleted, because of the high capture threshold of the left ventricular lead. The patient was then given dual site RV pacing (RV outflow tract+RV apex) in place of CRT, which showed similar efficacy at 12 weeks follow-up.

Do we need pacemakers resistant to magnetic resonance imaging?

Manufacturers of pacemakers (PM) and of magnetic resonance imaging (MRI) devices state that MRI scanning of PM wearers is contraindicated. This paper tries to summarise which effects can interfere with PM, what can be hazardous, and how treatment of PM in MRI can be modified to guarantee compatibility.</AbstractText>All PM tested were from deceased patients. Reed contact thresholds and reactions were investigated in low magnetostatic fields and compared with those in strong magnetostatic fields. Influence of gradient fields on PM and heating due to radiofrequency (RF) pulses were estimated. Thirty Legal Medicine Departments were questioned whether deaths of PM patients during MRI are known.</AbstractText>Reed contacts are influenced above 0.7 mT. In MRI fields only 28% of the PM in magnet mode remained so in all orientations. Of synchronous PM, 76% remained synchronous in all orientations. Gradient fields can influence sensing but cannot stimulate. Power density and temperature rise produced by RF fall rapidly with distance. Our question revealed six deaths. All suffered from sick-sinus-syndrome and all were not PM dependent. In three cases ventricular fibrillation was proven as the cause of death.</AbstractText>Asynchronous pacing due to magnetostatic and gradient fields may be problematic in patients with spontaneous rhythm. To avoid them, PM triggered MRI scan restricted to refractory period is proposed. Neither inhibition of PM nor heating of the electrode poses real risks. So far, we have examined eight patients 12 times in MRI triggered mode without problems.</AbstractText>

n-3 Fatty acids and ventricular arrhythmias in patients with ischaemic heart disease and implantable cardioverter defibrillators.

To investigate the relationship between serum content of n-3 polyunsaturated fatty acids (PUFA) and the incidence of ventricular arrhythmias in patients with an implantable cardioverter defibrillator (ICD).</AbstractText>We included 98 patients with ischaemic heart disease and an ICD. The numbers of ventricular fibrillation (VF) and ventricular tachycardia (VT) events were assessed during a 12-month period and related to the concentration of n-3 PUFA in serum phospholipids.</AbstractText>Patients with more than one arrhythmic event had significantly lower n-3 PUFA levels compared with patients without arrhythmias (mean 7.1% vs 9.2%, P&lt;0.01). Dividing the patients into quintiles according to their n-3 PUFA level those with the lowest content of n-3 PUFA had more ventricular arrhythmias than patients with the highest concentration of n-3 PUFA (mean 1.3 event vs 0.2 event, P&lt;0.05).</AbstractText>Patients with a low content of n-3 PUFA in serum had a higher incidence of ventricular arrhythmias compared with patients with high serum levels of n-3 PUFA. The data suggest that the protection offered by n-3 PUFA against sudden cardiac death observed in previous studies is mediated by a direct antiarrhythmic effect of n-3 PUFA.</AbstractText>

Comparing the global mRNA expression profile of human atrial and ventricular myocardium with high-density oligonucleotide arrays.

The knowledge of chamber-specific gene expression in human atrial and ventricular myocardium is essential for the understanding of myocardial function and the basis for the identification of putative therapeutic targets in the treatment of cardiac arrhythmia and heart failure. In this study the gene expression pattern of human left atrial and ventricular myocardium was analyzed.</AbstractText>Global mRNA expression patterns with high-density oligonucleotide arrays between left atrial and left ventricular myocardium of 6 patients with heart failure undergoing heart transplantation were compared. Clustering of microarray data confirmed chamber-specific gene expression profiles. Genes similarly expressed in all patients were further analyzed, and data were confirmed by means of real-time polymerase chain reaction and Western blot analysis.</AbstractText>Of 22,215 genes examined, 7115 transcripts were found to be expressed in all 12 human myocardial samples. One hundred twenty-five genes were differentially expressed between left atrial and left ventricular specimens in all patients examined. Novel genes preferentially expressed in human atria were identified. Interestingly, several potassium channels of subfamily K are more highly expressed in atria than in ventricles. Members of the potassium inwardly rectifying channel of subfamily J were found to be more highly expressed in human ventricular myocardium. Finally, chronic atrial fibrillation was associated with reduced atrial expression of the potassium channel TWIK-1, suggesting potential contribution of the corresponding current to electrical remodeling.</AbstractText>Human atria and ventricles show specific gene expression profiles. Our data provide the basis of a comprehensive understanding of chamber-specific gene expression in diseased human hearts and will support the identification of therapeutic targets in the treatment of arrhythmia and heart failure.</AbstractText>

Cardioprotective effects of [5-(2-methyl-5-fluorophenyl)furan-2-ylcarbonyl]guanidine (KR-32568) in an anesthetized rat model of ischemia and reperfusion heart injury.

The effects of a novel sodium/hydrogen exchanger-1 (NHE-1) inhibitor, KR-32568, were studied in an anesthetized rat model of 30 min ischemia/2.5 h reperfusion heart injury. KR-32568 dose-dependently inhibited NHE-1-mediated rabbit platelet swelling induced by intracellular acidification. In our anesthetized rat model, KR-32568 reduced infarct size from 67 (control) to 43 and 24% at 0.1 and 1.0 mg/kg (i.v. bolus, given 10 min before ischemia), respectively. KR-32568 at the same doses also significantly reduced the total number of ventricular premature beats during ischemia/reperfusion from 530 (control) to 266 and 115 beats, ventricular tachycardia (VT) incidence from 51 (control) to 21 and 8, VT duration from 238 s (control) to 63 and 33 s, ventricular fibrillation (VF) incidence from 17 (control) to 8 and 0, and VF duration from 85 s to 18 and 1 s. These results indicate that KR-32568 may exert potent cardioprotective effects in rats via inhibition of sodium/hydrogen exchanger-1.

Implantation of an "extracardiac" internal cardioverter defibrillator in a 6-month-old infant.

In infants and small children, ICD implantation is a challenge due to technical limitations and a significant number of complications. This report describes ICD implantation in a 6-month-old infant (body weight 5.5 kg). A completely extracardiac defibrillation system was implanted using a transvenous lead subcutaneously in the back below the left scapula as the defibrillation electrode and an active-can device in the right upper abdomen. Defibrillation threshold of implantation was &lt; or =10 J. During the follow-up of 3 months, 8 adequate ICD discharges were noted. The technique described seems feasible to facilitate ICD implantation in small infants.

Shortness of breath, syncope, and cardiac arrest caused by systemic mastocytosis.

During a 3-month period, a 33-year-old man presented to the emergency department on 4 occasions with dyspnea, palpitations, and syncope. His initial presentation was accompanied by acute myocardial injury and ventricular fibrillation. An extensive evaluation spanned the 3 months and included echocardiography, cardiac catheterization, electrophysiology study, tilt-table evaluation, pulmonary angiography, electroencephalography, and serum and urine analysis. Diagnosis eluded clinicians until a rash was recognized to be urticaria pigmentosa, and biopsy of the rash then implicated mastocytosis. Since the initiation of pharmacotherapy nearly 5 years ago, the patient has remained asymptomatic. This case demonstrates that systemic mastocytosis can present as recurrent syncope and even as cardiac arrest. Diagnosis of this rare but potentially fatal disease is made particularly challenging by its protean manifestations.

Demographic and temporal trends in out of hospital sudden cardiac death in Belfast.

To determine the epidemiology of out of hospital sudden cardiac death (OHSCD) in Belfast from 1 August 2003 to 31 July 2004.</AbstractText>Prospective examination of out of hospital cardiac arrests by using the Utstein style and necropsy reports. World Health Organization criteria were applied to determine the number of sudden cardiac deaths.</AbstractText>Of 300 OHSCDs, 197 (66%) in men, mean age (SD) 68 (14) years, 234 (78%) occurred at home. The emergency medical services (EMS) attended 279 (93%). Rhythm on EMS arrival was ventricular fibrillation (VF) in 75 (27%). The call to response interval (CRI) was mean (SD) 8 (3) minutes. Among patients attended by the EMS, 9.7% were resuscitated and 7.2% survived to leave hospital alive. The CRI for survivors was mean (SD) 5 (2) minutes and for non-survivors, 8 (3) minutes (p &lt; 0.001). Ninety one (30%) OHSCDs were witnessed; of these 91 patients 48 (53%) had VF on EMS arrival. The survival rate for witnessed VF arrests was 20 of 48 (41.7%): all 20 survivors had VF as the presenting rhythm and CRI &lt; or = 7 minutes. The European age standardised incidence for OHSCD was 122/100,000 (95% confidence interval 111 to 133) for men and 41/100,000 (95% confidence interval 36 to 46) for women.</AbstractText>Despite a 37% reduction in heart attack mortality in Ireland over the past 20 years, the incidence of OHSCD in Belfast has not fallen. In this study, 78% of OHSCDs occurred at home.</AbstractText>

Clinical, pathological, and biochemical studies in a patient with propionic acidemia and fatal cardiomyopathy.

A patient diagnosed at 9 months with a milder form of propionic acidemia was functioning at a near normal intellectual level and a normal neurological level at age 8. After 2-week history of feeling "poorly" but functioning normally, she became acutely ill and succumbed to heart failure and ventricular fibrillation in 12 h. At post-mortem the heart was hypertrophied and had low carnitine levels, despite carnitine supplementation and repeatedly normal plasma carnitine levels. The findings in this patient provide a possible mechanism for the cardiac complications that are becoming more apparent in propionic acidemia.

Influence of ventricular pacing on myocardial oxygen tension.

The influence of heart rate on cardiac output, oxygen consumption, and myocardial activity has been widely investigated. However, the influence of heart rate on myocardial oxygen tension (pO2) remains unclear. Since the introduction of flexible pO2 micro catheters to measure partial oxygen tension in a working muscle, it is possible to investigate the influence of heart rate on myocardial oxygen tension.</AbstractText>Intraoperatively, a flexible pO2 micro catheter was positioned in the mid-myocardium of 8 male farm pigs. The heart rate was varied via an external pacer from base rate up to fibrillation and the corresponding myocardial pO2 was measured.</AbstractText>Within 2 min, the myocardial pO2 adjusted to a change in heart rate. In this animal model, an optimal myocardial pO2 was observed at 109 bpm. A further increase in heart rate led to a decrease in myocardial pO2. When the heart rate was reaching the level of a fibrillation, pO2 dropped to zero.</AbstractText>In young healthy pigs--with a normal blood vessel regulation and the pharmacologic and experimental conditions used in this study--a significant relation between myocardial pO2 and heart rate was observed. Myocardial oxygen tension increased during cardiac pacing until a heart rate of 109 bpm. Thereafter a decline of pO2 occurred. Each change in heart rate resulted in a corresponding change of pO2 within roughly 2 min.</AbstractText>

Assessment of left ventricular function by Doppler tissue imaging in patients with atrial fibrillation following acute myocardial infarction.

We studied tissue Doppler parameters in patients with atrial fibrillation following acute myocardial infarction, and their relation to P wave durations and P dispersion.</AbstractText>Echocardiographic examination was performed in 84 consecutive patients with first anterior acute myocardial infarction. In addition to other conventional echocardiographic parameters, the peak systolic (Sm), early diastolic (Em) and late diastolic (Am) velocities were obtained at the lateral corner of the mitral annulus by pulsed wave tissue Doppler. The Em/Am ratio and the ratio of early diastolic mitral inflow velocity to Em (E/Em), which is a marker of diastolic filling pressure, were calculated. Electrocardiogram was recorded from all patients on admission; P wave measurements were also performed.</AbstractText>Atrial fibrillation occurred in 20 (23.8%) of 84 patients. The patients with atrial fibrillation had significant reduction of Em (5.6+/-1.5 vs. 8.7+/-2.7 cm/s, p &lt; 0.001), Em/Am (0.61+/-0.27 vs. 0.84+/-0.23, p = 0.001) and Sm (7.1+/-1.0 vs. 8.3+/-1.9 cm/s, p &lt; 0.001) values compared with those without. The E/Em ratio (14.45+/-4.62 vs. 7.47+/-2.79, p &lt; 0.001), P maximum (102+/-11 vs. 95+/-11 ms, p = 0.02) and P dispersion (35+/-7 vs. 26+/-7 ms, p &lt; 0.001) were significantly higher in patients with atrial fibrillation than in those without. In all patients, P dispersion showed significant correlation with Em (r = -0.33, p = 0.002), Sm (r = -0.40, p &lt; 0.001) and E/Em (r = 0.32, p = 0.003). When E/Em &gt; or = 10 was used as cutpoint, atrial fibrillation could be predicted with a sensitivity of 90%, and a specificity of 84%.</AbstractText>The patients with atrial fibrillation following acute myocardial infarction have reduced systolic and diastolic mitral annular velocities and increased E/Em ratio, P maximum and P dispersion values compared to those without. P dispersion is correlated with systolic and diastolic left ventricular function after acute myocardial infarction. The E/Em ratio appears to be a useful parameter for assessing the risk of atrial fibrillation occurrence after anterior acute myocardial infarction.</AbstractText>

Effects of long-term beta-blocker therapy on P-wave duration and dispersion in patients with rheumatic mitral stenosis.

P-wave dispersion (PWD), has been defined as the difference between maximum and minimum P-wave duration. Prolonged P-wave duration and increased PWD have been reported to be related with increased risk for atrial fibrillation (AF). AF is the most common sustained arrhythmia encountered in patients with rheumatic mitral stenosis (MS). Beta-blockers are the mainstay of therapy in patients with rheumatic MS to control ventricular rate both during sinus rhythm and AF. In the present study, we aimed to evaluate the effect of long-term beta-blocker therapy on P-wave duration and PWD in patients with rheumatic MS.</AbstractText>Study population includes 46 patients (group I, 8 men, 38 women, mean age = 34+/-8 years) with newly diagnosed moderate-to-severe rheumatic MS who have not taken any medication before and prescribed oral beta-blocker therapy and 46 healthy control subjects without any cardiovascular disease (group II, 8 men, 38 women, mean age = 35+/-7 years). Mitral valve area, maximum and mean diastolic mitral gradients, left atrial diameter, and systolic pulmonary artery pressure were evaluated by transthoracic echocardiography before initiation of beta blocker therapy and repeated at the end of the first month. Baseline maximum and minimum P-wave duration and PWD were determined on 12-lead electrocardiogram recorded for each patient and control subject and repeated at the end of the first month after initiation of beta-blocker therapy in patient group.</AbstractText>Maximum P-wave duration and PWD were found to be significantly higher in patients with MS than those in control subjects (Maximum P-wave duration: 128+/-7 ms vs. 104+/-4 ms and PWD: 52+/-6 ms vs. 27+/-3 ms, p &lt; 0.001 for both). Both groups had comparable minimum P-wave duration (75+/-4 ms vs. 76+/-4 ms, p = 0.093). Maximum P-wave duration and PWD were found to be significantly decreased by long-term beta blocker therapy (Maximum P-wave duration; 128+/-7 ms vs. 122+/-6 ms, p &lt; 0.001, PWD; 52+/-6 ms vs. 47+/-5 ms, p &lt; 0.001). However, there was no significant difference between the values of minimum P wave duration measured before and at the end of the first month of beta-blocker therapy (75+/-4 ms vs. 75+/-3 ms, p = 0.678). Statistically significant decrease were detected on maximum and mean mitral gradient and systolic pulmonary artery pressure and resting heart rate at the end of the first month of beta-blocker therapy. However, only the change in resting heart rate was found to be significantly correlated with the decrease in maximum P-wave duration and PWD (Maximum P-wave duration: r = 0.327, p = 0.026, PWD: r = 0.378, p = 0.01).</AbstractText>We have shown for the first time that long-term beta-blocker therapy causes a significant decrease in maximum P-wave duration and PWD in patients with rheumatic MS.</AbstractText>

Effects of Na(+) and K(+) channel blockade on vulnerability to and termination of fibrillation in simulated normal cardiac tissue.

Na(+) and K(+) channel-blocking drugs have anti- and proarrhythmic effects. Their effects during fibrillation, however, remain poorly understood. We used computer simulation of a two-dimensional (2-D) structurally normal tissue model with phase I of the Luo-Rudy action potential model to study the effects of Na(+) and K(+) channel blockade on vulnerability to and termination of reentry in simulated multiple-wavelet and mother rotor fibrillation. Our main findings are as follows: 1) Na(+) channel blockade decreased, whereas K(+) channel blockade increased, the vulnerable window of reentry in heterogeneous 2-D tissue because of opposing effects on dynamical wave instability. 2) Na(+) channel blockade increased the cycle length of reentry more than it increased refractoriness. In multiple-wavelet fibrillation, Na(+) channel blockade first increased and then decreased the average duration or transient time (&lt;T(s)&gt;) of fibrillation. In mother rotor fibrillation, Na(+) channel blockade caused peripheral fibrillatory conduction block to resolve and the mother rotor to drift, leading to self-termination or sustained tachycardia. 3) K(+) channel blockade increased dynamical instability by steepening action potential duration restitution. In multiple-wavelet fibrillation, this effect shortened &lt;T(s)&gt; because of enhanced wave instability. In mother rotor fibrillation, this effect converted mother rotor fibrillation to multiple-wavelet fibrillation, which then could self-terminate. Our findings help illuminate, from a theoretical perspective, the possible underlying mechanisms of termination of different types of fibrillation by antiarrhythmic drugs.

On-pump/beating-heart myocardial protection for isolated or combined coronary artery bypass grafting in patients with severe left ventricle dysfunction: assessment of myocardial function and clinical outcome.

Myocardial protection in coronary artery bypass grafting (CABG) with severe left ventricular (LV) dysfunction is still a surgical dilemma. Preoperative myocardial infarction (MI) and postoperative low output syndrome are serious complications in cases of inadequate protection of the heart, which has limited myocardial reserve. The aim of this study was to evaluate myocardial function and clinical outcome after on-pump/beating-heart CABG in patients with severe LV dysfunction.</AbstractText>Between March 2001 and March 2004, clinical, operative, and postoperative data were prospectively collected from patients with LV ejection fraction (EF) &lt; 30% who underwent on-pump/beating-heart CABG and associated procedures.</AbstractText>There were 46 patients and the mean patient age was 58.38 +/- 9.23. The mean EF was 25.6 +/- 2.8%. Operating time was 275 +/- 63 minutes. The frequency of distal anastomosis was 3.06 +/- 1.04. Twenty-four patients required aneurysmectomy in addition to CABG, and 2 of the 24 required mitral repairs. Inotropic support was required in 14 patients (30%) and 5 of them (10.9%) also required IABP. The LV EF improved significantly after the operation when compared to preoperative measurements (25.6 +/- 2.8 versus 33.64 +/- 4.69, P &lt; .05). Hospital mortality rate was 4.3% (2 of the 46 patients). No mortality was observed at a mean followup of 16 months after discharge from the hospital.</AbstractText>On-pump/beating-heart CABG technique is effective in protecting myocardial functions in patients with severe LV dysfunction. The main advantage of the on-pump/beating-heart technique is the ability it provides one to perform complete revascularization, and intracavitary procedures with low morbidity and mortality even in impaired LV function.</AbstractText>

Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: a meta-analysis.

This study was designed to identify all randomized clinical trial data evaluating angiotensin-converting enzyme inhibitors or angiotensin receptor blockers for the prevention of atrial fibrillation (AF), to estimate the magnitude of this effect and to identify patient subgroups most likely to benefit.</AbstractText>Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) reduce morbidity and mortality in patients with heart failure, vascular disease, and hypertension. Several reports suggest that they may also prevent the development of AF.</AbstractText>A systematic review of the literature was performed to identify all reports of the effect of ACEIs or ARBs on the development of AF. Eligible studies had to be randomized, controlled, parallel-design human trials of an ACEI or ARB that collected data on the development of AF.</AbstractText>A total of 11 studies, which included 56,308 patients, were identified: 4 in heart failure, 3 in hypertension, 2 in patients following cardioversion for AF, and 2 in patients following myocardial infarction. Overall, ACEIs and ARBs reduced the relative risk of AF by 28% (95% confidence interval [CI] 15% to 40%, p = 0.0002). Reduction in AF was similar between the two classes of drugs (ACEI: 28%, p = 0.01; ARB: 29%, p = 0.00002) and was greatest in patients with heart failure (relative risk reduction [RRR] = 44%, p = 0.007). Overall, there was no significant reduction in AF in patients with hypertension (RRR = 12%, p = 0.4), although one trial found a significant 29% reduction in patients with left ventricular (LV) hypertrophy. In patients following cardioversion, there appears to be a large effect (48% RRR), but the confidence limits are wide (95% CI 21% to 65%).</AbstractText>Both ACEIs and ARBs appear to be effective in the prevention of AF. This benefit appears to be limited to patients with systolic left ventricular dysfunction or LV hypertrophy. The use of these drugs following cardioversion appears promising but requires further study.</AbstractText>

Assessment of left ventricular systolic function in patients with chronic atrial fibrillation and dilated cardiomyopathy using the ratio of preceding to prepreceding R-R intervals.

The objective of this study was to determine the relation between left ventricular (LV) systolic function and the ratio of preceding (RR1) to prepreceding (RR2) R-R intervals in patients with chronic atrial fibrillation (AF) and dilated cardiomyopathy. LV systolic function (Emax) was examined using a conductance catheter with a micromanometer in 13 patients with chronic AF and dilated cardiomyopathy. We calculated Emax as a load-independent index of LV contractility and compared it with RR1, RR2, and the ratio of RR1/RR2. We analyzed 50+/-13 cardiac cycles (range 18-61) in each patient. Average heart rate was 80+/-13 beats/min, and ejection fraction over all cardiac cycle in each patient measured by conductance catheter was 31+/-8%. Emax was positively correlated with RR1 and RR1/RR2 in all patients, and negatively correlated with RR2 in all patients. In each patient, correlation coefficients of Emax with RR1/RR2 were greater than those with either RR1 or RR2. Furthermore, Emax at RR1/RR2=1 in the linear regression line reflected average Emax over all cardiac cycles in each patient. In conclusion, we have shown that LV contractility correlated positively with RR1/RR2 in patients with chronic AF and dilated cardiomyopathy, and LV contractility at RR1/RR2=1 represents the average value of contractility over all cardiac cycles.

Abnormalities on ECG and telemetry predict stroke outcome at 3 months.

ECG is a useful tool in monitoring vital functions in patients with acute stroke; however, fairly little evidence is available concerning the prevalence and the prognostic impact of ECG findings in patients with acute cerebral infarction and acute intracerebral haemorrhage (ICH).</AbstractText>This analysis was based on data from 692 patients with acute cerebral infarction, 155 patients with intracerebral haemorrhage (ICH), and 223 patients with transient ischaemic attack (TIA), who were admitted to hospital within 6 h of symptom onset. A 12 lead ECG was obtained on admission, and the patient was on telemetry for the first 12-24 h of hospitalisation.</AbstractText>ECG abnormalities were observed in 60% of patients with cerebral infarction, 50% of patients with ICH, and 44% of patients with TIA. In multivariate analyses 3-month mortality in patients with ischaemic stroke was predicted by atrial fibrillation OR 2.0 (95% CI 1.3-3.1), atrio-ventricular block OR 1.9 (95% CI 1.2-3.9), ST-elevation OR (2.8, 95% CI 1.3-6.3), ST-depression OR 2.5 (95% CI 1.5-4.3), and inverted T-waves OR 2.7 (95% CI 1.6-4.6). This was independent of stroke severity, pre-stroke disability and age. In patients with ICH, sinus tachycardia OR 4.8 (95% CI 1.7-14.0), ST-depression OR 5.2 (95% CI 1.1-24.9), and inverted T-wave 5.2 (95% CI 1.2-22.5) predicted poor outcome. None of the changes reached significance in patients with TIA. In patients with severe cerebral infarction or ICH, heart rate did not decrease within the first 12 h after admission, which was the case in patients with mild to moderate stroke. Rapid heart rate predicted 3-month mortality in multivariate testing OR 1.7 (95% CI 1.02-2.7).</AbstractText>ECG abnormalities are frequent in acute stroke and may predict 3-month mortality.</AbstractText>

[Non-cardiac surgery for patients with arrhythmia].

Arrhythmia is the most common perioperative cardiac complication during noncardiac surgery. Most perioperative arrhythmia is benign, but fatal arrhythmia can occur, requiring emergency care. Arrhythmia is divided into tachycardia and bradycardia. Both arrhythmias often result in cardiac failure. Ischemic heart disease often causes premature ventricular contraction or ventricular tachycardia. Hypertensive heart disease or valvular heart disease can lead to atrial fibrillation or supraventricular tachycardia. Although patients may not have cardiac disease, hypoxia, hypovolemia, electrolyte disturbance, acidosis, and hypothermia can also cause arrhythmia. Patients with pacemakers or implantable cardiodefibrillators (ICDs) are affected by electric cauterization, which interferes with the sensing and inhibits the pacing of pacemakers as well as ICDs If this occurs, the mode of pacemakers and ICDs must be reset during surgery.

Interventional approach to reduce thromboembolic risk in patients with atrial fibrillation ineligible for oral anticoagulation.

The annual incidence of stroke in patients with nonrheumatic atrial fibrillation averages 5% per year and increases with age, left ventricular dysfunction, hypertension, diabetes or prior stroke. Since in nonrheumatic atrial fibrillation 91% of left atrial thrombi are located in the left atrial appendage, in patients ineligible for oral anticoagulation it was suggested the percutaneous closure of left atrial appendage as a therapeutic option to reduce embolic risk. In this article we report our initial experience with this procedure, which was uneventful and efficacious at short-term follow-up. In conclusion, the interventional approach in patients with atrial fibrillation ineligible for oral anticoagulation seems feasible and promising, and deserves further investigation.

Crisis management during anaesthesia: cardiac arrest.

Cardiac arrest attributable to anaesthesia occurs at the rate of between 0.5 and 1 case per 10 000 cases, tends to have a different profile to that of cardiac arrest occurring elsewhere, and has an in-hospital mortality of 20%. However, as individual practitioners encounter cardiac arrest rarely, the rapidity with which the diagnosis is made and the consistency of appropriate management varies considerably.</AbstractText>To examine the role of a previously described core algorithm "COVER ABCD-A SWIFT CHECK", supplemented by a sub-algorithm for cardiac arrest, in the management of cardiac arrest occurring in association with anaesthesia.</AbstractText>The potential performance of this structured approach for each the relevant incidents among the first 4000 reported to the Australian Incident Monitoring Study (AIMS) was compared with the actual management as reported by the anaesthetists involved.</AbstractText>There were 129 reports of cardiac arrest associated with anaesthesia among the first 4000 AIMS incident reports. Identified aetiological factors were grouped into five categories: (1) anaesthetic technique (11 cases with this category alone; 32 with this and one or more of the other categories, representing 25% of all 129 cardiac arrests); (2) drug related (16; 32, 25%); (3) associated with surgical procedure (9; 29, 22%); (4) associated with pre-existing medical or surgical disease (30; 82, 64%); (5) unknown (8; 14, 11%). The "real life" presentation and management of cardiac arrest in association with anaesthesia differs substantially from that detailed in general published guidelines. Cardiac rhythms at the time were sinus bradycardia (23%); asystole (22%); tachycardia/ventricular tachycardia/ventricular fibrillation (14%); and normal (7%), with a further third unknown. Details of treatment were recorded in 110 reports; modalities employed included cardiac compression (72%); adrenaline (61%); 100% oxygen (58%); atropine (38%); intravenous fluids (25%), and electrical defibrillation (17%). There were no deaths or permanent morbidity in the 11 cases due solely to anaesthetic technique. 24 of the 25 deaths occurred in patients with significant pre-existing medical or surgical disease.</AbstractText>Because there are often multiple contributing factors to a cardiac arrest under anaesthesia, a complete systematic assessment of the patient, equipment, and drugs should be completed. The "COVER ABCD-A SWIFT CHECK" algorithm was judged to be a satisfactory process in this context and should be carried out even if the cause of the cardiac arrest is already thought to have been found. The diagnosis and management of cardiac arrest in association with anaesthesia differs considerably from that encountered elsewhere. The outcome is generally good, with most patients leaving hospital alive and apparently well.</AbstractText>

[The survey on radiofrequency catheter ablation in Chinese military hospitals].

To analyze the cumulative data of radiofrequency catheter ablation (RFCA) in the treatment of tachyarrhythmias in Chinese military hospitals.</AbstractText>Chinese PLA Cardiology Association sponsored the registration and statistical analysis. RFCA results were registered from January 1, 1993 to December 30, 2000 and from January 1, 2001 to December 30, 2003 respectively.</AbstractText>(1) A total of 14 599 patients from 42 hospitals underwent RFCA, RFCA was successful in 14 092 of 14 599 (success rate 96.5%) with a complication rate 0.5% (72/14599) and recurrence rate 2.8% (400/14 599). (2) The number of patients with accessory pathway (AVRT) and AV nodal reentrant tachycardia (AVNRT) were 8344 and 4822 respectively. (3) High success rate was maintained in AVNRT and AVRT ablation, success rate was significantly improved in the treatment of PVCs. Atrial fibrillation and non-idiopathic ventricular tachycardia ablation presented high recurrence rate with 27% and 21.3% respectively. The total number of complication was 72 cases, in which complete AV block and cardiac tamponade accounted for 31.9% (23/72) and 26.4% (19/72) respectively.</AbstractText>RFCA for the treatment of tachyarrhythmias was rapidly developed in Chinese military hospitals. Improving the level of technical training and practice will play an important role in reducing complication and recurrence rate.</AbstractText>

[Sixty-four cases of percutaneous coronary angioplasty on saphenous vein bypass grafts].

To evaluate the early clinical result of percutaneous transluminal coronary intervention (PCI) and stenting on saphenous vein grafts.</AbstractText>Percutaneous intervention was performed in 91 saphenous vein grafts in 64 patients. The data of clinical results during operation and hospitalization and that of other interventional assisting device were recorded in database and were analyzed.</AbstractText>The success rate of operation was 95.3%, non-Q wave myocardial infarction occurred in 1 patient (1.6%) and temporary no-reflow phenomenon occurred in 4 patients (6.3%) during operation. Reduced antegrade flow and ventricular fibrillation happened in 1 patient after stenting and normal antegrade flow obtained after cardiac compression and tracheal intubation and insertion of IABP. The distal protection devices were used in 7 patients (10.9%), X-sizer extraction system in 4 patients. Platelet glycoprotein IIb/IIIa receptor blockers were administered in 25 patients (35.9%). Non-Q wave myocardial infarction occurred in two cases, the incidence of major adverse clinical event was 3.1% during the period of hospitalization.</AbstractText>The instant success rate of PTCA and stenting of saphenous vein bypass grafts is high and recent clinical result is promising, but the middle and long term results remain to be further followed. The use of distal embolic protection device and GPIIb/IIIa receptor blockers may improve its prognosis.</AbstractText>

The treatment of cardiac causes of sudden death, syncope, and seizure.

The treatment for pediatric causes for sudden cardiac death can either be general and supportive or, in 2005, can be much more etiology specific. While antiarrhythmic therapy and activity restriction have been for years the mainstay of therapy, newer technologies such as radiofrequency ablation and automatic implantable cardioverter defibrillators (AICDs) are now more commonly applied for certain disease entities. The evolving role for clinical genetic testing to determine the specific etiology of pediatric sudden cardiac death continues to evolve. Further improvements in risk stratification will allow us to determine which patients are at greatest risk, so that aggressive treatment can be delivered to these subgroups. In the future, there may be gene-specific therapies and/or genetic modification.

The Long QT and Brugada syndromes: causes of unexpected syncope and sudden cardiac death in children and young adults.

Inherited Long QT and Brugada syndromes cause syncope and sudden cardiac death due to ventricular tachyarrhythmias. Diagnosis may be difficult and the syncopal events are commonly misdiagnosed as neurally mediated (vaso-vagal) episodes or as "seizures". The details of the events (onset, offset, sequelae, precipitating factors) and knowledge of the ECG features are key to the correct diagnosis, and in assisting the neurologist in discriminating these two life-threatening disorders from neurally mediated (vaso-vagal) syncope and in discerning when a "seizure" might be due to a lethal cardiac arrhythmia. Very effective treatments are available and prompt, correct diagnosis and appropriate treatment are life-saving.

Clinical predictors of defibrillation threshold in patients with implantable cardioverter-defibrillators.

Safety of patients with malignant ventricular arrhythmias, treated with implantable cardioverter defibrillators (ICD), depends on the possibility of immediate and effective intracardiac defibrillation. It is especially important in those patients in whom there is a risk of increased defibrillation threshold (DFT) of ventricular fibrillation (VF). Thus, it is important to know whether some clinical parameters may predict a high DFT.</AbstractText>To assess the relationship between DFT and clinical, demographic and anthropometric parameters, type and progression of underlying disease as well as antiarrhythmic therapy used in ICD recipients.</AbstractText>The study group consisted of 168 patients (47 females, 121 males, mean age 55+/-15 years, range 15-82 years) who were selected to receive an ICD. DFT was systematically tested during ICD implantation in all patients. Various clinical, demographic, anthropometric and echocardiographic parameters were analysed as the function of DFT value, examining their accuracy in predicting a high (&gt; or =15 J) or a low (&lt;15 J) DFT, using logistic regression model.</AbstractText>Univariate analysis revealed that DFT value was significantly related to the following parameters: idiopathic VF, dilated cardiomyopathy, amiodarone therapy and the use of beta blockers. There was a significant correlation between DFT and LVEDD, height, LVEF and impedance of defibrillating system. Multivariate analysis showed that amiodarone therapy, height, impedance of defibrillating system and LVEDD were independently related to the DFT value. Parameters which predicted a high (&gt; or =15 J) DFT, consisted of amiodarone therapy (p=0.005), height (p=0.01), LVEDD (p=0.01), LVEF (p=0.03), dilated cardiomyopathy (p=0.01) and body surface area (p=0.049). Amiodarone therapy occurred to be the only parameter which independently predicted a high DFT (odds ratio 2.78; 95% confidence interval 1.19-6.5).</AbstractText>Tall stature, enhanced LVEDD, decreased LVEF and amiodarone therapy increase the risk of a high DFT in ICD recipients. Chronic amiodarone therapy increases three times the risk of elevated DFT. In patients with already implanted ICD in whom amiodarone is started, reassessment of DFT following administration of a loading dose of the drug is required.</AbstractText>

Waveform analysis of ventricular fibrillation to predict defibrillation.

Ventricular fibrillation occurs during many cases of cardiac arrest and is treated with rescue shocks. Coarse ventricular fibrillation occurs earlier after the onset of cardiac arrest and is more likely to be converted to an organized rhythm with pulses by rescue shocks. Less organized or fine ventricular fibrillation occurs later, has less power concentrated within narrow frequency bands and lower amplitude, and is less likely to be converted to an organized rhythm by rescue shocks. Quantitative analysis of the ventricular fibrillation waveform may distinguish coarse ventricular fibrillation from fine ventricular fibrillation, allowing more appropriate delivery of rescue shocks.</AbstractText>A variety of studies in animals and humans indicate that there is underlying structure within the ventricular fibrillation waveform. Highly organized or coarse ventricular fibrillation is characterized by large power contributions from a few component frequencies and higher amplitude. Amplitude, decomposition into power spectra, or probability-based, nonlinear measures all can quantify the organization of human ventricular fibrillation waveforms. Clinical data have accumulated that these quantitative measures, or combinations of these measures, can predict the likelihood of rescue shock success, restoration of circulation, and survival to hospital discharge.</AbstractText>Many quantitative ventricular fibrillation measures could be implemented in current generations of monitors/defibrillators to assist the timing of rescue shocks during clinical care. Emerging data suggest that a period of chest compressions or reperfusion can increase the likelihood of successful defibrillation. Therefore, waveform-based prediction of defibrillation success could reduce the delivery of failed rescue shocks.</AbstractText>

Agonal respirations during cardiac arrest.

This review examines the physiologic understanding and clinical implications of agonal respirations during cardiac arrest.</AbstractText>Agonal respirations originate from lower brainstem neurons as higher centers become increasingly hypoxic during cardiac arrest. No single layperson descriptor consistently identifies agonal respirations; rather, laypersons use a collection of terms to describe the abnormal breathing of agonal respirations. Animal studies demonstrate that agonal respirations can produce clinically important ventilation, oxygenation, and circulation. In human studies, agonal respirations are apparent in 40% of persons suffering out-of-hospital cardiac arrest. Agonal respirations are associated with witnessed events, ventricular fibrillation, and survival, suggesting that agonal respirations are a marker of an arrest's early phase and may potentially directly affect cardiopulmonary function. Although agonal respirations appear to exert favorable cardiopulmonary effects, they may paradoxically inhibit rescue efforts by preventing arrest recognition. A standardized dispatch approach can help dispatchers identify agonal respirations by distinguishing normal and abnormal breathing in the unconscious patient. Future study should consider how information about agonal respirations might be integrated into the resuscitation to optimize outcomes.</AbstractText>Agonal respirations have physiologic and care implications. Efforts to identify agonal respirations and integrate this information into resuscitation care may improve outcome from cardiac arrest.</AbstractText>

Delaying shock for cardiopulmonary resuscitation: does it save lives?

Out-of-hospital cardiac arrest claims more than 450,000 lives annually in North America. Many communities have dedicated significant resources to provide rapid defibrillator response for patients in ventricular fibrillation. In spite of these efforts, mortality from out-of-hospital cardiac arrest has not improved significantly. Emerging evidence suggests some patients in ventricular fibrillation arrest may be harmed by immediate defibrillation.</AbstractText>Recent laboratory studies have shown benefit in performing a period of chest compressions (cardiopulmonary resuscitation) prior to defibrillation in models with more than 4 minutes of induced ventricular fibrillation. During the initial 4 minutes the heart is more amenable to electrical defibrillation. Between 4-10 minutes, chest compressions create some coronary perfusion and fill the left ventricle to prepare the heart for electric shock. These findings, in conjunction with most emergency medical service response times reported to be 5-8 minutes, have prompted human investigation into a strategy of chest compression first. A recent randomized controlled trial reported a fivefold increase in survival for patients with more than 5 minutes of VF who received 3 minutes of chest compressions prior to defibrillation compared with those who had not.</AbstractText>Current guidelines call for rapid defibrillation as the most important 'link' in the 'chain of survival'. For most ventricular fibrillation patients who have professional rescuers arrive after 5-8 minutes of ventricular fibrillation, however, immediate defibrillation is likely to be ineffective. Counterintuitively, these patients may benefit from a period of chest compressions prior to being shocked.</AbstractText>

Appropriate and inappropriate ventricular therapies, quality of life, and mortality among primary and secondary prevention implantable cardioverter defibrillator patients: results from the Pacing Fast VT REduces Shock ThErapies (PainFREE Rx II) trial.

Implantable cardioverter defibrillators (ICDs) reduce mortality in primary and secondary prevention. Quality of life, mortality, appropriate therapies for specific ventricular rhythms, and inappropriate therapies for supraventricular tachycardia (SVT) were compared among 582 patients (primary prevention=248; secondary prevention=334) in PainFREE Rx II, a 634-patient prospective, randomized study of antitachycardia pacing or shocks for fast ventricular tachycardia (FVT).</AbstractText>ICDs were programmed identically with 3 zones (ventricular tachycardia [VT] &lt;188 bpm; FVT=188 to 250 bpm; ventricular fibrillation [VF] &gt;250 bpm) but randomized to antitachycardia pacing or shock as initial therapy for FVT. All treated episodes with electrograms were adjudicated. Primary prevention patients had lower ejection fractions and more coronary artery disease. beta-Blocker use, antiarrhythmic drug use, and follow-up duration were similar. Over 11+/-3 months, 1563 treated episodes were classified as VT (n=740), FVT (n=350), VF (n=77), and SVT (n=396). The distribution of VT, FVT, and VF was not different between primary and secondary prevention patients (respectively, VT 52% versus 54%, FVT 35% versus 35%, and VF 14% versus 10%). More secondary prevention patients had appropriate therapies (26% versus 18%, P=0.02), but among these patients, the median number of episodes per patient was similar. Inappropriate therapies occurred in 15% of both groups and accounted for similar proportions of all detected and treated episodes (46% in primary prevention patients versus 34% in secondary prevention patients, P=0.09). Quality of life improved modestly in both groups, and mortality was similar.</AbstractText>Primary prevention patients are slightly less likely to have appropriate therapies than secondary prevention patients, but episode density is similar among patients with appropriate therapies. SVT resulted in more than one third of therapies in both groups, but quality of life and mortality were similar.</AbstractText>

Ibutilide--recent molecular insights and accumulating evidence for use in atrial flutter and fibrillation.

Ibutilide is a 'pure' class III antiarrhythmic drug, used intravenously against atrial flutter and fibrillation. At a cellular level it exerts two main actions: induction of a persistent Na+ current sensitive to dihydropyridine Ca2+ channel blockers and potent inhibition of the cardiac rapid delayed rectifier K+ current, by binding within the channel pore cavity upon channel gating. Ibutilide has been shown to terminate atrial flutter and fibrillation in animal studies, with some risk of ventricular pro-arrhythmia. Experimental models of hypertrophy/heart failure show altered sensitivity to ibutilide, with increased dispersion of repolarisation and incidence of pro-arrhythmia. Patient trials show that ibutilide is effective at terminating atrial arrhythmias when given alone, and that it can increase effectiveness and reduce energy requirements of electrical cardioversion. The risk to patients of polymorphic ventricular tachycardia necessitates careful patient selection and monitoring during and after treatment. An ibutilide analogue, trecetilide, requires further investigation but may offer a less readily metabolised and pro-arrhythmic alternative to ibutilide.

[An algorithm study on telecardiogram diagnosis based on multivariate autoregressive model and two-lead ECG signals].

In view of the time delay caused by reconstruction of signals at remote sites, a direct classification method with high accuracy suitable for telediagnosis of electrocardiogram (ECG) signals is studied.</AbstractText>The data for analysis and classification was obtained from MIT-BIH database, including 300 samples each of normal sinus rhythm (NSR), atria premature contraction (APC), premature ventricular contraction (PVC), ventricular tachycardia (VT), ventricular fibrillation (VF) and superventricular tachycardia (SVT). An multivariate autoregressive (MAR) model based technique that could combine the signals of two ECG leads was presented to classify the ECGs directly, including MAR modeling performed on ECGs, and quadratic discrimination function (QDF) based classification by using MAR coefficients and K-L MAR coefficients.</AbstractText>Besides quick and convenient diagnosis, the accuracy of the proposed classification algorithm was as high as 98.3%-100%.</AbstractText>The MAR modeling based technique is suitable for telecardiogram diagnosis. Comparing with single-lead ECGs, better classification results can be obtained through the combination of two-lead ECG signals.</AbstractText>

Epidermolysis bullosa simplex associated with muscular dystrophy and cardiac involvement.

We report a new clinical variant of epidermolysis bullosa simplex with muscular dystrophy (EBS-MD) that was associated with cardiac involvement. A 33-year-old patient had atrial fibrillation, pericardial effusion, and hypokinetic left ventricular cardiac walls. The muscle biopsy material revealed diffuse endomysial fibrosis and small atrophic muscle fibers with rounded contours. A positive desmin expression with abnormal localization in the subsarcolemmal groups was observed. We concluded that patients with EBS-MD should be investigated carefully when there are associated cardiac findings.

Heart failure.

Although heart failure is common, disabling, and deadly, there are now many effective treatments, at least for patients with low left-ventricular ejection fraction. For all, angiotensin-converting-enzyme inhibitors and beta blockers are the essential disease-modifying treatments, improving symptoms, reducing hospital admissions, and increasing survival. Implantable cardioverter defibrillators also improve survival. For patients with persistent symptoms, angiotensin-receptor blockers and aldosterone antagonists have additional benefits. These treatments are now preferred to digoxin, although this drug can still be useful at an earlier stage in patients with atrial fibrillation. In some patients with persistently severe symptoms and a wide QRS on the electrocardiogram, cardiac resynchronisation therapy also reduces mortality and morbidity. The role of other markers of ventricular dys-synchrony is under investigation. There is growing evidence that left-ventricular assist devices are indicated in some patients with end-stage heart failure. Organised delivery of care also improves outcome. However, there is still no firmly evidence-based treatment for heart failure with preserved ejection fraction. Many new pharmacological, device, and surgical treatments for heart failure are currently under evaluation in clinical trials, and other approaches, including stem-cell treatment, are at an earlier stage of investigation.

[The pulmonary toxicity of amiodarone: six-case report].

To report the clinical features and the prognosis, the methods of diagnosis and treatment, and the early detection of the pulmonary toxicity induced by amiodarone.</AbstractText>The clinical course, the findings of X-ray and CT and the results of treatment were summarized and analyzed in six patients with amiodarone-induced pulmonary toxicity.</AbstractText>Five males, one female, aged 62 - 69 (66.0 +/- 2.4) years. Amiodarone was used because of paroxysmal atrial fibrillation in five patients and ventricular arrhythmia in one. The loading dose was 7 g and the maintaining dose was 0.2 g/d or less. Pulmonary toxicity was recognized at the times in 0.5 - 4.0 (2.1 +/- 1.3) years after amiodarone therapy. Dyspnea occurred, crack rales were audible in both lower parts of the lungs, and the chest X-ray showed grid-like changes in case one. No symptom was found in the others. Their diagnosis was made according to the pulmonary intestinal changes by high-resolution computerized tomography when the lung marking was increased or deranged by chest X-ray during the regular follow-up. Pulmonary function examination showed that the restrictive ventilation and the CO diffusing capacity decreased in case one, while the CO diffusing capacity was normal in the others. The decreased obstructive ventilation capacity was found in case six. Amiodarone was discontinued in all the cases after the diagnosis of induced pulmonary toxicity. One patient was treated with corticosteroid, three with azithromycin, and the another two patients were not treated with drug. During 0.1 - 5.0 year period of follow-up the symptoms were markedly attenuated in case one, and no new symptoms and radiography findings were found in the others.</AbstractText>Pulmonary toxicity is a serious adverse effect of amiodarone. The typical feature is pulmonary intestinal fibrosis and thick pulmonary intestine in the early stage. Corticosteroid treatment seems effective. It would be helpful for early diagnosis to take chest X-ray examination regularly and CT examination in suspicions cases during the therapy. The prognosis may be good in the early diagnosed cases.</AbstractText>

[The electrophysiological study and implantable cardioverter defibrillator therapy for the patients with Brugada syndrome].

Clinical observation of electrophysiological study and implantable cardioverter defibrillator (ICD) therapy in patients with Brugada syndrome.</AbstractText>Ten patients (all male) with Brugada wave (spontaneous or propafenone test positive in ECG) underwent electrophysiological study (EPS). The mean age was (41 +/- 10) years. They had no structural heart disease with echocardiogram and the angiogram work-up. The ICD implanted in the patients with EPS-induced ventricular fibrillation in those who were available.</AbstractText>Three patients had the history of familial sudden cardiac death (SCD). Four patients had repeated syncope episodes, two of them had documented ventricular fibrillation during syncope episodes. The AH and HV intervals were 50 - 124 (86 +/- 21) ms and 41 - 84 (58 +/- 15) ms. The ventricular fibrillation was induced in four patients with syncope and atrioventricular reentry tachycardia in one patient with palpitation. Three patients had spontaneous or inducible atrial fibrillation. The ICD implanted in three patients with inducible ventricular fibrillation. Due to economic issue, one patient without ICD implantation had got SCD during follow-up. The patient with atrioventricular reentry tachycardia underwent a successful left atrioventricular accessory pathway ablation.</AbstractText>The Brugada patients with syncope and high rate of inducible ventricular fibrillation in EPS are the high risk population for SCD, in whom ICD should implant promptly to prevent SCD.</AbstractText>

[Combined cardiac resynchronization and implantable cardioversion defibrillation].

To examine the efficacy and safety of implantation of the device with combined cardiac resynchronization therapy (CRT) and implantable cardioversion defibrillation (ICD) capabilities.</AbstractText>Eleven patients aged 48 - 80 (71.6 +/- 9.5) years, 7 male and 4 female, were included in the study. All patients had either a history of aborted sudden cardiac death, ventricular tachyarrhythmia, or induced ventricular tachycardia during cardiac electrophysiological study, whose left ventricular ejection fractions were 35% or less and QRS durations were 120 or longer. The patients were implanted a Medtronic INSYNC II MARQUIS(TH) 7289. All left ventricular leads were implanted in left lateral or left posterior lateral side-branches of coronary sinus. The procedures were performed in general anesthesia status. The AV interval was optimized guided by ECHO in all the patients in the day after the procedure.</AbstractText>All procedures were successfully completed without major complications. The fluoroscopy time was 19 - 73 (44.7 +/- 19.9) min. Atrial lead amplitude, resistance and threshold were 0.5 - 3.5 (2.47 +/- 0.77) mV, 410 - 749 (590 +/- 126) Omega and 0.9 - 3.0 (1.37 +/- 0.71) V respectively. Right ventricular septal lead amplitude, resistance and threshold were 6.8 - 15.8 (11.00 +/- 3.48) mV, 387 - 750 (586 +/- 116) Omega and 0.4 - 1.0 (0.69 +/- 0.21) V respectively. The amplitude, resistance and threshold of left ventricular leads were 1.2 - 25 (15.37 +/- 5.15) mV, 423 - 812 (602 +/- 125) Omega and 0.3 - 5.0 (1.62 +/- 1.59) V respectively. The defibrillation thresholds (DFT) of 20 J were obtained in 3 patients, 6 J in 3 patients, and 15 J, 12 J and 3 J in one patient respectively. One of the 11 patients with failed old device did not obtain successful DFT after lead and device replacement and was defibrillated externally during DFT test. The another one did not obtain successful DFT because of abnormal ST-T changes in ECG. All devices were programmed to maximum of 30 J and discharged from the hospital in 48 hours except the one who failed to obtain DFT. The patients with mitral regurgitation improved after the AV optimization.</AbstractText>Implantation of device with CRT and ICD features is safe even in aging patients. The long time outcomes of the clinical efficacy of this combined device remain to be observed.</AbstractText>

[Percutaneous coronary intervention combined cardiac resynchronization therapy for refractory heart failure secondary to ischemic cardiomyopathy].

To evaluate the efficacy and safety of percutaneous coronary intervention (PCI) combined cardiac resynchronization therapy (CRT) for refractory heart failure secondary to ischemic cardiomyopathy (ICM).</AbstractText>PCI and CRT were performed in 7 ICM patients confirmed by angiography with NYHA class IV, QRS duration &gt;/= 130 ms in 6 of them, III degrees AVB in 1 patient, fast ventricular heart rate Af in 1 patient, ventricular fibrillation history in 2 patient. All of them had their LVEDD &gt;/= 55 mm, and LVEF &lt;/= 0.40 detected by UCG. PCI was performed first in 5 patients, and their follow-up angiography showed no restenosis 6 months after PCI, then CRT was given. CRT was performed first in 2 patients and 2 weeks later PCI was combined.</AbstractText>The procedures of PCI and CRT were performed successfully in all patients. Five patients received right atrial and biventricular pacing, one patient with Af received biventricular pacing and atrial-ventricular node radiofrequency ablation at the same procedure, and the another one patient received CRTD. One out of seven patients died of re-AMI 4 months after the combination therapy, and the other 6 patients had been alive 5 - 41 (23.2 +/- 13.8) months during the follow-up period. The heart function of the 7 patients had further improved after PCI and CRT combined therapy compared to that of PCI or CRT only. Their NYHA class decreased from IV to II, 6-minute walking distance increased steadily, and mitral regurgitation reduced and QRS duration shortened significantly. The LVEDD decreased and LVEF increased significantly in 2 patients without ventricular aneurysm, and slight improvement or no change were in the other 5 patients.</AbstractText>For patients with refractory heart failure secondary to ICM, the combination of PCI and CRT could obviously improve their heart function, quality of life and prognosis, which also very safe in perforation.</AbstractText>

Reality of out of hospital cardiac arrest.

The high mortality rates associated with out of hospital cardiac arrest, particularly those occurring in the home, stress the need for early treatment in the form of publicly accessible external defibrillators.

Temporary left ventricular pacing improves haemodynamic performance in patients requiring epicardial pacing post cardiac surgery.

In the 1990s, sequential atrio-ventricular pacing demonstrated haemodynamic benefit relative to right ventricular pacing in patients with sinus rhythm requiring pacing post cardiopulmonary bypass. The benefit of biventricular pacing has been demonstrated in non-surgical patients with severe left ventricular dysfunction. It was hypothesised that left ventricular pacing would increase cardiac output in surgical patients. We report the findings of a prospective trial of left ventricular pacing with active lead placement on the anterior or posterior left ventricular surface, compared to standard practice of active lead placement on the right ventricular surface.</AbstractText>Twenty five patients with left ventricular dysfunction underwent pacing with active lead placement on the right ventricle (control), the anterior left ventricle and the posterior left ventricle in random order, with each pacing mode of 10 min duration, following cardiopulmonary bypass. Haemodynamic parameters were measured with a thermodilution pulmonary artery catheter. Patients provided their control values.</AbstractText>In the 25 patients studied, pacing with the active lead posteriorly on the left ventricle increased cardiac index from 2.74 to 3.08 l/min per m2 (P=0.019). Significant increases in mean arterial pressure with the use of this pacing mode were observed. There were no complications relating to application or removal of the left ventricle pacing leads.</AbstractText>Left ventricular pacing with active lead placed on the postero-lateral left ventricular wall affords haemodynamic benefit to cardiac surgical patients.</AbstractText>

The perplexing complexity of cardiac arrhythmias: beyond electrical remodeling.

Cardiac arrhythmias continue to pose a major medical challenge and significant public health burden. Atrial fibrillation, the most prevalent arrhythmia, affects more than two million Americans annually and is associated with a twofold increase in mortality. In addition, more than 250,000 Americans each year suffer ventricular arrhythmias, often resulting in sudden cardiac death. Despite the high incidence and societal impact of cardiac arrhythmias, presently there are insufficient insights into the molecular mechanisms involved in arrhythmia generation, propagation, and/or maintenance or into the molecular determinants of disease risk, prognosis, and progression. In addition, present therapeutic strategies for arrhythmia abatement often are ineffective or require palliative device therapy after persistent changes in the electrical and conduction characteristics of the heart have occurred, changes that appear to increase the risk for arrhythmia progression. This article reviews our present understanding of the complexity of mechanisms that regulate cardiac membrane excitability and cardiac function and explores the role of derangements in these mechanisms that interact to induce arrhythmogenic substrates. Approaches are recommended for future investigations focused on providing new mechanistic insights and therapeutic interventions.

Glucose and insulin influences on heart and brain in cardiac surgery.

The elective global ischemia of on-pump coronary artery bypass surgery contributes to the incidence of postoperative mortality, complications, and use of resources. In addition to cardiopulmonary bypass and techniques for myocardial protection such as aortic cross clamp, ventricular fibrillation, and cardioplegia, the administration of systemic glucose-insulin-potassium (GIK) in the perioperative period may act as both a metabolic modulator and potential inodilator. GIK may therefore serve to protect the myocardium and promote adequate cardiac and hemodynamic performance that would improve patient recovery. Cell, tissue, and animal experiments have determined a number of mechanisms of action by which this may be achieved, with increasing focus on insulin as the key component. The original concepts centered on GIK during or after ischemia switching metabolism away from that based on non-esterified fatty acids toward a more favorable glucose-based metabolism and thus improving the efficiency of adenosine triphosphate production and glycogen preservation. Insulin's ability to reduce intracellular fatty acid metabolism may also reduce cellular membrane damage. More recently other mechanisms have also been suggested, including osmotic, oxygen free radical scavenging, and antiapoptotic and anti-inflammatory effects. However, trials that have examined the role of GIK in cardiac surgery have been small, open label, and involved a wide variety of regimens. They have demonstrated improved glycogen preservation, reduced infarct size, reduced incidences of dysrhythmias, need for inotropic agents, and low cardiac output state, and overall reduced lengths of stay. The perceived need to achieve strict blood glucose control to reduce neurologic injury and improve overall mortality have conflicted with its practical difficulties, particularly during cold cardiopulmonary bypass, and the exact role of supplemental glucose administration and resulting hyperglycemia require re-examination.

Increased cortical cerebral blood flow with LUCAS; a new device for mechanical chest compressions compared to standard external compressions during experimental cardiopulmonary resuscitation.

LUCAS is a new device for mechanical compression and decompression of the chest during cardiopulmonary resuscitation (CPR). The aim of this study was to compare the efficacy of this new device with standard manual external chest compressions using cerebral cortical blood flow, cerebral oxygen extraction, and end-tidal CO2 for indirect measurement of cardiac output. Drug therapy, with adrenaline (epinephrine) was eliminated in order to evaluate the effects of chest compressions alone.</AbstractText>Ventricular fibrillation (VF) was induced in 14 anaesthetized pigs. After 8 min non-intervention interval, the animals were randomized into two groups. One group received external chest compressions using a new mechanical device, LUCAS. The other group received standard manual external chest compressions. The compression rate was 100 min(-1) and mechanical ventilation was resumed with 100% oxygen during CPR in both groups. No adrenaline was given. After 15 min of CPR, external defibrillatory shocks were applied to achieve restoration of spontaneous circulation (ROSC). Cortical cerebral blood flow was measured continuously using Laser-Doppler flowmetry. End-tidal CO2 was measured using mainstream capnography.</AbstractText>During CPR, the cortical cerebral blood flow was significantly higher in the group treated with LUCAS (p = 0.041). There was no difference in oxygen extraction between the groups. End-tidal CO2, an indirect measurement of the achieved cardiac output during CPR, was significantly higher in the group treated with the LUCAS device (p = 0.009). Restoration of spontaneous circulation was achieved in two animals, one from each group.</AbstractText>Chest compressions with the LUCAS device during experimental cardiopulmonary resuscitation resulted in higher cerebral blood flow and cardiac output than standard manual external chest compressions. These results strongly support prospective randomised studies in patients to evaluate this new device.</AbstractText>

Details of the initial management of cardiac arrest occurring in the workplace in a French urban area.

Our goal was to evaluate the details and management of cardiac arrest (CA) occurring in the working environment.</AbstractText>We conducted a 10-year retrospective study based on the medical records of the Garches mobile intensive care unit. CA occurring in the workplace ("Inside W." group) was matched with two CA outside the workplace ("Outside W." group), with regard to sex, age and year of occurrence. The Chain of Survival and prognosis factors were analysed in a bi-multivariate analysis.</AbstractText>From 1993 to 2002, 72 CA were included in the "Inside W." group, with 79% arising from suspected cardiac aetiology (there was a similar proportion in the "Outside W." group). Some variables in the cardiac aetiology patients were higher in the "Inside W." group compared to the "Outside W." group (P &lt; 0.05): early external chest compression [(ECC), 37%, n = 20 versus 16%, n = 16)] and ventricular fibrillation as initial recorded rhythm (40%, n = 33 versus 16%, n = 16). The proportion of use of automated external defibrillator (AED) was similar in the two groups. The workplace was not associated with a better outcome, with 9% patients discharged alive compared to 4% n = 6, P &gt; 0.05. Early ECC and defibrillation attempted with an AED were associated with patients discharged alive from the intensive care unit in a multivariate analysis (P &lt; 0.05), but not the workplace and cardiac aetiology.</AbstractText>Although our study did not support that concept that the workplace was a safer place, there was a better chain of survival for CA applied within workplace settings. Basic Life Support teaching and installation of AEDs could be helpful, though further cost-effectiveness studies are needed.</AbstractText>

Evolution of a community-wide early defibrillation programme experience over 13 years using police/fire personnel and paramedics as responders.

In November 1990, a 2-year trial period was initiated in which police officers in the city of Rochester, Minnesota, were trained in the operation of automated external defibrillators (AEDs). Following the trial, the program was expanded as the city grew in population and area. In 1998 firefighters also were equipped with AEDs, bringing to a total 18 AEDs with police and fire personnel, in addition to paramedic capability.</AbstractText>From November 1990 to December 2003, all adult patients with atraumatic cardiac arrest with ventricular fibrillation (VF) as the presenting rhythm were included for analysis. Call-to-shock time intervals, restoration of spontaneous circulation after defibrillation shocks only (without need for vasoactive or inotropic drug administration), and neurologically intact survival (overall performance category (OPC) 1 or 2) were study end-points.</AbstractText>One hundred and ninety-three patients presented in VF. Of these, 80 (41%) were discharged neurologically intact. Of the 159 VF patients whose arrest was bystander-witnessed 73 (46%) were discharged. Survival from non-VF arrest was very low (5%). Assessment of VF survivors demonstrated a quality of life, adjusted for age, gender, and disease, similar to that of the general population.</AbstractText>These data demonstrate that a relatively high survival can be obtained in a city of this size and area employing a non-tiered community-wide approach within the emergency medical services (EMS) system.</AbstractText>

International Resuscitation Network Registry: design, rationale and preliminary results.

There is a lack of high-quality information about the effectiveness of resuscitation interventions and international differences in structure, process and outcome after out-of-hospital cardiac arrest and cardiopulmonary resuscitation because data are not collected uniformly. An internet-based international registry could make such evaluations possible, and enable the conduct of large randomized controlled trials of resuscitation therapies. A prospective international cohort study was performed that included 571 infants, children and adults (a) who experienced cardiac arrest requiring chest compressions or external defibrillation, (b) outside the hospital in the study communities and (c) upon whom resuscitation was attempted by EMS personnel. Cardiac arrest was defined as lack of responsiveness, breathing or movement in individuals for whom the EMS system is activated for whom an arrest record is completed. All data were collated via a secure and confidential web-based method by using automated forms processing software with appropriate variable range checks, logic checks and skip rules. Median number of missing responses for each variable was 0 (interquartile range 0, 0). Twenty-seven percent of the patients had a first recorded rhythm of ventricular fibrillation or ventricular tachycardia, 60% had a witnessed arrest, and 34% received bystander CPR. Mean time from call to arrival on scene was 7.1+/-5.1 min. Six percent of the patients survived to hospital discharge. The resuscitation process was highly variable across centers, and survival and neurological outcome were also significantly and independently different across centers. This study shows that it is possible to collect data prospectively describing the structure, process and outcome associated with cardiac arrest in multiple international sites via the internet. Therefore, it is feasible to conduct adequately powered randomized trials of resuscitation therapies in international settings.

[Magnetic resonance imaging in a patient with pacemaker].

The patient is a 24-year-old female with a dual-chamber pacemaker, who had intracranial hypertension, progressive visual loss, and several inconclusive cranial tomographies. She underwent magnetic resonance imaging, even though that diagnostic method is absolutely contraindicated in patients with pacemakers.

Myocardial compliance was not altered after acute induction of atrial fibrillation in sheep.

Although left ventricular (LV) contractility in atrial fibrillation (Af) is known to change in a beat-to-beat fashion, little is known about the changes in LV compliance in Af.</AbstractText><AbstractText Label="MATERIAL/METHODS" NlmCategory="METHODS">We experimentally induced tachycardic Af (average heart rate - 154 beats per minute) in 18 sheep. LV volume and pressure were simultaneously monitored using a conductance catheter. LV end-diastolic volume (V(ED)) and pressure (P(ED)) were plotted in a beat-to-beat fashion and fitted to the following exponential equation (P(ED)=gamma x e(b x V(ED))) in each animal. A random effects model was constructed to determine if the intercepts and slopes differ.</AbstractText>In all animals, those plots after the induction of Af fit quite well to the exponential function (r=0.834+/-0.184) by gating short preceding interval (RR1) beats. By simply taking the natural logarithm of both sides in the equation, the linear relationship (ln(P(ED)) =alpha+ betaxV(ED), where a = lng) was observed in all animals before (normal sinus rhythm, NSR) and after the induction of Af. Only two of 18 intercepts and four of 18 slopes deviate between NSR and Af. Most interestingly, the random effects model clearly detailed that the average animal had intercepts and slopes that were not discernibly different between NSR and Af.</AbstractText>Unlike LV contractility, myocardial compliance did not change after the acute induction of Af. These interesting results may give us insights into the understanding of the physiology in acute rapid Af.</AbstractText>

Angiotensin-converting enzyme inhibitor therapy inhibits the progression from paroxysmal atrial fibrillation to chronic atrial fibrillation.

Atrial fibrillation is a progressive disease, which in the paroxysmal form (PAF) becomes more frequent and finally becomes chronic (CAF). A retrospective analysis of patients with PAF was conducted to examine the hypothesis that angiotensin-converting enzyme inhibitors (ACEI) will prevent the progression to CAF.</AbstractText>On the basis of their treatment, 95 patients with PAF were divided into 2 groups: 42 patients treated with ACEI for hypertension throughout the period of treatment and follow-up (ACEI group) and 53 patients not given ACEI (non-ACEI group). Cardiac rhythms were assessed either from the medical records or the electrocardiograms recorded every 2-4 weeks at follow-up visits. The mean follow-up time was 8.3+/-3.5 years. There was no significant difference in the use of antiarrhythmic drugs, left atrial diameter or left ventricular ejection fraction between the 2 groups. The Kaplan-Meier curve for the time to occurrence of CAF showed a lower incidence of CAF in the ACEI group and demonstrated that the 5-year probability for persistence of PAF without progression to CAF was 88.3%, but 47.5% in the non-ACEI group.</AbstractText>These results indicate that ACEI will prevent progression from PAF to CAF.</AbstractText>

Heart Failure with Preserved Systolic Function.

At least 30% of patients with congestive heart failure have preserved systolic function in the absence of significant valvular heart disease. These patients have diastolic dysfunction. Patients are frequently older and hypertensive. The rate of hospitalization in these patients is similar to that in patients with systolic dysfunction. Mortality is intermediate between that of patients with systolic dysfunction heart failure and normal subjects. Diagnosis requires a clear demonstration of the presence of the heart failure syndrome, normal systolic function, and the absence of valvular disease that could increase left atrial pressures. The diagnosis is supported by evidence of diastolic dysfunction that, from a practical point of view, will be provided most frequently by tissue Doppler imaging. Few randomized data are available on efficacy of therapeutic approaches. Acute treatment centers on reducing central blood volume with diuretics and nitrates and controlling heart rate, particularly in the setting of atrial fibrillation. Further treatment centers on reversing underlying pathophysiologic changes, particularly left ventricular hypertrophy. Control of hypertension and antagonism of the renin-angiotensin-aldosterone system appear to be promising therapeutic approaches.

Is hypertension a prothrombotic state?

Hypertension is complicated by thrombosis-related events (such as myocardial infarction and stroke), and despite the high vascular pressures, these thrombotic occlusive events paradoxically occur more often than hemorrhagic episodes. The predisposition for thrombogenesis is increased in hypertension, which leads to changes in the platelets, endothelium, and matrix metalloproteinases and their inhibitors, as well as the coagulation and fibrinolytic pathways, which help promote the induction and the maintenance of this prothrombotic or hypercoagulable state. Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. These changes can, to a certain degree, be reversed by the treatment of hypertension, although the effects may be inconsistent. The evidence for antithrombotic therapy is less consistent, but in "high risk" hypertensive patients, antiplatelet therapy is useful.

Cardiac arrest in a soccer player: a unique case of anomalous coronary origin detected by 16-row multislice computed tomography coronary angiography.

Anomalous origin of the coronary arteries may be present in otherwise normal subjects without clinical significance, but can also be the cause of myocardial ischemia and sudden death in both adults and teenagers. In particular, the origin of the left main coronary artery or left anterior descending artery from the right sinus of Valsalva or right coronary artery may result in compression of the vessel during or immediately after exercise. We present a unique case of coronary anomaly with four separate coronary ostia originating from the right coronary sinus in a soccer player with sudden cardiac arrest. Multislice contrast-enhanced computed tomography has emerged as a valid noninvasive method for the diagnosis of coronary artery anomaly.