Significance of aborted cardiac arrest and sustained ventricular tachycardia in patients referred for treatment therapy of advanced heart failure.

Cardiac arrest in patients with heart failure may be the result of remediable factors such as pulmonary edema, drug toxicity, or electrolyte abnormalities, or it may be due to primary arrhythmias. The relation of prior aborted cardiac arrest or sustained ventricular tachycardia to subsequent prognosis was assessed in 458 consecutive patients referred for management of advanced heart failure (left ventricular ejection fraction 0.2 +/- 0.07). All patients received tailored vasodilator and diuretic therapy and were then followed as outpatients. Patients were divided into four groups: 388 patients (85%) with no prior cardiac arrest or sustained ventricular tachycardia, 31 patients (7%) with a primary arrhythmia cardiac arrest, 22 patients (5%) with a secondary cardiac arrest, and 17 patients (4%) with sustained ventricular tachycardia without cardiac arrest. Patients with cardiac arrest resulting from a primary arrhythmia were usually treated with antiarrhythmic drugs (25 patients), and five patients received an implantable defibrillator. After hospital discharge actuarial 1-year sudden death risk (17%) and total mortality (24%) rates for the group with primary arrhythmia were similar to corresponding values in patients with no history of cardiac arrest or sustained ventricular tachycardia (17% and 30%, respectively). In patients with a secondary cardiac arrest as a result of exacerbation of heart failure (11 patients), torsade de pointes (10 patients), or hypokalemia (one patient), therapy focused on removal of aggravating factors. Actuarial 1-year sudden death (39%) and total mortality (54%) rates for the group with secondary arrest were higher than for patients without a history of cardiac arrest (p = 0.003 and 0.005, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Tachycardiomyopathy in patients with and without subacute cardiac pathology. Experiences at the Cardiovascular Center of Merida, Venezuela]

We report our experiences with tachycardia-induced cardiomyopathy. Nine patients (3-56 years old) had incessant supraventricular tachycardia and congestive heart failure. The cardiac eco-Doppler evidenced a significant increase of cardiac volumes and mild tricuspid and mitral regurgitation. The ejection fraction (EF) was 0.31 +/- 0.12, the end diastolic volume was 162 +/- 48 cc and the end systolic volume, 116 +/- 54 cc. Four patients had accessory pathways, 3 atrial flutter, 1 A-V nodal reentrant tachycardia, and 1 ectopic atrial tachycardia. Two patients had Chagasic myocarditis. Only in one chagasic patient a decreased number of tachycardia episodes was achieved, this patient died. The autopsy revealed cerebellar and pulmonary emboli. In the other 8 patients the arrhythmia was well controlled. In these, the ventricular volumes decreased, the EF increased to 0.51 +/- 0.14 (p = 0.00006), and the congestive heart failure remitted. We conclude that incessant tachycardia produces a symptomatic dilated cardiomyopathy in patients with and without structural heart disease. The arrhythmia control is followed by an increase in cardiac function and a remission of heart failure symptoms.     

Clinical experience in seventy-seven patients with the automatic implantable cardioverter defibrillator

Seventy-seven patients with drug-refractory sustained ventricular tachycardia (VT) (28 patients) or ventricular fibrillation (VF) (49 patients) underwent implantation of an automatic cardioverter defibrillator (AICD). The 67 men and 10 women, with a mean age of 60 +/- 12 years (range 18 to 79), had coronary artery disease (60 patients), idiopathic cardiomyopathy (eight patients), mitral valve prolapse (four patients), hypertensive heart disease (one patient), Ebstein's anomaly (one patient), long QT syndrome (one patient), and primary electrical disease (two patients). The mean left ventricular ejection fraction was 35 +/- 16% (range 10% to 75%). Sustained VT/VF was induced in 64 patients (83%) at baseline electrophysiologic testing. A mean of 4.1 +/- 1.3 antiarrhythmic drugs failed to control the arrhythmia. Associated surgery at AICD implantation included coronary artery bypass in 19 patients, coronary bypass with aneurysmectomy in six patients, and aneurysmectomy alone in one patient. Five patients had only prophylactic patches implanted during aneurysmectomy or coronary bypass and the AICD device was subsequently implanted under local anesthesia to prevent arrhythmia recurrence or to control persistently inducible VT. Operative mortality was 2.6% with two deaths from intractable VF. Fifty-two patients (69%) continued receiving antiarrhythmic drugs to suppress spontaneous VT. During a mean follow-up of 15 +/- 13 months (range 1 to 63), six patients died: two suddenly due to probable pulse generator failure (greater than 2 years old), one of acute myocardial infarction, two of heart failure, and one of respiratory failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic value of early electrophysiologic studies for ventricular tachycardia recurrence in patients with coronary artery disease treated with amiodarone

Amiodarone was used in 86 patients with ventricular tachycardia (VT) (67 patients) or ventricular fibrillation (19 patients) secondary to coronary artery disease. The mean +/- standard deviation left ventricular ejection fraction was 30 +/- 12% (range 8 to 65%). Prior trials with 4 +/- 1.2 alternate antiarrhythmic agents had been unsuccessful. Amiodarone was loaded at dosages of 1,200 to 1,800 mg/day, with maintenance dosages of 400 to 600 mg/day. Drug efficacy was evaluated by programmed stimulation at 10 to 14 days in 68 patients. In 38 patients sustained VT or ventricular fibrillation was inducible (group I), whereas 30 patients (group II) had either no inducible VT (8) or had nonsustained VT induced (22). Holter monitoring was used to assess drug efficacy in 18 patients (group III). All patients were evaluated at 3- to 6-month intervals with Holter monitors for efficacy and a standard protocol for toxicity. During a long-term follow-up of 18 +/- 16 months, sudden death occurred in 5 patients and nonfatal arrhythmia recurrences were detected in 16. The actuarial probability of freedom from fatal and nonfatal arrhythmia recurrences at 24 months was 0.52 for group I, 0.97 for group II and 0.68 for group III. The mode of induction, rate change or hemodynamic tolerance of the induced ventricular tachycardia did not predict arrhythmia recurrence. Among the clinical variables analyzed, only an ejection fraction of less than or equal to 30% was identified as a significant predictor of arrhythmia recurrence. Nonsudden cardiac death occurred in 21 patients, including 19 from heart failure and 2 from myocardial infarction. Noncardiac death occurred in 7 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Concomitant beta-blocker therapy is associated with a lower occurrence of ventricular arrhythmias in patients with decompensated heart failure

BACKGROUND: Ventricular arrhythmias are nearly universally present in patients with advanced congestive heart failure (CHF) and represent an important cause of mortality in these patients. One of the putative mechanisms for the salutary effects of beta-blockers on sudden death mortality in heart failure is their ability to suppress ventricular arrhythmias. However, supporting data in patients with CHF are sparse, especially in the setting of excessive neurohumoral activation associated with symptomatic decompensated heart failure. METHODS AND RESULTS: We studied 236 patients (159 men; mean age, 61 +/- 14 years) admitted for decompensated CHF. Fifty patients were receiving beta-blockers at the time of the study. The severity of ventricular arrhythmia was assessed by 24-hour Holter recordings by using several prospectively defined measures of ventricular ectopy. All measures of ventricular ectopy were lower in patients receiving beta-blockers. The average hourly total premature ventricular beats (PVCs), hourly ventricular couplets, repetitive PVCs, and frequency of ventricular tachycardia episodes were 15% (P =.02), 75% (P <.05), 72% (P <.05), and 87% (P =.01) lower in patient receiving beta-blockers, respectively. In a multivariate regression analysis, the negative relationship between beta-blockers and the average hourly PVCs (P =.03), the frequency of ventricular pairs (P =.03), repetitive PVCs (P <.05), and ventricular tachycardia episodes (P =.01) remained significant and independent. CONCLUSIONS: Concomitant beta-blocker therapy during heart failure decompensation is associated with a marked reduction in complex ventricular ectopy and episodes of ventricular tachycardia. This effect of beta-blockers may play an important protective role by preventing serious ventricular arrhythmias during transient increases in sympathetic activity.     

Beneficial effects of low dose amiodarone in patients with congestive cardiac failure: a placebo-controlled trial

The effects of amiodarone in a low dosage (200 mg every 8 h for 2 weeks, then 200 mg/day) was assessed in a double-blind placebo-controlled trial in 34 patients with a history of severe congestive heart failure but no sustained ventricular arrhythmia. Left ventricular ejection fraction, treadmill exercise tolerance and 48 h electrocardiographic monitoring were assessed before and repeatedly after beginning amiodarone or placebo therapy over 6 months, and side effects were monitored. In patients receiving amiodarone, the ejection fraction increased significantly from 19 +/- 7 to 29 +/- 15% at 6 months (p less than 0.01 from baseline), but not significantly in 14 placebo-treated patients (18 +/- 5 to 22 +/- 9%). Exercise tolerance increased significantly in amiodarone-treated patients (median 433 s to 907 s, p less than 0.05), but not significantly in placebo-treated patients (757 to 918 s). Nonsustained ventricular tachycardia was present in 88% of amiodarone-treated patients before, but in only 21% of patients after 6 months of treatment (p = 0.06); it was seen in 43% of placebo-treated patients at baseline and in 50% after 6 months. Fifty percent of amiodarone-treated patients had side effects (principally nausea) and the drug was withdrawn in 28% of cases; no life-threatening effects were seen. Low dose amiodarone appears to have a multifaceted potential to produce benefits in arrhythmia control, exercise tolerance and ventricular function in patients with a history of severe congestive heart failure, but better control of side effects (principally nausea) appears essential. Effects on mortality could not be determined from this study; such assessment requires a larger cohort of patients.     

Late potentials in idiopathic dilated cardiomyopathy

Twenty-five patients with idiopathic dilated cardiomiopathy were investigated in order to evaluate the role of late ventricular potentials as possible markers of ventricular tachycardia or sudden cardiac death. Holter monitoring showed ventricular tachycardia in 9 patients (group A) all of whom had late ventricular potentials, (mean +/- SD length 37.22 +/- 15.83 ms and mean +/- SD voltage 5.62 +/- 2.78 microV). Mean +/- SD ejection fraction in this group was 20 +/- 9.39%. In 16 patients (group B), without ventricular tachycardia, means +/- SD ejection fraction 27.5 +/- 8.17%; late ventricular potentials were recorded in 2 patients. During the follow-up period (means +/- SD 11.53 +/- 7.19 months), 3 patients underwent heart transplantation, 2 patients underwent pace-maker implantation and 2 patients from the ventricular tachycardia group died one from sudden cardiac death and the other from progressive heart failure. No significant differences were found in the ejection fraction either between the ventricular tachycardia and the non-ventricular tachycardia group, or between the late ventricular potentials and the non-late ventricular potential groups. Negative data were also obtained when we tried to find a correlation between the ejection fraction and late ventricular potential length and/or voltage. Good results were observed with regard to sensitivity (100%), specificity (87%) and predictive accuracy (81%) but follow-up data did not specify a definite prognostic value for late ventricular potentials. The Authors conclude that late ventricular potentials are markers of patients with idiopathic dilated cardiomyopathy who are prone to ventricular tachycardia. However, the role of late ventricular potentials in sudden cardiac death is still uncertain.     

Dilated cardiomyopathy induced by ectopic atrial tachycardia

The deleterious effect of chronic or incessant supraventricular tachycardia on ventricular function is well-known and it has been demonstrated than can ultimately lead to dilated cardiomyopathy if unrecognized. Any variety of supraventricular tachycardia with chronic evolution may lead to left ventricular dysfunction, ectopic atrial tachycardia because of its persistent nature, often incessant and poorly responsive to antiarrhythmic drugs is a frequent cause of reversible congestive heart failure in patients without other demonstrable organic heart disease. Five patients (aged 14 to 52 years) were referred with symptoms of heart failure, NYHA functional class II (one patient), class III (one patient) and class IV (3 patients) associated with an incessant ectopic atrial tachycardia. Four patients underwent radiofrequency catheter ablation of the ectopic focus and one patient was treated with amiodarone. All patients were successfully treated and the echocardiographic assessment of left ventricular function indicated regression of the cardiomyopathy picture with recovery of systolic function, (mean left ventricular ejection fraction 39.2 +/- 6.1% before vs mean 62.4 +/- 4.8% after (p < 0.01). The clinical and echocardiographic picture of cardiomyopathy induced by incessant ectopic atrial tachycardia is reversible after successful treatment. This stresses the necessity of recognizing such arrhythmia as cause of primary heart failure.     

Bedside programmed ventricular stimulation for sudden death risk stratification

BACKGROUND: Patients with myocardial infarction and left ventricular dysfunction are at risk for sudden death. This research was conducted to determine the applicability and safety of a bedside programmed stimulation protocol to determine the risk for sudden death in these patients. METHODS: Four hundred and twelve patients with acute myocardial infarction were studied. Left ventricular ejection fraction was evaluated by means of an echocardiogram. Ventricular arrhythmia, late potentials and heart rate variability were determined by means of Holter recordings. Fifty patients (60 +/- 14-year-old; 85% male) presented a left ventricular ejection fraction lower than 0.40 (0.36 +/- 0.10) associated with late potentials, low heart rate variability or ventricular arrhythmia greater than Lown I. After a central venous access was placed under fluoroscopy guidance and ECG monitoring, a quadripolar catheter was advanced to the right ventricular apex to perform programmed ventricular stimulation with up to three extrastimuli. The patients were followed-up to determine in-hospital morbidity and/or mortality. RESULTS: No patient suffered complications. Ventricular tachycardia or ventricular fibrillation was induced in six patients. All of them received amiodarone and in five an automatic cardioverter-defibrillator was implanted. After a 22 +/- 6 month follow-up, five patients had received appropriate discharges from the implanted device and none had suffered from arrhythmic sudden death. CONCLUSION: Bedside programmed stimulation is a safe and useful means for sudden death risk stratification in post myocardial infarction patients. It moreover presents the advantage of being cheaper than conventionally used procedures.     

Effect of spironolactone on ventricular arrhythmias in congestive heart failure secondary to idiopathic dilated or to ischemic cardiomyopathy

Epidemiologic studies have shown an important increase in the high mortality of patients with congestive heart failure (CHF) despite optimal medical management. Ventricular arrhythmia was recognized as the most common cause of death in this population. Electrolyte imbalance, myocardial fibrosis, left ventricular dysfunction, and inappropriate neurohumoral activation are presumed responsible for sudden cardiac death. In this study, we focused on the deleterious effects of the overproduction of aldosterone that occurs in patients with CHF. Secondary hyperaldersteronism can be part of several factors thought to be responsible for sudden cardiac death. We randomized 35 patients (32 men, aged 48 +/- 9 years) with systolic dysfunction (ejection fraction 33 +/- 5%) and New York Heart Association class III CHF secondary to dilated or ischemic cardiomyopathy into 2 groups. The treatment group received spironolactone, an aldosterone receptor antagonist, along with standard medical management using furosemide, angiotensin-converting enzyme inhibitors, and digoxin. The control group received only the standard medical treatment. Holter monitoring was used to assess the severity of ventricular arrhythmia. After 20 weeks, patients who received spironolactone had a reduced hourly frequency of ventricular premature complexes (VPCs) (65 +/- 18 VPCs/hour at week 0 and 17 +/- 9 VPCs/hour at week 16) and episodes of nonsustained ventricular tachycardia (VT) (3.0 +/- 0.8 episodes of VT/24-hour period at week 0, and 0.6 +/- 0.3 VT/24-hour period at week 16). During monitored treadmill exercise, a significant improvement in ventricular arrhythmia was found in the group receiving spironolactone (39 +/- 10 VPCs at week 0, and 6 +/- 2 VPCs at week 16). These findings suggest that aldosterone may contribute to the incidence of ventricular arrhythmia in patients with CHF, and spironolactone helps reduce this complication.     

Analysis of terminal arrhythmias stored in the memory of pacemakers from patients dying suddenly.

AIMS: Stored electrograms or marker channels are available in most of modern cardiac pacemaker models. We sought to analyse these information to uncover terminal events of pacemaker patients dying suddenly. Method and results We made post-mortem pacemaker (PM) interrogations in 19 patients dying suddenly out of hospital between the years 1997 and 2005 (mean age 59 +/- 13 years, 90% males). The systems had activated arrhythmia monitoring algorithms. Indications of pacing were sick sinus syndrome in seven, AV-block in five, and heart failure due to asynchrony in seven cases. The interrogated pacemakers were CHORUS 7034 (n = 12), CONTAK TR (n = 2), and INSYNC III (n = 5). For interpretation stored marker channels and electrograms were analysed. The mean observation time after PM implantation prior death was 2.11 +/- 1.44 years, the mean left ventricular ejection fraction from the last available echo examination in the year prior death was 27.5 +/- 8%, mean age was 63 +/- 12 years. In 17/19 cases (89%), a tachycardia (most likely ventricular tachycardia) was found correlating to the time of death. The mean cycle length of the terminal arrhythmia was 307 +/- 144 (250-344) ms, corresponding to a heart rate of 195 +/- 95 (174-240) bpm. We found no evidence of specific pacemaker-related problems such as electronic failure, battery depletion, or undersensing. CONCLUSIONS: Post-mortem analysis of arrhythmia monitoring of pacemaker patients revealed tachycardias (most likely ventricular tachycardia) to be related to sudden death. These findings give some insight in mechanisms of terminal events in this group.     

Sudden Cardiac Death in Dilated Cardiomyopathy – Therapeutic Options

BACKGROUND: Despite routine use of angiotensin-converting enzyme (ACE) inhibitors, beta-blockers and spironolactone in patients with heart failure due to dilated cardiomyopathy (DCM), these patients still have a considerable annual mortality rate of 5-10%. Sudden unexpected death accounts for up to 50% of all deaths and is most often due to rapid ventricular tachycardia or ventricular fibrillation and less often due to bradyarrhythmias or asystole. THERAPEUTIC OPTIONS: The use of beta-blockers in patients with heart failure has been shown to improve overall mortality considerably. This survival benefit has been demonstrated for bisoprolol, metoprolol and carvedilol. Therefore, one of these three beta-blocking agents should be administered routinely starting with low doses in all patients with New York Heart Association (NYHA) class II or III heart failure in addition to ACE inhibitors, unless there is a contraindication to beta-blocker use. In addition, NYHA class IV heart failure patients have been shown to benefit from carvedilol therapy, if tolerated. The conflicting results of GESICA and CHF-STAT studies do not support a strategy of "prophylactic" amiodarone therapy in patients with DCM in order to prevent sudden cardiac death. Despite growing evidence that implantable cardioverter defibrillator (ICD) therapy results in improved overall survival py preventing sudden cardiac death in patients at high risk for serious arrhythmic events, arrhythmia risk stratification with regard to prophylactic ICD implantation remains highly controversial in patients with DCM. CONCLUSION: This review describes potential arrhythmia mechanisms in DCM and summarizes the results of antiarrhythmic drug trials and of prophylactic ICD trials in patients with heart failure as well as our knowledge concerning arrhythmia risk stratification in patients with DCM.     

Polymorphous ventricular tachycardia associated with acute myocardial infarction

BACKGROUND. During a 2.9-year period, 11 patients developed polymorphous ventricular tachycardia 1-13 days after acute anterior (seven patients) or inferior (four patients) myocardial infarction. None of the 11 patients had sinus bradycardia (mean heart rate, 90 +/- 23 beats/min), but three had a sinus pause immediately before the onset of polymorphous ventricular tachycardia. In all 11 patients, the QT interval and corrected QT interval (QTc) were normal or minimally prolonged (QT, 385 +/- 34 msec; QTc, 442 +/- 40 msec). None had significant hypokalemia (mean serum potassium concentration, 4.3 +/- 0.5 meq/l) or a grossly abnormal serum magnesium or calcium concentration (2.1 +/- 0.4 and 8.9 +/- 0.7 mg/dl, respectively). METHODS AND RESULTS. Immediately before the onset of polymorphous ventricular tachycardia, symptoms and/or electrocardiographic changes consistent with recurrent myocardial ischemia occurred in nine of 11 patients. One patient died before drug therapy could be initiated. Lidocaine was used in 10 patients and proved to be effective in only one. Intravenous procainamide was used in six patients: one improved, and five had recurrence of polymorphous ventricular tachycardia. Bretylium was used in five patients and was ineffective in all cases. Overdrive pacing was used in four patients and failed to suppress recurrent arrhythmias in all cases. Four patients with persistent polymorphous ventricular tachycardia unresponsive to lidocaine, procainamide, or bretylium responded to intravenous amiodarone. One patient with polymorphous ventricular tachycardia that was consistently preceded by ST segment elevation responded to intravenous nitroglycerin. Two patients with persistent polymorphous ventricular tachycardia and obvious recurrent ischemia unresponsive to pharmacological intervention responded to emergency coronary revascularization. A third patient who experienced recurrent angina and polymorphous tachycardia was initially stabilized with pharmacological therapy but subsequently underwent elective revascularization and has remained stable without antiarrhythmic therapy. CONCLUSIONS. Post-myocardial infarction polymorphous ventricular tachycardia is not consistently related to an abnormally long QT interval, sinus bradycardia, preceding sinus pauses, or electrolyte abnormalities. This arrhythmia has a variable response to class I antiarrhythmics but may be suppressed by intravenous amiodarone therapy. It is often associated with signs or symptoms of recurrent myocardial ischemia. Furthermore, coronary revascularization appears to be effective in preventing the recurrence of polymorphous ventricular tachycardia when associated with recurrent postinfarction angina.     

Antiarrhythmic efficacy and hemodynamic effects of cibenzoline in patients with nonsustained ventricular tachycardia and left ventricular dysfunction

This was a prospective single-blind, placebo-controlled study of cibenzoline in 21 patients with five or more runs of nonsustained ventricular tachycardia (VT) and left ventricular dysfunction (mean left ventricular ejection fraction 36 +/- 24%). Ambulatory electrocardiographic monitoring revealed a baseline of 616 +/- 431 runs of VT/day on placebo. Of the 18 patients tolerating the drug, 14 (77%) patients initially had a 75% or greater reduction in VT (177 +/- 164 runs of VT/day, p less than .05). A repeat ambulatory electrocardiogram documented long-term suppression of VT in 13 of 14 patients at 1 month (2.1 +/- 1.3 runs VT/day, p less than .01), in 10 of 14 patients at 3 months (2.5 +/- 1.9 runs VT/day, p less than .01), and in nine of 14 patients at 6 months (1.5 +/- 0.8 runs VT/day, p less than .01). Aggravation of arrhythmia or drug failure was seen in four of 18 (22%) patients (new onset of sudden cardiac death, two patients; sustained VT, two patients). Hemodynamic measurements were obtained with the use of right heart catheterization in patients at rest and exercising during the placebo phase and after 60 hr of oral cibenzoline. Group hemodynamic variables, both measured and derived, showed no detrimental effect of cibenzoline. However, in three of 21 patients (mean ejection fraction 21%), cibenzoline was discontinued due to severe depression of left ventricular function. Caution is recommended in the use of cibenzoline in patients with left ventricular ejection fractions of less than 25%.     

Significance of timing programmed electrical stimulation after acute myocardial infarction

To assess the influence of time on the inducibility by programmed electrical stimulation of ventricular arrhythmias after acute myocardial infarction, 18 patients were studied on day 5 and day 24 after infarction with a stimulation protocol employing a maximum of three right ventricular extrastimuli during sinus rhythm and at three paced cycle lengths. All patients were without documented sustained ventricular arrhythmia (sustained ventricular tachycardia or ventricular fibrillation) before the investigation. Sustained ventricular arrhythmia was induced in two patients on day 5, but in nine on day 24 after infarction. This difference in incidence was statistically significant (p less than 0.05), as was the change in the distribution ratio of induced sustained ventricular arrhythmia from day 5 to day 24 (p less than 0.05). The types of arrhythmia induced on day 24 were sustained ventricular tachycardia with a mean cycle length of 207 ms in six cases (five monomorphic, one polymorphic), and ventricular fibrillation in three cases. These nine patients did not differ from the remaining nine patients in maximal serum creatine kinase, infarct site, number of stenosed coronary arteries, global left ventricular ejection fraction (47 +/- 7% versus 46 +/- 10%) and results of 24 hour ambulatory electrocardiographic (Holter) monitoring, but they had a significantly shorter right ventricular effective refractory period (223 +/- 10 ms versus 259 +/- 28 ms; p less than 0.05). During the follow-up period of 24 +/-5 months no patient died, had syncopal attacks or developed spontaneous episodes of sustained ventricular arrhythmia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical experience in patients with implantable cardioverter defibrillators

Forty patients (36 men and 4 women) with life-threatening arrhythmia received an implantable cardioverter defibrillator (ICD). Mean age was 63 years (range, 46 to 80 years). All patients had structural heart disease, with coronary artery disease in 32 patients, idiopathic cardiomyopathy in 7 patients, and hypertensive heart disease in 1 patient. Mean left ventricular ejection fraction was 29 +/- 13%. The clinical arrhythmia was out-of-hospital cardiac arrest in 14 patients (35%), symptomatic sustained ventricular tachycardia in 21 patients (53%), and episodes of syncope without documented spontaneous ventricular arrhythmia but ventricular tachycardia that was easily provoked at the time of electrophysiologic testing in 5 patients (13%). Sustained ventricular tachycardia was induced in 37 patients (93%) at basic electrophysiologic testing. The average number of drug failures was 2.9 +/- 1.4 per patient. One patient (2.5%) died perioperatively because of intractable ventricular tachycardia and ventricular fibrillation. During a median follow-up period of 5.5 months (range 2-21 months) 2 sudden deaths occurred. No patient had a serious complication during the follow-up period. Ten patients (25%) received antiarrhythmic drugs to suppress spontaneous ventricular tachycardia. Appropriate shock treatment was received by 18 patients (45%), and inappropriate shock treatment was received by 2 patients (5%). Several issues regarding use of the ICD must be considered, but the device seems to be useful, and it is associated with an acceptable rate of complications and good long-term success at the present time.     

Effects of carvedilol on the hemodynamics and its tolerance in elderly patients

Clinical trials have shown that beta-blockers can produce symptomatic improvement and decrease the risk of death in chronic heart failure patients. However, the side effects of beta-blockers including worsening heart failure, AV-block, contracting peripheral vessels and unfavorable effects on glucose and cholesterol metabolism tend to make physicians hesitate to prescribe beta-blockers for elderly patients. Carvedilol is a novel non-selective beta-blocker without intrinsic sympathomimetic activity (ISA) and has vasodilating effect through blocking alpha 1 receptor. We examined the effects of carvedilol on cardiac parameters in order to clarify whether beta-blocker may affect left ventricular function in elderly Japanese patients with hypertension, angina pectoris, or both. We examined the hemodynamic effect of carvedilol in 16 patients with hypertension, angina patients or both, aged 65 and over (75.5 +/- 5.6 y.o.). After 12 weeks treatment with 10-20 mg daily oral administration, echocardiography was performed and hemodynamic parameters were calculated to evaluate their cardiac functions. Blood pressure was significantly decreased, especially in systolic pressure (163.8/87.6 +/- 15.6/11.2 mmHg to 141.6/76.9 +/- 16.6/11.7 mmHg, p < 0.001/p < 0.01, respectively). Ejection fraction increase (65.8 +/- 11.8% to 71.2 +/- 11.4%, p < 0.05) accompanied heart rate decrease (72.0 +/- 16.1 bpm to 63.9 +/- 11.4 bpm, p < 0.05). Carvedilol increased ejection fraction and decreased blood pressure safely in elderly patients with hypertension, angina pectoris, or both. Taking the condition of each patient into consideration, alpha-beta-blocker can be beneficial in elder patients.     

Prognosis of idiopathic dilated cardiomyopathy

Previous reports in referral populations have emphasized the poor prognosis of dilated cardiomyopathy. This study evaluated mortality and morbidity in patients presenting at a referral center between 1989 and 1993. One hundred seventy-two consecutive patients were studied. At presentation, 82 were in New York Heart Association functional class III/IV. Mean (+/- SD) left ventricular end-diastolic dimension was 69 +/- 11 mm, ejection fraction was 25 +/- 10%, VO2 max was 21 +/- 9 mL/min/kg, and sodium was 136 +/- 9 mM. Treatments included vasodilators (n = 157, 92%), anticoagulation (n = 50, 29%), amiodarone (n = 52, 30%), and cardiac defibrillator (n = 5, 3%). During the follow-up period (mean, 26 +/- 29 months), 16 patients died and 60 developed progressive heart failure; 46 (27%) required cardiac transplantation. The majority of the patients (102, 59%) were stable or improved. Established prognostic determinants (left ventricular end-diastolic dimension, ejection fraction, sodium, and arrhythmia) were of low predictive value for the development of progressive heart failure or sudden death. The 1- and 2-year probabilities of death or transplantation was 16 and 21%, respectively (death only 6 and 7%, respectively). These observations are subject to referral bias, but suggest that the majority of patients can remain stable. Any improvement in survival compared to earlier experience can be due to earlier diagnosis, availability of transplantation, and new heart failure management strategies.     

Limited clinical utility of endomyocardial biopsy in patients presenting with ventricular tachycardia without apparent structural heart disease.

To determine the cardiac pathology underlying ventricular tachyarrhythmias, endomyocardial biopsy was performed in 14 patients, 10 men and 4 women, with a mean age of 40 years (range 17-63) and no apparent structural heart disease, presenting with high-density symptomatic nonsustained ventricular tachycardia (VT) (n = 4), sustained VT (n = 6), and ventricular fibrillation (n = 4). The absence of coronary or valvular heart disease was documented by cardiac catheterization. The mean left ventricular ejection fraction was 56 +/- 10%. Noninvasive assessment of the ventricular arrhythmia was made in all patients with Holter monitoring and/or exercise testing, while invasive evaluation with programmed electrical stimulation was performed in 13 patients. Biopsy findings included subendocardial and interstitial fibrosis in 7 patients, and monocytes containing periodic acid Schiff (PAS) positive vacuoles in 1 patient; biopsy was normal in 6 patients. There was no relationship between the presence or absence of pathologic abnormalities on biopsy and left ventricular ejection fraction, presenting or induced arrhythmias, or prognosis. Pathologic evidence supporting a specific treatable diagnosis was not present in any biopsy. Drugs to suppress spontaneous (3 patients) or induced (8 patients) VT were instituted, while 2 patients were not treated. In 1 patient who was resuscitated from out-of-hospital cardiac arrest an automatic defibrillator was implanted. In 24.6 months of mean follow-up there was 1 nonfatal arrhythmia recurrence, 1 noncardiac death, and 1 sudden death in a patient with fibrosis on biopsy, an ejection fraction of 45%, and both inducible and spontaneous sustained VT suppressed with an antiarrhythmic agent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of programmed ventricular stimulation in patients surviving complicated acute myocardial infarction: a prospective study.

In survivors of complicated myocardial infarction, the inducibility of sustained ventricular tachycardia may help identify a subset that is at increased risk for subsequent sudden cardiac death or spontaneous sustained ventricular tachycardia. We performed prehospital discharge programmed ventricular stimulation in 86 survivors of acute myocardial infarction complicated by heart failure, angina pectoris, or nonsustained ventricular tachycardia. These patients also underwent cardiac catheterization with coronary angiography and 24-hour ambulatory ECG recording. Programmed ventricular stimulation induced sustained ventricular tachycardia in 19 patients (22%) and ventricular fibrillation in six (7%) and did not induce these arrhythmias in 61 patients (71%). During an average follow-up of 18 +/- 13 months, 11 patients had arrhythmic events (seven sudden death and four nonfatal spontaneous sustained ventricular tachycardia) and 10 patients had nonsudden cardiac death. The total cardiac mortality rate was 20%. Arrhythmic events occurred in 32% of the 19 patients with inducible sustained ventricular tachycardia compared with 7% of the remaining 67 patients (p less than 0.003). By multivariate analysis the occurrence of arrhythmic events was independently predicted by both inducible sustained ventricular tachycardia and Killip class III or IV heart failure. The risk of arrhythmic events was 4.4% in the absence of both variables versus 38.4% (p less than 0.001) when both variables were present. The total cardiac mortality rate was best predicted by low left ventricular ejection fraction (less than 30%). Thus programmed ventricular stimulation is useful in risk stratification of survivors of complicated acute myocardial infarction. The prognostic utility appears to be particularly high in patients with infarction complicated by Killip class III or IV heart failure.