enalapril and Tachycardia--Ventricular

Ventricular arrhythmias are considered to be related to left ventricular (LV) dysfunction. ACE inhibitors though improve LV function their beneficial role on exercise-induced ventricular arrhythmias is not established. To study the effects of ACE inhibitors on exercise capacity vis-a-vis their role on exercise-induced ventricular arrhythmias, 25 patients of congestive heart failure (CHF) of various etiologies in NYHA Class II and III were subjected to a prospective randomised controlled trial. The control group comprising of 12 patients received conventional treatment (digitalis and diuretics) and the test group was given enalapril/captopril in addition as tolerated. They were followed up for 3 months. Exercise testing on treadmill and monitoring of clinical and biochemical parameters were done at the beginning and end of study in all cases. Ventricular arrhythmias observed during exercise and post-exercise for 10 minutes was analysed using Lown's grading for frequency and severity of ventricular arrhythmia. The mean exercise duration showed significant improvement on ACE inhibitor as compared to the control group (p < 0.05) however there was no significant change in the grades of arrhythmia. Serum electrolytes and other bio-chemical parameter were within normal range. It is concluded that effect of ACE inhibitor on improving functional capacity in CHF is independent of it's any effect on exercise-induced ventricular arrhythmias.

Topics: Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Captopril; Enalapril; Exercise Test; Exercise Tolerance; Female; Heart Failure; Humans; Male; Middle Aged; Physical Endurance; Prospective Studies; Reference Values; Tachycardia, Ventricular

In this study 24-h Holter electrocardiographic recordings were used to measure the effects of an angiotensin converting enzyme inhibitor, enalapril given for 4 weeks, on the frequency of cardiac arrhythmias in 24 patients (14 patients had enalapril, 30 patients had placebo) with congestive heart failure (New York Heart Association Functional Class 3) receiving maintenance therapy with digoxin and furosemide. Although the placebo group had no change in the frequence of arrhythmias, enalapril-treated patients showed significant decrease in the frequency of premature ventricular complexes couplet, bigemine VPS and ventricular tachycardia. Moreover, it was observed that six cases of atrial fibrillation returned to sinus rhythm. During enalapril treatment, some patients experienced increased serum potassium levels, but there was no change in serum digoxin levels. We also observed echocardiographic improvement in left ventricular function as well as clinical symptoms of congestive heart failure. Finally we observed that there was an antiarrhythmic effect of enalapril in congestive heart failure. We thought that the antiarrhythmic effect of enalapril in congestive heart failure was probably due to hemodynamic improvement.

Topics: Aged; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Digoxin; Double-Blind Method; Electrocardiography, Ambulatory; Enalapril; Female; Heart Failure; Heart Rate; Humans; Male; Middle Aged; Myocardial Contraction; Placebos; Potassium; Tachycardia, Ventricular; Ventricular Function, Left

Patients with heart failure have a high prevalence of serious arrhythmias and sudden cardiac-death.. Male patients aged 18-75 years with chronic heart failure were randomized to enalapril or hydralazine-isosorbide dinitrate. Short-term (4-hour to 8-hour) Holter tape recordings were performed before randomization, at 3 months, at 1 year, and yearly thereafter. Of 804 patients randomized to therapy, 715 had Holters at baseline. Couplets were noted in 56% versus 60% and ventricular tachycardia (VT) (three or more consecutive ventricular premature beats) in 27% versus 29% of patients randomized to enalapril versus hydralazine-isosorbide dinitrate, respectively. The presence of VT at 3 months, 1 year, and 2 years predicted significantly higher mortality during the subsequent year (p < 0.0001, p < 0.001, and p < 0.037, respectively). In the enalapril group, VT prevalence decreased by 27% at 1 year (p < 0.02). A decrease in prevalence of VT was not seen in the hydralazine-isosorbide dinitrate group. New VT was seen in 11% of enalapril patients versus 24% of hydralazine-isosorbide dinitrate patients at 1 year (p < 0.002). When compared with hydralazine-isosorbide dinitrate at 1 and 2 years, there was a 52% and 49% reduction, respectively, in sudden deaths in the enalapril group. Thus, at 1 and 2 years, the decrease in sudden deaths in the enalapril group coincided with the decrease in VT prevalence and the decrease in new VT emergence.. In patients with heart failure, VT and couplets predict increased mortality. When compared with hydralazine-isosorbide dinitrate, enalapril decreases both the persistence of baseline VT at 3 months and the emergence of new VT at 1 and 2 years. The reduction in VT prevalence parallels a reduction in sudden death. The effect of enalapril on survival over hydralazine-isosorbide dinitrate may be related to its ability to reduce prevalence of ventricular arrhythmia.

Topics: Death, Sudden, Cardiac; Drug Therapy, Combination; Electrocardiography, Ambulatory; Enalapril; Heart Failure; Humans; Hydralazine; Isosorbide Dinitrate; Male; Middle Aged; Prevalence; Risk Factors; Tachycardia, Ventricular

Topics: Angiotensin-Converting Enzyme Inhibitors; Arrhythmias, Cardiac; Dipeptides; Double-Blind Method; Electrocardiography, Ambulatory; Enalapril; Exercise Test; Female; Heart Failure; Humans; Lisinopril; Male; Middle Aged; Stroke Volume; Tachycardia, Ventricular; Ventricular Function, Left

The combination of ventricular tachycardia (VT) and severe left ventricular dysfunction presents a serious challenge in management of acute fulminant myocarditis (AFM). We report a case of a 17-month-old girl with AFM, presented with hypotension and VT, successfully treated with respiratory and inotropic support, high-dose intravenous immunoglobulin, and amiodarone. The myocardial function improved significantly within 2 weeks of treatment. The clinical course was complicated by significant amiodarone-induced hepatotoxicity, disseminated intravascular coagulation, and deep-vein thrombosis. She was later diagnosed with congenital dysfibrinogenemia and treated with chronic Lovenox therapy.

Topics: Acute Disease; Amiodarone; Angiotensin-Converting Enzyme Inhibitors; Anti-Arrhythmia Agents; Drug Therapy, Combination; Electrocardiography; Enalapril; Female; Follow-Up Studies; Humans; Immunoglobulins, Intravenous; Immunologic Factors; Infant; Myocarditis; Tachycardia, Ventricular; Ventricular Function, Left

Atrial structural remodeling creates a substrate for atrial fibrillation (AF), but the underlying signal transduction mechanisms are unknown. This study assessed the effects of ACE inhibition on arrhythmogenic atrial remodeling and associated mitogen-activated protein kinase (MAPK) changes in a dog model of congestive heart failure (CHF).. Dogs were subjected to various durations of ventricular tachypacing (VTP, 220 to 240 bpm) in the presence or absence of oral enalapril 2 mg. kg(-1). d(-1). VTP for 5 weeks induced CHF, local atrial conduction slowing, and interstitial fibrosis and prolonged atrial burst pacing-induced AF. Atrial angiotensin II concentrations and MAPK expression were increased by tachypacing, with substantial changes in phosphorylated forms of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and p38-kinase. Enalapril significantly reduced tachypacing-induced changes in atrial angiotensin II concentrations and ERK expression. Enalapril also attenuated the effects of CHF on atrial conduction (conduction heterogeneity index reduced from 3.1+/-0.4 to 1.9+/-0.2 ms/mm, P<0.05), atrial fibrosis (from 11.9+/-1.1% to 7.5+/-0.4%, P<0.01), and mean AF duration (from 651+/-164 to 218+/-75 seconds, P<0.05). Vasodilator therapy of a separate group of VTP dogs with hydralazine and isosorbide mononitrate did not alter CHF-induced fibrosis or AF promotion.. CHF-induced increases in angiotensin II content and MAPK activation contribute to arrhythmogenic atrial structural remodeling. ACE inhibition interferes with signal transduction leading to the AF substrate in CHF and may represent a useful new component to AF therapy.

Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Atrial Fibrillation; Dogs; Electrophysiology; Enalapril; Endomyocardial Fibrosis; Heart Atria; Heart Failure; Hemodynamics; Hydralazine; Isosorbide Dinitrate; Mitogen-Activated Protein Kinases; Renin-Angiotensin System; Signal Transduction; Tachycardia, Ventricular