One hundred and one patients with sustained unimorphic ventricular tachycardia underwent programmed ventricular stimulation with one of two protocols. Fifty patients underwent programmed stimulation with protocol A, which consisted of burst overdrive pacing, single, double, and triple extrastimuli at the right ventricular apex, right ventricular outflow tract, or septum, and then at the left ventricular apex. Fifty-one patients underwent programmed stimulation with protocol B, which consisted of burst overdrive pacing, single and double extrastimuli at the right ventricular apex, right ventricular outflow tract or septum, and at the left ventricular apex, followed by triple extrastimuli at these sites. The stimulation protocol was continued until sustained ventricular tachycardia or rapid, polymorphic ventricular tachycardia greater than 10 sec in duration was induced. With protocol A, clinical and nonclinical ventricular tachycardia was induced in 76% and 36% of patients, respectively; with protocol B, clinical and nonclinical ventricular tachycardia was induced in 85% and 38% of patients, respectively. Direct-current countershock for sustained polymorphic ventricular tachycardia was required in 10% of patients studied under protocol A, compared with in 2% of patients studied under protocol B. With protocol A, near-maximal yield of induced clinical (72%) and nonclinical ventricular tachycardia (30%) was attained after the use of triple extrastimuli at the first stimulation site. The yield of stimulation at a second right ventricular site and of left ventricular stimulation was only an additional 2% each. With protocol B, triple extrastimuli increased the yield of induced clinical ventricular tachycardia from 61% to 85%.(ABSTRACT TRUNCATED AT 250 WORDS)

Minoxidil, a potent predominant arterial dilator, improves hemodynamics over the short term in patients with heart failure. In random double-blind fashion 17 patients with chronic left heart failure were given minoxidil (nine patients) or placebo (eight patients) in addition to digoxin and diuretics for 3 months. Cardiac index and heart rate increased and mean arterial pressure and systemic vascular resistance fell within 4 hr of minoxidil administration. Right heart and pulmonary arterial pressures were unchanged over the short term but rose after long-term minoxidil. After 3 months of minoxidil treatment, systemic vascular resistance was still reduced (11.7 +/- 6.3[SD] vs 17.1 +/- 3.1 U at baseline; p less than .05). Hemodynamics were similar at baseline and remained unchanged during placebo treatment. Mean left ventricular ejection fraction rose from 29.6 +/- 17.7% to 42.7 +/- 22.3% (p less than .05) after 3 months of minoxidil treatment (this result was influenced largely by responses in two patients), and remained unchanged (at 25.1 +/- 16.6%) after 3 months of placebo. Exercise duration and maximal oxygen uptake during exercise were unchanged during minoxidil or placebo treatment. Total clinical events, including increased need for diuretics, angina, ventricular arrhythmias, worsening heart failure, and death were all more frequent during minoxidil vs placebo administration (21 vs seven total events; p less than .01). Thus, despite improving hemodynamics and left ventricular function, long-term minoxidil administration was associated with a poorer clinical course in patients with chronic left ventricular failure. Furthermore, this experience demonstrates that improvement of left ventricular function alone cannot be reliably interpreted as proof of clinical efficacy of therapeutic interventions in patients with heart failure.

The significance and treatment of ventricular premature beats (VPBs) in patients without sustained ventricular tachycardia (VT), sudden death, or syncope remains unclear. We undertook a prospective study of programmed electrical stimulation (up to two extrastimuli and burst pacing) in 73 patients (age 60 +/- 10 years) with high-grade VPBs who had no evidence of sustained VT, sudden death, or syncope as determined by 48 hr of monitoring in the cardiac care unit and 48 hr Holter monitoring. Fifty-six patients (76.7%) had atherosclerotic heart disease, 10 (13.7%) had cardiomyopathy or valvular heart disease, and seven (9.6%) had no evident heart disease. Thirty-seven patients (50.7%) had Lown grade IVB VPBs, 30 (41.1%) had Lown grade IVA VPBs, and six (8.2%) had Lown grade III VPBs. Programmed electrical stimulation identified two groups of subjects: group 1 comprised 20 patients (27%) in whom VT or ventricular fibrillation was induced, group 2 comprised 53 patients (73%) in whom no ventricular arrhythmia or only two to four repetitive ventricular responses were induced. There was a significant difference between the presence of atherosclerotic heart disease, old myocardial infarction, and ejection fraction of less than 40% in group 1 compared with group 2. However, there was no significant difference in the grade of VPBs between the two groups. Seventeen of 20 patients from group 1 were placed on antiarrhythmic therapy (defined by programmed electrical stimulation), whereas group 2 patients were randomly assigned to prophylactic antiarrhythmic therapy. A total of 70 patients were followed up for 30 +/- 15 months. The incidence of sustained VT and/or sudden death (31.5% vs 2%; p less than .001) was significantly higher in group 1 compared with group 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Three hundred and one patients who had been hospitalized for acute myocardial infarction, were less than 70 years old, were in sinus rhythm, and did not have complete bundle branch block were stratified before discharge according to age, size of infarction, and type of ventricular arrhythmias as determined on a 6 hr electrocardiogram (ECG). They were thereafter randomly assigned to double-blind treatment with 100 mg bid metoprolol or placebo. Repeat 6 hr ECGs were recorded 3 days and 1, 6, and 12 months after treatment had begun. In the placebo group there was a significant increase in the proportion of patients with complex premature ventricular complexes (PVCs) (i.e., multiform, paired and R-on-T PVCs, or ventricular tachycardia) as well as increased numbers of PVCs in the patients during the follow-up. In contrast, an initial decrease in the number of PVCs (p less than .001) was found in the metoprolol group, whereas the complexity of PVCs was constant in those patients who continued on metoprolol therapy throughout the follow-up period. We conclude that the increase in complexity and number of PVCs that is part of the natural clinical course after myocardial infarction is counteracted by long-term treatment with metoprolol.

To elucidate the mechanisms of reduction of left ventricular end-diastolic pressure by nifedipine in certain individuals, we evaluated cardiac and peripheral hemodynamic responses in 32 patients after they were randomly assigned to nifedipine (20 mg sublingually) or to placebo treatment. Forearm plethysmography was performed during cardiac catheterization with micromanometers. No hemodynamic parameters were changed after placebo. Left ventricular end-diastolic pressure declined by 14% (p less than .02) after nifedipine in patients with impaired left ventricular function, but was unchanged in those with normal function; indexes of peripheral venous hemodynamics (forearm venous tone, forearm volume change) were not affected. In those patients with abnormal left ventricular function, forearm vascular resistance decreased 36% and forearm blood flow increased 31% (p less than .0005 for both), while neither changed in those with normal function. Cardiac output increased by 10% in patients with impaired left ventricular function but was unchanged in the remainder, while calculated total systemic resistance fell by 24% in those with abnormal left ventricular function (p less than .002 for both). Thus, reduction of left ventricular preload by nifedipine is not attributable to venous pooling, but rather this beneficial effect appears to be attributable to improved left ventricular systolic function in response to afterload reduction, particularly in patients with impaired left ventricular function.

To determine whether adding blood to a cardioplegic solution affects myocardial preservation, a randomized prospective study was carried out in 60 patients undergoing coronary revascularization to compare the effects of crystalloid potassium cardioplegics (group C) and potassium cardioplegic solutions to which blood has been added (group B) on markers of myocardial metabolism (lactate, inorganic phosphate, base deficit release, glucose and lactate uptake, oxygen extraction), myocardial damage (creatine kinase [CK]-MB levels), and cardiac performance (cardiac index and left atrial pressure). The solution with added blood had a significantly (p less than .05) greater oxygen content, a lower pH, and higher concentrations of potassium, calcium, sodium, and glucose. In group B patients there was a suggestion (p less than .06) of greater uptake of oxygen during the beginning of the initial cardioplegic infusion. During reperfusion there was no evidence of differential release of the metabolites of anaerobiosis and myocardial oxygen extraction and glucose and lactate uptake were similarly depressed in both groups. Likewise, CK-MB release after bypass was the same in both groups. Prompt, adequate functional recovery of cardiac index and left atrial pressure was observed in both groups. It was concluded that although there may be more oxygen available from the blood-containing solution during early infusion, there is no evidence that under the conditions of this investigation adding blood to cardioplegic solution improves myocardial preservation.

Eleven patients with severe left ventricular impairment (mean ejection fraction 24%) and moderate impairment of exercise tolerance underwent a double-blind, placebo-controlled, cross-over trial of the orally administered beta-agonist prenalterol. Exercise hemodynamics and tolerance were measured during bicycle and treadmill exercise after 2 weeks of therapy with placebo or prenalterol. Cardiac index, ejection fraction, and stroke work index were not improved and exercise duration and peak oxygen consumption were not significantly different during the two treatments. During prenalterol treatment heart rate during exercise was consistently reduced. These results show that prolonged therapy with prenalterol does not improve hemodynamics or exercise tolerance and is associated with a diminished heart rate response to exercise.

Defibrillation/cardioversion thresholds were measured in 33 patients undergoing defibrillator implants. Each patient had a 12 cm2 patch placed near the left ventricular apex via a thoracotomy and a 10 cm2 spring lead placed pervenously at the right atrial-superior vena caval junction. Ventricular tachycardia of stable morphology, polymorphic ventricular tachycardia, or ventricular fibrillation was induced four times in each patient and 1, 5, 10, and 25 J truncated exponential shocks with 60% tilt were given in a random sequence. The conversion rate was constant (77%, 86%, 87%, 85%) with increasing energy for ventricular tachycardia but progressively increased for polymorphic ventricular tachycardia and ventricular fibrillation (8%, 33%, 58%, 92%). The ventricular tachycardia acceleration rates for 1, 5, 10, and 25 J were 23%, 14%, 10%, and 15%. Patients not reliably converted with 25 J may require repositioning of leads or two patches. We conclude that for the spring-patch electrodes, increasing energy from 1 to 25 J improves the conversion rate for polymorphic ventricular tachycardia and ventricular fibrillation; the ventricular tachycardia conversion rate is constant. Acceleration of ventricular tachycardia occurs at all energies. Defibrillator implantation requires extensive intraoperative electrophysiologic testing to ensure safe and reliable termination of ventricular tachycardia and fibrillation.

The efficacy of intracoronary urokinase and streptokinase were compared in 80 patients with acute myocardial infarction in a prospective, randomized, double-blind study. Urokinase was infused into the occluded coronary artery at 6000 U/min, and streptokinase was infused at 2000 U/min. Maximal duration of infusion was 2 hr. The frequency of successfully opening the artery was similar for patients receiving urokinase (27 of 45, 60%) and those receiving streptokinase (20 of 35, 57%). Fibrinogen levels after infusion were measured in 63 patients. Nineteen of 29 streptokinase recipients had fibrinogen levels less than 100 mg/dl compared with levels of two of 34 urokinase recipients (p less than .001). Five of 45 (11%) patients receiving urokinase and 10 of 35 receiving streptokinase (29%) had bleeding complications (p less than .05). Major bleeding after early coronary artery bypass surgery was more frequent in the streptokinase group (four of five compared with a similar group of patients receiving urokinase (none of five). This study demonstrates that while urokinase and streptokinase have equal intracoronary thrombolytic efficacy, patients receiving urokinase have less systemic fibrinolysis and less perioperative bleeding with early surgery than do patients receiving streptokinase.

In "post hoc" subgroup analyses, a simple classification system for patients, based on the presence or absence of findings indicative of electrical and/or mechanical complications early during short-term hospitalization, was applied to the data from the Beta-Blocker Heart Attack Trial (BHAT). In the largest subgroup of BHAT patients who had no reported complications, the 25 month mortality was low and the observed benefit of propranolol therapy small. Patients with electrical complications only had intermediate mortality and a pronounced effect of treatment was observed. Those with mechanical complications had the highest mortality and experienced an intermediate relative benefit of beta-blocker treatment. They also reported the most adverse effects. Post hoc analyses should always be interpreted cautiously. It is important to determine whether these findings are present in other completed beta-blocker trials. On the basis of these analyses alone it is suggested that the present practice of prescribing beta-blockers in postinfarction patients should not be altered.

A prospective randomized trial was conducted to evaluate the effects of exercise-based cardiac rehabilitation after myocardial revascularization surgery (MRS) on work capacity (measured in mets) and left ventricular function as determined from ejection fraction (LVEF). Twenty-eight patients undergoing MRS were randomly assigned to experimental (aerobic exercise, n = 19) or control (muscle relaxation and low-level exercise, n = 9) groups. Patients were studied before surgery (T1) and 2 (T2), 8 (T3), and 24 (T4) weeks after surgery with first-pass radionuclide angiography both while they were at rest and during maximal upright cycle ergometric exercise. Subsets of patients were also studied at T2, T3, and T4 at a standard workload of 75 W, and during maximal exercise 1 year after surgery (T5). Work capacity improved in both groups although significantly more so in the experimental group (3.9, 3.8, 6.0, and 7.3 mets and 3.7, 3.7, 4.9, and 5.7 mets at T1, T2, T3, and T4 in the experimental and control groups, respectively). The differences between groups were significant by T3. Peak exercise LVEF increased significantly in both groups from T1 to T2 then decreased at T3 and remained unchanged through T5. Peak exercise LVEF at T3 to T5 remained significantly above that observed at T1. LVEF responses were not related to the exercise program. During a standard workload, heart rate decreased, blood pressure increased, and LVEF did not change in either group. After conclusion of the formal protocol (T4), work capacity and LVEF did not change for either group throughout an additional 6 months (T5).(ABSTRACT TRUNCATED AT 250 WORDS)

Preliminary clinical and laboratory observations suggest that nifedipine might prevent progression of threatened myocardial infarction by reversing coronary spasm or might limit necrosis during the course of acute myocardial infarction. We screened 3143 patients with ischemic pain of greater than 45 min duration and randomly assigned 105 eligible patients with threatened myocardial infarction and 66 with acute myocardial infarction to receive nifedipine (20 mg orally every 4 hr for 14 days) or placebo plus standard care. Treatment was started 4.6 +/- 0.1 hr after the onset of pain. Infarct size index was calculated by the MB-creatine kinase (CK) method and expressed as CK-geq/m2 +/- SE. The incidence of progression to infarction among patients with threatened myocardial infarction was not significantly altered by nifedipine (36 of 48 [75%] for placebo-treated and 43 of 57 [75%] for nifedipine-treated patients). Furthermore, infarct size index was similar among placebo- and nifedipine-treated patients (16.9 +/- 1.5 MB-CK-geq/m2, n = 65, and 17.0 +/- 1.5 MB-CK-geq/m2, n = 68, respectively) with threatened myocardial infarction who exhibited infarction and for those with acute myocardial infarction. Among the 171 eligible patients randomly assigned to drug or placebo, 6 month mortality did not differ significantly (8.5% for placebo vs 10.1% for nifedipine, NS), but mortality in the 2 weeks after randomization was significantly higher for nifedipine-treated patients (0% for placebo compared with 7.9% for nifedipine, p = .018).(ABSTRACT TRUNCATED AT 250 WORDS)

To characterize the potential of nifedipine in the therapy of unstable angina pectoris we implemented a blinded, randomly assigned, titrated schedule of conventional therapy (propranolol, if not contraindicated, and isosorbide dinitrate) or nifedipine for 14 days in 126 patients hospitalized in a coronary care unit for ischemic chest pain of less than 45 min duration. There were no significant differences between conventionally and nifedipine-treated patients with regard to (1) the time to relief of pain as judged by life table analysis, (2) the decrease in anginal attacks per 24 hr from day 0 to day 2 (-2.5 +/- 0.4 for conventional therapy vs; -2.8 +/- 0.3 for nifedipine), (3) the decrease in the number of nitroglycerin tablets consumed per 24 hr (-2.0 +/- 0.5 for conventional vs -2.1 +/- 0.4 for nifedipine therapy), (4) the percentage of patients requiring morphine on day 1 (13% for conventional vs 21% for nifedipine therapy), or (5) the percentage of patients who developed infarction (14% in both groups). Among the 27 patients who did not respond to initial conventional (n = 13) or nifedipine therapy (n = 14), five in each group became pain free when the opposite therapy (either nifedipine or conventional therapy) was added. In the subgroup of 67 patients who were receiving propranolol before randomization, addition of nifedipine was more effective in controlling pain than was an increase in conventional therapy (p = .026). In the subgroup of 59 patients not receiving prior propranolol, initiation of conventional therapy produced more rapid pain relief than initiation of nifedipine therapy alone (p less than .001), which tended to increase heart rate. Thus, for the study population as a whole therapy with nifedipine alone was equivalent to conventional therapy for unstable angina, although this overall equivalence may result from a combination of superiority of nifedipine therapy in patients previously receiving beta-blocker therapy and superiority of beta-blocker therapy in patients not previously receiving beta-blockers.

To determine the influence of adjunctive treatment with coumadin or aspirin on recurrence rate after percutaneous transluminal coronary angioplasty (PTCA), 248 patients in whom PTCA was assessed to be a primary success were randomized to either 325 mm aspirin daily or to coumadin treatment sufficient to maintain a prothrombin time 2 to 2.5 times the control value. The follow-up protocol included stress testing and coronary angiographic examinations 3 to 6 months after PTCA. All patients were followed for at least 9 months. Of the 122 patients randomized to coumadin 44 (36%) had recurrent stenoses as opposed to 34/126 (27%) of patients on aspirin, a difference that did not reach statistical significance at the .05 level. However, patients with at least a 6 month history of angina demonstrated a significantly different response to adjunctive treatment in that 19/43 (44%) of coumadin patients as compared with 10/48 (21%) of aspirin patients had recurrent stenoses (p less than .05). Thus, coumadin was not shown to be more effective than aspirin as adjunctive treatment after PTCA, while aspirin was shown to be superior to coumadin in patients with a longer history of angina.

In a randomized double-blind trial we sought to determine whether short-term therapy with ticlopidine (250 mg bid for 14 days) inhibited platelet deposition on Dacron aortic bifurcation grafts that had been in place a year or longer. A total of 10 men, 42 to 69 years old, underwent indium-111 platelet imaging during both placebo and drug phases of the trial at 24, 48, and 72 hr after the injection of labeled platelets. Platelet accumulation was quantitated by a graft/blood ratio that compared background-corrected activity of indium-111-labeled platelets in the graft with whole-blood activity of indium-111-labeled platelets. Additionally, blinded qualitative visual analysis of the unprocessed images was used to compare graft area activity with activity in adjacent native arteries. Ticlopidine significantly prolonged the template bleeding time from 5.3 +/- 0.5 to 17.1 +/- 3.1 min (+/- SEM) (p = .003). However, by quantitative analysis there was no significant reduction in platelet deposition in the graft during ticlopidine therapy compared with placebo at 24 hr (graft/blood ratio 2.3 +/- 0.4 vs 2.6 +/- 0.3), 48 hr (3.1 +/- 0.5 vs 3.2 +/- 0.4), or 72 hr (3.9 +/- 0.7 vs 4.0 +/- 0.6) after injection of labeled platelets. By visual analysis, nine patients had positive results for abnormal platelet deposition when on placebo that were unchanged when on ticlopidine. The tenth patient had an equivocal result for abnormal platelet deposition when on placebo and a negative result for abnormal platelet deposition when on ticlopidine.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of clonidine, naloxone, and their combination on arterial blood pressure (BP), heart rate (HR), and hemodynamic and biochemical parameters were examined in 29 patients with essential hypertension. Treatment for 3 days with 0.3 mg/day clonidine reduced BP and HR, and these effects were quickly reversed by a single injection of 0.4 mg iv naloxone in 17 of the patients (responders), but not in the remaining 12 (nonresponders). Responders had higher control values for cardiac output, stroke index, plasma renin activity (PRA), and plasma epinephrine levels than did nonresponders. Basal BP was similar in the two groups, but clonidine decreased BP, PRA, and plasma epinephrine more in responders than in nonresponders. Naloxone given during placebo treatment had no significant effects. During clonidine treatment naloxone increased BP, HR, total peripheral resistance, PRA, and plasma epinephrine and norepinephrine, and decreased stroke volume in responders, whereas in nonresponders its only effect was a small increase in HR. It is concluded that in a subset of hyperadrenergic, hypertensive patients the antihypertensive effect of clonidine involves a naloxone-reversible inhibition of central sympathetic outflow, probably mediated by the release of an endogenous opioid.

The National Heart, Lung and Blood Institute Type II Coronary Intervention Study, a double-blind, placebo-controlled trial, evaluated the efficacy of reduction in cholesterol levels induced by cholestyramine on progression of coronary artery disease (CAD). The rate of CAD progression in patients treated with cholestyramine plus diet was compared with that of patients treated with placebo plus diet. CAD progression was defined angiographically. Significant decrease in total cholesterol (TC) and low-density lipoprotein cholesterol (LDLc) and increases in high-density lipoprotein cholesterol (HDLc), as well as in HDLc/TC and HDLc/LDLc ratios, were observed with cholestyramine. HDLc change was due to increase in HDL2A and HDL2B. When the relationship between CAD progression and lipid changes was examined independent of specific treatment group, a significant inverse relationship was found between progression at 5 years and the combination of an increase in HDLc and a decrease in LDLc; changes in HDLc/TC and HDLc/LDLc were the best predictors of CAD change. While the testing of these relationships independent of treatment group was not part of the initial study design, the trends were observed in both the placebo-treated and cholestyramine-treated groups. Moreover, with multivariate analysis, the effect of cholestyramine treatment on CAD progression was eliminated by adding changes in HDLc/TC to the regression model. These findings support the hypothesis that increases in HDLc and decreases in TC (or LDLc) can prevent or delay CAD progression.

In the National Heart, Lung and Blood Institute Type II Coronary Intervention Study, patients with Type II hyperlipoproteinemia and coronary artery disease (CAD) were placed on a low-fat, low-cholesterol diet and then were randomly allocated to receive either 6 g cholestyramine four times daily or placebo. This double-blind study evaluated the effects of cholestyramine on the progression of CAD as assessed by angiography. Diet alone reduced the low-density lipoprotein cholesterol 6% in both groups. After randomization, low-density lipoprotein cholesterol decreased another 5% in the placebo group and 26% in the cholestyramine-treated group. Coronary angiography was performed in 116 patients before and after 5 years of treatment. CAD progressed in 49% (28 of 57) of the placebo-treated patients vs 32% (19 of 59) of the cholestyramine-treated patients (p less than .05). When only definite progression was considered, 35% (20 of 57) of the placebo-treated patients vs 25% (15 of 59) of the cholestyramine-treated patients exhibited definite progression; the difference was not statistically significant. However, when this analysis was performed with adjustment for baseline inequalities of risk factors, effect of treatment was more pronounced. Of lesions causing 50% or greater stenosis at baseline, 33% of placebo-treated and 12% of cholestyramine-treated patients manifested lesion progression (p less than .05). Similar analyses with other end points (percent of baseline lesions that progressed, lesions that progressed to occlusion, lesions that regressed, size of lesion change, and all cardiovascular end points) all favored the cholestyramine-treated group, but were not statistically significant. Thus, although the sample size does not allow a definitive conclusion to be drawn, this study suggests that cholestyramine treatment retards the rate of progression of CAD in patients with Type II hyperlipoproteinemia.

This placebo-controlled, double-blind, longitudinal crossover study compares the efficacy of disopyramide and ethmozine, a new investigational drug, in suppressing frequent (40 or more per hour) ventricular premature depolarizations (VPDs) in 27 patients completing a 37 day protocol. Although both drugs significantly reduced VPDs relative to placebo, ethmozine was a superior antiarrhythmic drug in ach9eving near-total abolition of VPDs (30% of patients), which was never observed during disopyramide dosing (p less than .05). At the 80% VPD reduction level, ethmozine was effective in 56% of all patients compared with an effectiveness in only 22% of patients during disopyramide therapy (p less than .05). The mean peak plasma level of ethmozine was 0.66 +/- 0.8 micrograms/ml, which significantly fell to a trough level of 0.1 +/- 0.08 micrograms/ml (p less than .001). Mean peak and trough plasma levels of disopyramide exhibited less fluctuation (2.6 +/- 0.9 micrograms/ml vs 2.2 +/- 0.9 micrograms/ml). Ethmozine had no effect on the QT interval, whereas disopyramide prolonged it significantly. Importantly, while disopyramide produced serious side effects in 30% of patients, ethmozine was well tolerated with no statistically significant side effects compared with placebo.

In a controlled, randomized, double-blind study we investigated the long-term effects of the beta 1-adrenoceptor agonist prenalterol in 16 patients with severe congestive heart failure (NYHA class III or IV). Previous to and 1 week, 3 months, and 6 months after continuous oral intake of 40 to 120 mg prenalterol a day, catheterization of the right heart combined with an ergometer test was carried out; M mode and two dimensional echocardiograms as well as systolic time intervals were also recorded. With prenalterol the heart rate increased within 1 week from 81 +/- 7 to 90 +/- 7 beats/min (mean +/- SD) (p less than .05) and remained increased after 3 months (93 +/- 9 beats/min, p less than .01) and 6 months (91 +/- 6 beats/min, p less than .05). After 1 week the cardiac index rose from 2.7 +/- 0.7 to 3.3 +/- 0.7 l/min/m2 (p less than .01), and after 3 and 6 months it fell again to 3.0 +/- 0.9 l/min/m2 and 2.9 +/- 0.7 l/min/m2, respectively. In the ergometer test the improvement in performance was not significant. The mean velocity of circumferential fiber shortening initially increased from 0.58 +/- 0.20 to 0.79 +/- 0.28 circumferences/sec (p less than .01), but dropped after 3 months to 0.62 +/- 0.31 circumferences/sec. The ejection fraction determined from the two-dimensional echocardiogram rose after 1 week from 20 +/- 10 to 27 +/- 12% (p less than .05), but decreased again after 3 months (23 +/- 11%) and 6 months (20 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)