Effects of verapamil and nifedipine on left ventricular function at rest and during exercise in patients with prinzmetal's variant angina pectoris

To assess the effects of verapamil and nifedipine on left ventricular function at rest and during exercise in patients with Prinzmetal's variant angina pectoris, 10 patients (6 men and 4 women with a mean age of 52 years) with variant angina were each treated for 2 month periods with placebo, verapamil (400 ± 80 mg/day, mean ± standard deviation [SD]) and nifedipine (82 ± 31 mg/day). During the final week of each 2 month treatment period equilibrium gated blood pool scintigraphy was performed at rest and during exercise. At rest, heart rate during verapamil therapy was lower than during treatment with nifedipine; systolic blood pressure and left ventricular volumes and ejection fraction were similar for the three interventions. The maximal work load achieved was similar during placebo, verapamil and nifedipine therapy. At the maximal work load common to all three exercise studies, heart rate and systolic blood pressure were lower with verapamil than with placebo and nifedipine; ventricular volumes and ejection fraction were similar with the three agents. Thus, in patients with variant angina and a wide range of left ventricular function at rest, neither verapamil nor nifedipine significantly alters left ventricular volumes or ejection fraction at rest or during exercise.     

Effect of verapamil and nifedipine on left ventricular function at rest and during exercise in patients with Prinzmetal''s variant angina pectoris

To assess the effects of verapamil and nifedipine on left ventricular function at rest and during exercise in patients with Prinzmetal's variant angina pectoris, 10 patients (6 men and 4 women with a mean age of 52 years) with variant angina were each treated for 2 month periods with placebo, verapamil (400 ± 80 mg/day, mean ± standard deviation [SD]) and nifedipine (82 ± 31 mg/day). During the final week of each 2 month treatment period equilibrium gated blood pool scintigraphy was performed at rest and during exercise. At rest, heart rate during verapamil therapy was lower than during treatment with nifedipine; systolic blood pressure and left ventricular volumes and ejection fraction were similar for the three interventions. The maximal work load achieved was similar during placebo, verapamil and nifedipine therapy. At the maximal work load common to all three exercise studies, heart rate and systolic blood pressure were lower with verapamil than with placebo and nifedipine; ventricular volumes and ejection fraction were similar with the three agents. Thus, in patients with variant angina and a wide range of left ventricular function at rest, neither verapamil nor nifedipine significantly alters left ventricular volumes or ejection fraction at rest or during exercise.     

Hemodynamic effects of nifedipine during upright exercise in stable angina pectoris and either normal or severely impaired left ventricular function

The immediate effects of sublingual nifedipine (20 mg) were evaluated in 18 men with stable, exercise-related angina pectoris and angiographically confirmed coronary artery obstructions, stratified at the time of left ventricular (LV) angiography according to the degree of LV dysfunction supine at rest (Group 1: n = 9, left ventricular end-diastolic pressure [LVEDP] less than 20 mm Hg; Group 2: n = 9, LVEDP greater than 20 mm Hg). At rest, in the upright posture in both groups, nifedipine reduced the systemic vascular resistance (p less than 0.01). The systemic arterial mean (p less than 0.05) and diastolic (p less than 0.01) pressures were reduced despite an increase in the cardiac output (p less than 0.05). Heart rate was increased only in Group 1 (p less than 0.05). Pulmonary artery occluded pressure was unchanged in both groups. During upright bicycle exercise in all patients, compared to control measurements, systemic arterial pressure (p less than 0.01) and vascular resistance (p less than 0.05) were similarly reduced, while exercise cardiac output response and LV filling pressure did not change after nifedipine. Heart rate was increased in Group 1 (p less than 0.05) and decreased in Group 2 (p less than 0.05). Stroke volume during exercise after nifedipine decreased 1 ml/m2 in Group 1 (p greater than 0.05) and increased 2 ml/m2 in Group 2 (p greater than 0.05) compared to control measurements; the between-group difference in the exercise heart rate and stroke volume responses after nifedipine were significant at the 5% level.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improvement in left ventricular diastolic function in patients with stable angina after chronic treatment with verapamil and nicardipine

A placebo-controlled double-blind randomized crossover studywas carried out to assess the effects of chronic therapy withtwo calcium antagonists on left ventricular diastolic functionin patients with stable angina. Ventricular function was assessedusing equilibrium radionuclide angiography and the data wasanalysed using an automated algorithm. The mean±SD ejectionfraction on placebo was 59±10% and this remained unchangedon both verapamil (59 ±9%; P = NS) and nicardipine (58±7%; P = NS). Verapamil increased the peak filling rateindex (P<0.001) and first one-third filling fraction (P<0.005).Nicardipine increased the peak filling rate index (P < 0.005),but did not alter the other diastolic indices. Early fillingrate index was not altered by either drug. Comparison of theeffects of nicardipine and verapamil revealed no significantdifferences in ejection fraction, peak filling rate index orearly filling rate index. However, verapamil showed a greaterimprovement in time to peak filling rate and first one-thirdfilling fraction (P<0.01, P<0.01, respectively) comparedwith nicardipine. Heart rate (P<0.002) and systolic bloodpressure (P<0.01) were also lower on verapamil than on nicardipine.These data suggest that left ventricular ‘relaxation’abnormalities may be detected in patients with chronic anginapectons before systolic dysfunction becomes apparent and thatthese abnormalities may be partially corrected by calcium antagonists.     

Randomized double-blind comparison of verapamil and nifedipine in chronic stable angina

A randomized double-blind crossover trial was performed in 32 patients with chronic stable angina to compare the antianginal actions of verapamil (120 mg 3 times daily) and nifedipine (20 mg 3 times daily). Efficacy was assessed using objective end points obtained by computer-assisted exercise testing and 24 hour ambulatory monitoring for S-T segment shift. Twenty-eight patients completed the trial. The mean exercise time to produce angina improved from 5.7 ± 0.3 minutes (mean ± standard error of the mean) in patients on placebo, to 7.9 ± 0.5 minutes in those on nifedipine and 10.0 ± 0.7 minutes in those on verapamil. Similar improvement was seen in all other objective variables. Generally, verapamil produced mild bradycardia and nifedipine mild tachycardia. Four patients complained of palpitations and angina after ingestion of nifedipine and were identified by ambulatory monitoring to have tachycardia and persistent S-T depression. These opposite effects on heart rate may explain the differences in efficacy between these 2 potent calcium ion antagonists.     

Effects of nifedipine on myocardial perfusion during exercise in chronic stable angina pectoris

Nifedipine may be effective in the treatment of stable angina by both decreasing myocardial oxygen demand and increasing myocardial oxygen supply. To determine the mechanism of action of nifedipine and its dose-response relation, 14 patients with stable angina were treated with nifedipine 10, 20 and 30 mg 4 times daily as single-agent therapy in a double-blind, randomized, placebo-controlled crossover trial. Treatment was continued for 1 week on each dose regimen and efficacy was determined using an exercise test at the end of each phase. Compared to placebo, a significant decrease of systolic blood pressure at peak exercise occurred with the nifedipine 20- and 30-mg regimens (p less than 0.05), accompanied by an increase in heart rate on the 10- and 20-mg regimens (p less than 0.005). There was no significant effect on the rate-pressure product compared to placebo at any exercise time on any of the nifedipine regimens. The times to onset of ST-segment depression and to angina were delayed significantly by all 3 dose regimens compared to placebo (p less than 0.02). There was a significant decrease in the magnitude of ST-segment depression at all exercise times by all dosage schedules of nifedipine compared with placebo (p less than 0.05), although there were no significant differences among the 3 dosage schedules. Data indicate that since nifedipine was effective in improving manifestations of myocardial ischemia during exercise without altering the double product at submaximal or maximal exercise, its beneficial mechanism of action may have been due to enhancing blood flow to ischemic zones or to favorably altering determinants of myocardial oxygen demand, which were not measured.     

Improved exercise performance in persons with stable angina pectoris receiving diltiazem

The effects of diltiazem, a calcium antagonist drug, were compared with those of placebo on exercise performance during a series of symptom-limited upright exercise tests. Ten patients with chronic stable angina were studied over a period of 7 weeks. The drug was administered in a random double-blind fashion and was evaluated at increasing dose levels of 120, 180 and 240 mg/day. Diltiazem was effective in increasing the total duration of exercise (p <0.001) and the time to the first onset of angina (p <0.02) and to the first appearance of 1 mm of S-T depression (p <0.02). These effects were most marked at the highest dose level of diltiazem. The heart rate was reduced at rest (p <0.05) and during submaximal exercise (p <0.001). There was a reduction in diastolic blood pressure during submaximal exercise (p <0.04) but no change in systolic pressure. Pressure-rate product was significantly reduced at submaximal (p <0.001) but not maximal exercise. The reduction in pressure-rate product is postulated as the mechanism by which diltiazem enhances duration of exercise. There was no reduction in electrocardiographic evidence of myocardial ischemia at peak exercise by either clinical observation or computer analysis of spatial electrocardiographic variables. Five of the six patients who continued to take the drug maintained or improved their exercise performance on follow-up study 8 to 10 months later.     

Effects of nifedipine on arterial oxygenation at rest and during exercise in patients with stable angina

The effects of nifedipine on arterial oxygenation and hemodynamics were studied at rest and during bicycle exercise in 12 men (mean age 55 years, range 41 to 67) with stable exertional angina. The study was conducted double-blind on 2 days, 1 week apart, using a placebo-controlled crossover design. On each day, measurements at rest were made before and 20 minutes after 20 mg sublingual nifedipine or placebo and were followed by measurements made during exercise. Compared with placebo, nifedipine reduced mean arterial pressure, systemic vascular resistance and pulmonary vascular resistance, and increased heart rate and cardiac output at rest and during exercise. It did not alter mean pulmonary artery or pulmonary artery wedge pressures at rest, but decreased them during exercise. Nifedipine decreased arterial oxygen tension (PaO2) from 96 +/- 10 to 90 +/- 13 mm Hg (p less than 0.05) at rest and from 99 +/- 11 to 92 +/- 12 mm Hg (p less than 0.005) at submaximal exercise (33 +/- 21 W), but did not alter it (100 +/- 12 versus 100 +/- 16 mm Hg, p = NS) at maximal exercise (68 +/- 30 W). The reduction in PaO2 was not due to alveolar hypoventilation, because nifedipine did not alter arterial carbon dioxide tension, or to changes in mixed venous oxygen tension, which nifedipine increased at rest (39 +/- 2 versus 43 +/- 3 mm Hg, p less than 0.001) and during submaximal exercise (31 +/- 4 versus 33 +/- 4 mm Hg, p less than 0.03) and maximal exercise (27 +/- 3 versus 31 +/- 3 mm Hg, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Calcium antagonist drugs in chronic stable angina. Comparison of verapamil and nifedipine.

The relative efficacy of two calcium antagonist drugs, verapamil, 120 mg three times a day and nifedipine, 20 mg three times a day, was examined in a double-blind randomised trial. Patients were assessed at the end of four week periods by a maximal treadmill exercise test, the frequency of anginal attacks, glyceryl trinitrate consumption, and side effects. Sixteen point praecordial maps were recorded at rest, immediately after exercise, and at minute intervals for 10 minutes. Total ST segment depression (epsilon ST) was used as a measure of myocardial ischaemia. Both verapamil and nifedipine increased maximal work capacity but epsilon ST at the termination of the test remained constant. Both drugs reduced the frequency of anginal attacks and glyceryl trinitrate consumption. Systolic blood pressure at rest and on exercise was reduced by both drugs. Verapamil and nifedipine were equally effective in treating angina, but side effects were more common with nifedipine.     

Effects of beta blockade on systolic and diastolic left ventricular function at rest and during exercise in patients with chronic stable angina pectoris

This study examined the effects of beta blockade with betaxolol, a cardioselective, lipid-soluble, beta-adrenergic-blocking agent, on rest and exercise systolic and diastolic left ventricular function in 15 patients, aged 40 to 70 years (mean = 52), with chronic stable angina pectoris. Each patient underwent three upright exercise studies at identical workloads; the first was a baseline study, the second was done 3 hours after a single oral dose, and the third was obtained after chronic therapy for 2 weeks. Beta blockade was evident by significant decreases in heart rate, systolic blood pressure, and diastolic blood pressure at rest and during exercise (p less than 0.04). Although there were no significant changes (at rest or during exercise) in mean left ventricular ejection fraction and peak filling rate, individual variations were seen after 3 hours and 2 weeks of therapy. During chronic therapy, the peak filling rate increased in three patients, decreased in five, and remained unchanged in seven. Also, discordant changes in systolic and diastolic functions were seen at rest and during exercise during both acute and chronic therapy. Thus, although acute and chronic beta blockade produces no significant changes in mean measurements of diastolic and systolic left ventricular performance, individual variations and discordant results are seen in many patients. The acute effects are generally consistent with the chronic effects, but exceptions are present.     

Abnormalities of left ventricular shape in patients with stable angina

In this study, left ventricular shape was evaluated quantitatively by calculating the power spectrum and the regional curvatures of angiographic outlines as seen in the right oblique anterior projection. Two groups of patients were studied: 16 normal subjects and 16 patients with stable angina who were selected because of normal left ventricular function (normal left ventricular volumes, pressures, ejection fraction and no regional wall motion abnormality at subjective analysis of ventriculograms). The two groups did not differ in terms of mean age of the patients. Regional curvatures were calculated using the Frenet-Serret formula starting from the mitral corner (point 1) and extending to the aortic corner (point 90). The power spectrum was calculated by means of Fourier analysis. The ventricular shape during diastole of the patients with angina differed significantly from that of the normal group in that there was a greater posterobasal curvature; a lower curvature of the inferior wall showing an inward convexity; a greater parietal curvature of the inferoapical region and a minor curvature of the anterobasal region. The power spectrum differed significantly from that of the normal subjects. The 1st and 2nd harmonics were reduced and the 3rd, 4th, 5th and 6th ones increased. The end-systolic contour of the group of patients with stable angina showed a higher amplitude of the 3rd and 5th harmonics and a lower amplitude of the 1st, 2nd, 9th, 10th and 11th harmonics with respect to the group of normal patients. Regional curvatures showed significant differences between the two groups in the antero-basal region. These modifications of left ventricular shape in patients with stable angina did not appear to be related to age and/or heart rate; to abnormalities in hemodynamics and wall motion; or to acute ischemia. Abnormalities of shape in patients with stable angina, therefore, may indicate a remodeling of the left ventricle due to the structural effects (myocardial and/or interstitial) of chronic ischemia.     

Effect of nifedipine on left ventricular function during exercise in patients with stable effort angina. Relation of its efficacy to the severity of coronary artery disease

To evaluate whether the effect of nifedipine on left ventricular function relates to the severity of coronary artery disease (CAD) or not, supine graded ergometer exercise testing was performed before and after sublingual administration of 10 mg nifedipine in 24 patients with stable effort angina. To minimize the effect of nifedipine on myocardial oxygen consumption, exercise before and after nifedipine was discontinued at the same target rate pressure product. Percent (%) left ventricular ejection fraction (EF) [EF during exercise/EF at rest.100] was measured before and after nifedipine by radionuclide angiocardiography. The angiographic degree of CAD was defined by Gensini's CAD scoring as follows: severe CAD: greater than or equal to 50, moderate: less than 50 greater than 20 and mild: less than or equal to 20. After nifedipine, left ventricular function (%EF) was improved in all 6 patients with mild CAD, but was worsened in all 9 patients with severe CAD. Maximal ST segment depression during exercise was improved in 5 of 6 patients with mild CAD, while improvement was induced in 5 of 9 patients with moderate CAD and in 3 of 9 patients with severe CAD. Jeopardy of coronary collateral vessels may have an influence on the effect of nifedipine. It is suggested that the effect of nifedipine on left ventricular function is influenced by the severity of CAD when most of its effect on myocardial oxygen consumption is eliminated.     

Effects of intravenous verapamil on left ventricular relaxation and filling in stable angina pectoris

Left ventricular (LV) diastolic function is often impaired in coronary artery disease (CAD). To assess whether verapamil could improve LV diastolic properties, 12 patients with CAD undergoing right- and left-sided cardiac catheterization, as well as simultaneous radionuclide angiography, were studied before and during intravenous administration of verapamil (0.1 mg/kg as a bolus followed by 0.007 mg/kg/min). The heart rate was kept constant by atrial pacing in both studies. LV pressure-volume relations were obtained. Verapamil decreased LV systolic pressure (130 +/- 22 to 117 +/- 16 mm Hg, p less than 0.01) and the end-systolic pressure/volume ratio (2.4 +/- 1.3 to 1.6 +/- 0.5 mm Hg/ml, p less than 0.05), and increased LV end-diastolic (13 +/- 4 to 16 +/- 4 mm Hg, p less than 0.02) and pulmonary capillary pressures (10 +/- 5 to 12 +/- 5 mm Hg, p less than 0.005). Despite such negative inotropic effects, cardiac index increased (3.4 +/- 0.7 to 3.9 +/- 0.6 liters/min/m2, p less than 0.02). The time constant of isovolumic relaxation shortened (63 +/- 14 to 47 +/- 9 ms, p less than 0.02); peak filling rate increased (370 +/- 155 to 519 +/- 184 ml/s, p less than 0.001; 2.6 +/- 1.1 to 3.3 +/- 0.9 end-diastolic counts/s, p less than 0.02; and 4.1 +/- 1.6 to 5.5 +/- 1.5 stroke counts/s, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of nifedipine on exercise-induced left ventricular dysfunction and myocardial hypoperfusion in stable angina

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 ± 42 seconds to 471 ± 50 seconds (p < 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 ± 3.6% to 52 ± 3.3%, p < 0.05) and at peak exercise (42 ± 3.3% to 47 ± 3.7%, p < 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 ± 2.3 to 3.0 ± 2.3, p < 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.     

Isradipine therapy in chronic stable angina pectoris--comparison with nifedipine.

Current available calcium antagonists, although useful in angina pectoris, are often poorly tolerated. We therefore compared isradipine, a new calcium antagonist, with nifedipine in 18 patients with angina. Patients sequentially received incremental doses of either isradipine (IS) 2.5-7.5 mg three times daily or nifedipine (NF) 10-30 mg three times daily for 6 weeks each, in a randomized double-blind crossover study. Both agents produced similar (P = 0.43) increases in maximum exercise duration (IS + 30%; NF + 34%) and an equivalent (P = 0.38) increase in time to onset of angina on exercise (IS + 53%; NF + 62%). Both IS and NF significantly reduced exercise-induced ST depression (-40% and -45%) to a similar degree (P = 0.48). NF significantly (P = 0.019) reduced angina attacks (-3.0 attacks.week-1; 26%) compared to IS (-0.4; 4%) whilst a similar but non-significant trend in favour of NF was also apparent in the consumption of sublingual glyceryl trinitrate (-0.1 tablets.week-1; 2% vs +1.3.week-1; 23%; P = 0.28). However, significantly (P less than 0.03) more patients experienced adverse events whilst taking NF than with IS (36 events in 16/18 (89%) v 18 in 9/18 (50%). Thus, IS and NF increased exercise tolerance and reduced exercise angina and ST depression equally well although NF use was associated with fewer anginal episodes and IS with fewer side effects.     

Improvement in exercise capacity and associated changes in hemodynamics and left ventricular function after the addition of metoprolol to nifedipine in patients with stable exertional angina

In 10 men with stable exertional angina, the changes in exercise capacity, hemodynamics, and left ventricular (LV) function were measured after 20 mg sublingual nifedipine (N) and again after adding 100 mg oral metoprolol (M). Nifedipine alone did not significantly improve exercise workloads (+18%) and duration (+21%), but the addition of metoprolol increased both parameters by a further 37 and 32%, respectively (both p less than 0.005 vs. N). After nifedipine the onset of angina was slightly delayed (5.14 +/- 2.41 min placebo (P), 6.00 +/- 2.31 min N, p less than 0.1) and occurred at higher workloads (36 +/- 17 W P, 43 +/- 8 W N, p less than 0.1). After the addition of metoprolol, the onset of angina was delayed substantially more (9.57 +/- 2.22 min, p less than 0.001 vs. P and N) and occurred at much higher workloads (62 +/- 20 W, p less than 0.001 vs. P and N). At rest (R) and during exercise (E), nifedipine decreased systemic vascular resistance (-36% R, -27% E, both p less than 0.001) and mean arterial pressure (-18% R, -21% E, both p less than 0.001), and increased heart rate (+15% R, +11% E, both p less than 0.001), Pulmonary artery wedge pressure on exercise increased less (22 +/- 7 mmHg P, 13 +/- 5 mmHg N, p less than 0.001). After adding metoprolol, the major change was a reduced heart rate (-25% vs. N at R and E, both p less than 0.001), and arterial pressure was unaltered. Pulmonary artery wedge pressure on exercise increased to 18 +/- 5 mmHg (p less than 0.05 vs. N). Exercise LV ejection fraction and volume did not change significantly after adding metoprolol despite marked improvement in angina. In this acute exercise study in patients with stable exertional angina, metoprolol added to nifedipine markedly improved exercise capacity by preventing the increase in heart rate seen with nifedipine. In our patients with relatively normal LV function at rest, the combination was safe and produced no deleterious effects on LV function.     

Combined therapy with verapamil and propranolol in chronic stable angina

The comparative efficacy of verapamil (360 mg daily) and propranolol (240 mg daily) was evaluated with computerized treadmill exercise in 22 patients with chronic stable angina in a placebo-controlled double-blind crossover study with 4 weeks on each active phase. Fourteen of these patients still had angina despite active drug therapy and they were further treated with a combination of verapamil (360 mg) and propranolol (120 mg) for 4 weeks. The mean exercise time for these patients taking placebo was 4.8 ± 0.22 minutes (mean ± standard error of the mean) and this increased to 6.8 ± 0.64 minutes with propranolol and 8.0 ± 0.5 minutes with verapamil. A further increase to 10.1 ± 0.88 minutes was observed with the combination of both drugs and seven patients became symptom-free. S-T segment criteria improved with both drugs, and combination therapy produced a further reduction in peak S-T depression. Electrocardiographic ambulatory monitoring showed no evidence of conduction defects and mean hourly heart rates were similar to those seen with propranolol alone. Left ventricular function indexes were not significantly different from those obtained with propranolol. Combination therapy with verapamil and propranolol appears to be efficacious in the treatment of selected patients with severe chronic stable angina. The patients need to be carefully monitored for adverse effects.     

Effects of nifedipine on left ventricular performance in unstable angina pectoris during a follow-up of 48 hours

In 1981, a large, double-blind, randomized, multicenter trial was started in The Netherlands to evaluate the therapeutic effects of nifedipine or metoprolol in patients with unstable angina. This study, called the Holland Interuniversity Nifedipine Trial (HINT), included several hundred patients to establish potential therapeutic effects. From December 1982 until January 1984 the effects of nifedipine on left ventricular (LV) performance in a subgroup of 37 HINT patients were studied using radionuclide techniques. All patients (18 treated with nifedipine, 19 with placebo) underwent radionuclide angiography and 33 underwent thallium-201 scintigraphy just before and 48 hours after the start of treatment with the experimental medication. Radionuclide angiographic studies were also performed 1 hour (29 patients) and 4 hours (31 patients) after the start of treatment. The thallium-201 images showed defects in 24 (73%) of the baseline images and in 21 (64%) of the 48-hour images. No significant differences were seen between patients receiving nifedipine or placebo in the incidence of new defects or in the disappearance of defects at 48 hours. Changes in thallium-201 images were not related to recurrence of myocardial ischemia or the development of acute myocardial infarction. Nineteen of the 37 patients (51%) with baseline blood pool images had a reduced LV ejection fraction (EF) (38 +/- 10%) and 18 patients (49%) had a normal LVEF of 56 +/- 5%. LVEF improved after 48 hours in 8 patients receiving nifedipine and in only 1 patient receiving placebo (p less than 0.02). This effect was not present at 1 and 4 hours after treatment.(ABSTRACT TRUNCATED AT 250 WORDS)