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The occurrence and significance of transient dilation of the left ventricle during dipyridamole stress-redistribution thallium-201 scintigraphy was studied in 73 patients who underwent both dipyridamole thallium-201 study and coronary angiography. Transient dilation ratio was calculated from planar anterior images by dividing the computer-derived left ventricular area on the initial image by that of the 4-hour image. In 11 patients with normal coronary arteriograms or less than 50% coronary stenosis, the transient dilation ratio was 0.98 +/- 0.046. An abnormal transient dilation ratio was defined as greater than or equal to 1.12, representing greater than or equal to 3 standard deviations above the mean normal value. When the 15 patients with an abnormal ratio were compared with the 58 with a normal ratio, the former group had a significantly higher frequency of 3 critical (greater than or equal to 90%) coronary stenoses (33 vs 5%), higher prevalence of collaterals (67 vs 24%), more extensive myocardial reversible defects by planar (71 vs 10%) or by single-photon emission computed tomography (87.5 vs 35%) imaging and a higher incidence of dipyridamole-induced anginal chest pain (53 vs 22%). No significant difference between the 2 groups was noted with respect to age, gender, prior myocardial infarction, single or double critical coronary stenosis, dipyridamole-induced ischemic electrocardiographic response and increased lung uptake. An abnormal transient dilation ratio of greater than or equal to 1.12 was a specific marker of multivessel (87%) or 3-vessel (85%) critical coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Twenty-two patients with stable angina were studied in a randomised double-blind, placebo-controlled crossover trial to compare the antianginal effects of nicardipine (30 mg) and verapamil (120 mg), each given three times a day. Efficacy was assessed using treadmill exercise testing and 24-hour ambulatory electrocardiographic monitoring performed after an initial 2-week placebo phase and at the end of each 4-week active treatment period. Exercise time (mean +/- standard error of mean) increased from 7.4 +/- 0.5 min on placebo to 8.4 +/- 0.7 min on nicardipine (P less than 0.05) and to 9.9 +/- 0.7 min on verapamil (P less than 0.001). Resting heart rate was decreased by verapamil (P less than 0.002) and increased by nicardipine (P less than 0.02). Exercise heart rate was increased on nicardipine (P less than 0.005) but heart rate gain was higher on verapamil (P less than 0.01). Blood pressure and peak ST segment depression were unaltered by either drug but the time to 1 mm ST segment depression increased on both drugs. Ambulatory heart rates were lower on verapamil than on nicardipine and patient subjective preference was in favour of verapamil. This study confirms that both nicardipine and verapamil improve exercise capacity, but verapamil produces a greater improvement in exercise tolerance and indices of myocardial ischaemia whilst nicardipine is associated with an increase in the number of episodes of ST segment depression on ambulatory monitoring.

In this single-blind, placebo-controlled trial, carvedilol, a nonselective beta-blocking and vasodilating agent was studied in six patients with chronic stable angina. All patients had reproducible treadmill exercise time without medical treatment and developed chest pain in association with ST-segment depression (greater than 1 mm at J + 80 msec) on exercise. None had a history of rest or unstable angina or myocardial infarction within three months prior to the study. In all patients, anti-anginal medication except sublingual nitroglycerin was discontinued for 10 days. The patients entered an initial two week-phase of placebo. They then received carvedilol, 25 mg and then 50 mg twice daily for two weeks on each dose, followed by another two week-placebo-phase. Radionuclide ventriculography was performed at the end of each phase at rest and during maximal symptom-limited exercise. Bicycle ergometry was carried out in the supine position with incremental workloads. Exercise time and workload were recorded at the end of the first phase and imaging was performed at the same time and workload throughout the trial. Carvedilol produced a dose-related reduction in rest and exercise heart rate and blood pressure. Peak exercise ST-segment change was reduced by both doses of carvedilol, but this did not achieve a level of significance. After the first placebo phase all patients had abnormal left ventricular wall motion and resting ejection fraction (range: 35% to 45%). Four out of six patients had significant improvement in wall motion abnormalities, in two patients there was no change, and none developed a deterioration in abnormal wall motion.(ABSTRACT TRUNCATED AT 250 WORDS)

A placebo-controlled double-blind randomized crossover study was carried out to assess the effects of chronic therapy with two calcium antagonists on left ventricular diastolic function in patients with stable angina. Ventricular function was assessed using equilibrium radionuclide angiography and the data was analysed using an automated algorithm. The mean +/- SD ejection fraction on placebo was 59 +/- 10% and this remained unchanged on both verapamil (59 +/- 9%; P = NS) and nicardipine (58 +/- 7%; P = NS). Verapamil increased the peak filling rate index (P less than 0.001) and first one-third filling fraction (P less than 0.005). Nicardipine increased the peak filling rate index (P less than 0.005), but did not alter the other diastolic indices. Early filling rate index was not altered by either drug. Comparison of the effects of nicardipine and verapamil revealed no significant differences in ejection fraction, peak filling rate index or early filling rate index. However, verapamil showed a greater improvement in time to peak filling rate and first one-third filling fraction (P less than 0.01, P less than 0.01, respectively) compared with nicardipine. Heart rate (P less than 0.002) and systolic blood pressure (P less than 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 angina pectoris before systolic dysfunction becomes apparent and that these abnormalities may be partially corrected by calcium antagonists.