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The effect on exercise tolerance of nitroglycerin (NTG) ointment was studied by exercise test on bicycle ergometer in a selected group of patients with effort angina and angiographically proven critical coronary lesions. NTG ointment (15 mg) and placebo were administered in a double-blind cross-over randomized trial on two consecutive days; exercise test was carried out before the administration of NTG ointment and placebo, and repeated after one hour, 2 and 1/2 hours and 4 hours. Compared to control and placebo tests, NTG ointment produced a highly significant increase of duration of exercise and of total work load in all tests, as well as a significant decrease of maximal ST segment depression. After NTG ointment administration resting systolic blood pressure showed a significant decrease after one hour, 2 and 1/2 hours and 4 hours, resting heart rate a significant increase after 2 and 1/2 and 4 hours, and peak exercise heart rate a significant increase after 4 hours. Double product at rest was unaffected by NTG ointment, while at peak exercise it showed a significant increase only after 4 hours. Our data show that in patients with effort angina NTG ointment produces an important increase of exercise capacity which persists at least for 4 hours after the administration. Therefore NTG ointment seems to be of high value in the treatment of effort angina.

The value of the dipyridamole test (0.75 mg/kg i.v.) in the diagnosis of angina pectoris was studied in 54 patients with angina pectoris (35 with angina on effort associated or not associated with rest angina and 19 with angina only at rest) and in 12 control subjects. The test induced electrocardiographic signs of ischemia (positive test) in 74% of patients with angina on effort, while it was negative in all cases with angina only at rest and in control subjects. All anginal patients with normal coronary arteries or less than 50% stenosis had a negative test; a positive response was observed in 36, 79 and 60% of cases with one-, two-or three-vessel disease, respectively. Hemodynamic changes with a marked arteriolar vasodilatation were observed both in the negative and in the positive tests. In the positive tests no significant change of double product, blood pressure and left ventricular end-diastolic pressure occurred before ischemia appeared. The results of the study show that dipyridamole as a diagnostic test in angina pectoris has a high specificity but a lower sensitivity than exercise test. The hemodynamic and eletrocardiographic findings in the positive tests suggest that dipyridamole-induced ischemia is due to a flow maldistribution with selective subendocardial ischemia secondary to the coronary arteriolar dilatation caused by the drug.

The purpose of this study was to focus on the clinical and angiographic characteristics of 113 patients with crescendo angina (Group I) as compared to 187 patients with angina of new onset (Group II), selected from a series of 474 consecutive subjects, admitted to our clinic between January 1976 and July 1983 because of recurrent episodes of spontaneous angina, who underwent cardiac catheterization and coronary angiography within one month of hospitalization. Group I patients showed a greater incidence of prior transmural myocardial infarction (p less than 0.01), arterial hypertension (p less than 0.01), multivessel disease (p less than 0.01) and a lower value of left ventricular ejection fraction (p less than 0.01) than Group II patients. In the latter group of patients anginal episodes were more frequently associated with S-T segment elevation than with S-T segment depression (p less than 0.001), while the opposite was found in patients with crescendo angina. Survival curves up to five years showed that medically treated patients with crescendo angina had a worse long-term prognosis than patients with unstable angina of new onset (p less than 0.01). On the contrary no difference was found between the surgically treated patients of the two groups. Our data suggest that the more diffuse involvement of the coronary tree associated with a more depressed left ventricular function may result in an unfavorable long-term prognosis in patients with crescendo angina as compared to those with unstable angina of new onset. Such a difference between the two groups was abolished by surgical treatment.

The effectiveness of nitroglycerin ointment in vasospastic angina pectoris at rest was evaluated in 10 patients selected for study. The study was performed after a 24 hour control period, and a randomized single-blind crossover experimental design was followed. Two percent nitroglycerin ointment (15 mg) or placebo ointment was administered every 6 hours for a period of 48 hours each; the first treatment period was followed by a second in which each preparation was used for a 24 hour period. All patients were hospitalized in the coronary care unit; an objective evaluation was carried out using a multichannel electrocardiographic recording to assure recognition of the painless ischemic episodes. Coronary angiography showed critical stenosis of one or two vessels in 9 of the 10 patients; spasm was demonstrated in 3. Results of the ergonovine test were positive in nine of nine patients. Nitroglycerin ointment produced a significant reduction in the mean daily number of episodes during the first (12.5 +/- 3.9 versus 0.5 +/- 0.4, p less than 0.02) as well as the second treatment period (10.6 +/- 3.8 versus 0.6 +/- 0.4, p less than 0.02). These results demonstrate that nitroglycerin ointment provides effective, long-lasting protection against angina due to coronary spasm.

The duration of effect of single oral doses of 10 and 20 mg of nifedipine was studied in 10 patients with angiographically proven coronary artery disease and with stable exercise-induced angina pectoris. In a randomized double-blind manner exercise tests were carried out 1 hour before and 1, 2, 4 and 6 h after the administration of placebo, nifedipine 10 mg(N10) and nifedipine 20 mg(N20). Compared with the placebo both N10 and N20 produced a statistically significant increase in exercise tolerance at 1(P less than 0.05), 2(P less than 0.01), 4(P less than 0.01) and 6(P less than 0.05) hours after N10 and at 1(P less than 0.01), 2(P less than 0.01), 4(P less than 0.01) and 6(P less than 0.05) hours after N20. At peak exercise the product of heart rate X systolic blood pressure (RPP) was significantly increased compared with placebo at 2, 4 and 6 h after N10 and at 2, 4 and 6 h after N20 with maximal ST-segment depression unchanged. At the same duration of exercise at which angina had occurred during control studies the RPP was unaffected by nifedipine while a statistically significant reduction of ST-segment depression was seen at 1, 2 and 4 h after N10 and at 1, 2 and 4 h after N20. Direct measurements of great cardiac vein flow during exercise in two patients showed that nifedipine is effective in preventing the abnormal increase of exercise-induced coronary tone in the area supplied by stenotic vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

The effectiveness of nifedipine in treating angina pectoris at rest was evaluated in 14 patients with frequent ischemic episodes associated with S-T segment elevation or depression. The trial consisted of (1) a 48 hour control period; (2) a placebo period and a period of treatment with nifedipine of 48 hours each; and (3) a second placebo period and a second period of treatment with nifedipine of 24 hours each. The efficacy of treatment was evaluated by continuous electrocardiographic recording to detect painless ischemic episodes. During coronary angiography coronary spasm was demonstrated in five patients. The ergonovine maleate test was positive in seven of eight patients. No statistically significant difference was found in the mean daily number of ischemic episodes between the control period and the first placebo period, or between the control and the second placebo periods. Nifedipine produced a highly significant reduction in the mean daily number of episodes compared with the response to placebo during the first as well as the second period. Nifedipine is effective in angina at rest caused by coronary arterial spasm. The prevention of ischemia may be related to the ability of nifedipine to decrease calcium-dependent coronary muscle tone and to prevent coronary spasm.