[Diagnostic possibilities in Prinzmetal (variant) angina pectoris].
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Ten coronary patients showing no signs of controlled myocardial infarction and responding with transient ST rise to bicycle-ergometric exercise were investigated. ST rise was also recorded from the same leads during a spontaneous attack and cold testing. Coronarography revealed mild coronary arterial lesions. No ST elevation was recorded when bicycle-ergometric test was repeated in the presence of obsidan or corinfar treatment, and the test was negative in most cases.
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A 54 years-old man with a history of migraine, suffered from chest pain together with ST-segment elevation related to the intake of drugs against migraine attacks. The coronary arteriography showed normal coronary arteries. We suggest coronary artery spasm as the most probable cause of ischemia. We conclude that vasoactive drugs against migraine must be utilized with caution, or even avoided in patients with chest pain suggestive of myocardial ischemia.
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To test the hypothesis that coronary spasm could be a coronary manifestation of systemic endothelial dysfunction and that the activity of coronary spasm could influence systemic endothelial function, we examined brachial flow-mediated, endothelium-dependent vasodilation and nitroglycerin-induced endothelium-independent vasodilation with high-resolution ultrasound in 11 men with variant angina pectoris (6 active and 5 inactive) without established coronary atherosclerosis. Endothelium-dependent vasodilation in peripheral circulation was preserved in men with active and inactive variant angina pectoris, suggesting that systemic endothelial dysfunction is not involved in either the pathogenesis or the activity of coronary spasm.
BACKGROUND: Plasma adiponectin is decreased in patients with coronary artery diseases, especially in patients with acute coronary syndrome (ACS). However, the correlation between plasma adiponectin and variant angina pectoris (VAP) has not been verified. Plasma adiponectin concentrations between VAP and other coronary artery diseases was compared in the present study. The association between plasma adiponectin concentration and VAP was also investigated. METHODS AND RESULTS: Plasma adiponectin concentrations in the VAP group (n=101) were compared with those of the ACS group (n=117), the stable angina pectoris group (n=108), and the normal coronary group (n=81). Plasma adiponectin concentrations in VAP and ACS were significantly lower than that of the normal coronary group (6.6+/-5.4 vs 5.2+/-4.0 vs 9.0 +/-6.2 microg/ml, p<0.001, respectively). Multivariate analysis indicated that plasma adiponectin (odds ratio (OR) 0.735, 95% confidence interval (CI) 0.621-0.855, p=0.011), smoking (OR 2.012, 95% CI 1.210-3.880, p=0.020), and age (OR 0.976, 95% CI 0.957-0.997, p=0.022) correlated independently with the development of VAP. CONCLUSIONS: Our results suggest that a decrease in plasma adiponectin concentration might be associated with the development of VAP.
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 months 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.
The clinical effects of nitrendipine, a new calcium antagonist, were investigated in a single-blind test on 21 patients with variant angina pectoris. The efficacy of the drug was evaluated on the basis of frequency of anginal attacks and Holter electrocardiographic findings during different treatment periods at doses of 10 mg once a day (period I) and 20 mg once a day (period II). The number of anginal attacks decreased significantly from a pretreatment level of 2.1 +/- 0.3 per day to 0.7 +/- 0.2 per day in treatment period I and 0.3 +/- 0.1 per day in treatment period II (p less than 0.01, p less than 0.001, respectively). The consumption of sublingual nitroglycerin tablets decreased significantly in both treatment periods in comparison with the observation period before treatment (p less than 0.01, p less than 0.001, respectively). In 20 patients with continuous ECG monitoring, the frequency of ST-segment elevation was 4.5 +/- 1.0 per day during the pretreatment period; it decreased significantly to 0.9 +/- 0.6 per day in treatment period I and 0.5 +/- 0.3 per day in treatment period II (p less than 0.01, p less than 0.001, respectively). The duration and the maximum magnitude of ST-segment elevation also improved significantly in both treatment periods. These results demonstrate the efficacy of nitrendipine in the treatment of variant angina at a single daily dose of 10 mg.
Twelve patients were entered prospectively into a randomized double-blind study comparing the efficacy of nifedipine and isosorbide dinitrate (ISDN) in the treatment of variant angina pectoris due to coronary artery spasm. Using the diary technique, both anginal episodes and nitroglycerin tablets consumed were recorded during the pretrial, no drug period, and both active drug phases. During the baseline pretrial period, an average of 1.1 anginal episodes/day occurred with reduction to 0.28/day during nifedipine treatment and 0.39/day during ISDN treatment. Headache was the major side effect during ISDN treatment, occurring in 9 of 11 (81%) patients; and nonheart failure related pedal edema during nifedipine treatment, occurring in 4 of 12 (33%) patients. Intolerable side effects necessitating cessation of treatment occurred in two patients during nifedipine treatment and in three patients during ISDN treatment. Patients preferred nifedipine over ISDN because of increased efficacy and fewer uncomfortable side effects. We conclude that both nifedipine and ISDN are effective therapy for coronary spasm, but that nifedipine was more effective and was preferred by the majority of patients.
A case of variant angina with angiographically "normal" coronary arteries is reported. The clinical picture had been dominated by chronic stable angina for six years, and this symptomatology was complicated by pain at rest and also during the night. Two years later the patient had a myocardial infarction.
A 30-year-old man with variant angina pectoris and ventricular arrhythmias had an angiographically demonstrable 60% obstructive lesion of the proximal left anterior descending coronary artery that was observed to progress to 100% during spasm. Control of pain and arrhythmia by pharmacologic means was unsuccessful. Aortocoronary saphenous vein-internal mammary coronary bypass was associated with an anteroseptal wall myocardial infarction and relief from both angina pectoris and arrhythmias. It is suggested that infarction of the ischemic myocardium played a role in the successful management of this case.
Six patients with Prinzmetal's variant angina were treated with oral verapamil administration. Before and after the initiation of therapy, ambulatory ECG monitoring was performed to assess objectively the response to therapy. With verapamil administration, the frequency of both chest pain and transient ST-segment deviations was sharply diminished.