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The pharmacologic and physiologic effects of the slow-channel calcium antagonists verapamil, nifedipine and diltiazem are reviewed. Relevant pathophysiologic features of various acute ischemic heart disease syndromes are also reviewed and the clinical applications of the slow-channel calcium antagonists to acute ischemic heart disease syndromes in patients are discussed.
Plasma levels and 24-hour urine excretion of fibrinopeptide A were measured in a consecutive series of 179 patients with angina pectoris. Sixty-four patients had stable angina and 115 patients had unstable angina. Urine was collected over 24 hours the day before coronary arteriography, and blood samples were taken at the end of urine collection. When the values of fibrinopeptide A in plasma and in the 24-hour urine specimens were compared, no significant correlation was found in patients with either stable (rs = 0.16, difference not significant) and unstable (rs = 0.07, difference not significant) angina. The concentrations of fibrinopeptide A in the plasma did not differ significantly when patients with stable angina (range 0.1 to 82.6, median 7.4 ng/mL) were compared with patients with unstable angina (range 0.2 to 61.7, median 14 ng/mL, p = 0.055), whereas fibrinopeptide A 24-hour urinary excretion was significantly higher in patients with unstable angina (range 0.3 to 38.1, median 11.8 micrograms/24 hr) than in patients with stable angina (range 0.4 to 38.1, median 3.8 micrograms/24 hr, p less than 0.001). Twenty-four-hour urine excretion of fibrinopeptide A in patients with unstable angina and angiographically documented intracoronary thrombi were higher than the corresponding values in patients with unstable angina without such angiographic characteristic (p less than 0.001). The largest increase in plasma and urine concentration of fibrinopeptide A was observed in patients whose first episode of angina at rest occurred within the previous 48 hours. We conclude that the cumulative thrombin activity, assessed by 24-hour urinary excretion of fibrinopeptide A, is a more useful index, compared with single fibrinopeptide A measurement in plasma, for discriminating between patients with stable and with unstable angina pectoris.
BACKGROUND: Coronary vasospasm-induced electrical and mechanical complications in patients with acute coronary syndrome and no hemodynamically significant coronary artery disease are rarely reported. METHODS: A total of 733 consecutive patients with acute coronary syndrome admitted to our hospital who subsequently underwent coronary angiography at our institution were enrolled. Patients who had documented complete atrioventricular block or ventricular fibrillation, no evidence of hemodynamically significant coronary artery disease on coronary angiogram, and no other (non-coronary) cardiac abnormalities were included. Patients were followed for subsequent cardiac events and mortality. RESULTS: Over a 6-year period at our institution, acute coronary syndrome complicated by life-threatening cardiac arrhythmias developed in six patients who had no hemodynamically significant coronary artery disease with corresponding intra-coronary ergonovine provocative coronary vasospasm. Acute myocardial infarction was diagnosed in five of these patients and variant angina pectoris in one. Complete atrioventricular block was the most common complication in these cases, followed by cardiogenic shock with or without right ventricular infarction, ventricular fibrillation, and severe sinus arrest. These complications were corrected with intravenous fluid, intravenous atropine or cardiac defibrillation. During a median follow-up period of 26 months, none of the patients expired or suffered nonfatal reinfarction. Two individuals who did not stop smoking during follow-up developed recurrent angina after self-discontinuation of calcium antagonists. CONCLUSIONS: Coronary vasospasm can be a cause of life-threatening cardiac arrhythmias in patients with acute coronary syndrome and no hemodynamically significant coronary artery disease. Coronary angiography with/without intra-coronary ergonovine testing is necessary in acute coronary syndrome patients to identify the underlying pathology and establish appropriate treatment in these cases.
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Two cases presenting with episodes of marked ST segment elevation occurring with, but most often without, anginal pain are reported. The changes were recorded through continuous ECG monitoring during Prinzmetal's angina and in the course of myocardial infarction. Such transient asymptomatic ECG abnormalities reveal silent acute myocardial ischemia and are often unrecognized. However, they may lead to severe arrhythmias or myocardial infarction, and sudden deaths occurring in the course of ischemic heart disease are likely to be explained on this basis. Transient episodes of silent ST segment elevation similar to those occurring in Prinztal's angina have been reported in various circumstances. They bring into discussion the delimitations of variant angina pectoris.
The calcium channel blockers initially were approved for the treatment of classical and variant angina pectoris. Recent studies indicate that these agents also are useful in such diverse conditions as pulmonary and systemic hypertension, hypertrophic cardiomyopathy, arrhythmias, asthma, Raynaud's syndrome, esophageal spasm, myometrial hyperactivity, cerebral arterial spasm, and migraine.
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Knowledge of the pathophysiology of myocardial ischemia has been greatly enhanced recently by new information on coronary artery spasm. This phenomenon accounts for the mechanism underlying the attacks of resting chest pain in Prinzmetal's angina and plays a role in almost all aspects of ischemic heart disease. The diagnosis of coronary artery spasm can be made presumptively with noninvasive methods, but definitive documentation is usually obtained in the cardiac catheterization laboratory. The nitrate derivatives and the calcium antagonists provide a safe and effective approach to therapy.
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We evaluated the association between coronary spasm and hyperinsulinemia (high immunoreactive insulin, IRI) in patients with angina pectoris. The study cohort comprised 30 patients with spastic angina pectoris, 30 patients with angina pectoris showing fixed-obstructive coronary sclerosis and 30 control subjects who were matched for body mass index, age and sex. A 75-gram oral glucose test was performed, and blood sugar and IRI were serially measured concomitant with serum total cholesterol, triglyceride and HDL cholesterol. The IRI level at 60 min, the peak IRI during the test, sigma IRI and sigma IRI/sigma blood sugar were significantly higher in the patients than in the controls. Total cholesterol and LDL cholesterol levels were significantly increased in patients showing fixed-obstructive coronary sclerosis compared to controls.
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Dopamine is widely used for the treatment of cardiogenic and hypovolemic shock. This study was undertaken to compare the response to dopamine in epicardial conduit coronary arteries of humans, Japanese monkeys, and dogs, and to determine the mechanism of vasoconstriction and vasodilation. In helical strips of coronary arteries from humans and monkeys partially contracted with prostaglandin F2 alpha, dopamine produced a concentration-related contraction; the human artery contraction was greater. The contractions were reversed to a relaxation by treatment with phentolamine. Relaxation of monkey arteries treated with the alpha adrenoceptor antagonist was not influenced by metoprolol, a beta 1 antagonist, or endothelium denudation, but was reversed to contraction by SCH23390, a dopamine1 receptor antagonist. On the other hand, dog coronary arteries responded to dopamine with a relaxation that was abolished by metoprolol, but not influenced by SCH23390 or butoxamine, a beta 2 antagonist. We conclude that dopamine in clinical doses elicits significant contractions, mediated possibly by alpha adrenoceptors, in human and monkey coronary arteries; thus, care has to be taken when the amine is used in patients with variant angina pectoris. Relaxation of monkey coronary arteries appears to be associated with activation of dopamine1 receptors, whereas those of the dog arteries are mediated mainly by beta 1 receptors.
Nifedipine antagonises influx of calcium through cell membrane slow channels, and sustained release formulations of the calcium channel blocker have been shown to be effective in the treatment of mild to moderate hypertension and both stable and variant angina pectoris. Preliminary findings also indicate that these formulations are effective in the treatment of Raynaud's phenomenon and hypertension in pregnancy, and that they reduce the frequency of ischaemic episodes in some patients with silent myocardial ischaemia. The exact mechanism of action of nifedipine in all of these disorders has not been defined. However, its potent peripheral and coronary arterial dilator properties, together with improvements in oxygen supply/demand, are of particular importance. A major goal of sustained release therapy is to permit reductions in the frequency of nifedipine administration, preferably to once daily, and thus improve patient compliance. Two new once-daily formulations--the nifedipine gastrointestinal therapeutic system (GITS) and a fixed combination capsule comprising sustained release nifedipine 20 mg and atenolol 50 mg--have exhibited marked antihypertensive efficacy. The GITS preparation has also been used effectively in the treatment of stable angina pectoris, and both formulations appear to be well tolerated. Sustained release nifedipine formulations are generally better tolerated than their conventionally formulated counterparts, particularly with regard to reflex tachycardia. Adverse effects seem to be dose related, are mainly associated with the drug's potent vasodilatory action, and include headache, flushing and dizziness. Generally, these effects are mild to moderate in severity and transient, usually diminishing with continued treatment. Thus, sustained release nifedipine formulations are useful and established cardiovascular therapeutic agents which have demonstrable efficacy in various forms of angina, mild to moderate hypertension and Raynaud's phenomenon. Further, promising results shown by the nifedipine GITS formulation, with its advantage of once daily administration suggest that it is likely to become one of the preferred nifedipine formulations for the treatment of hypertension and the various forms of angina.
Since the registration of sumatriptan (Imigran) in May 1991, the Netherlands Centre for Monitoring of Adverse Reactions to Drugs received 13 reports of substernal chest tightness or pain attributed to its use. These concerned 11 women and two men with an average age of 41 years, who developed angina-like symptoms mostly within one hour after oral or subcutaneous administration. Electrocardiography (in three patients) and echocardiography (in one patient), performed after resolution of the symptoms, were normal. With the exception of one patient, none had experienced such symptoms before. Although sumatriptan is an effective anti-migrainous drug, cautious use is strongly advised. Sumatriptan is contraindicated in patients with coronary artery disease or variant angina pectoris.
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Nitro derivates are effective agents for the treatment of myocardial ischemia. The effectiveness of these compounds in anginal disease is due to their ability to induce dilatation of veins which results in decreased left and right ventricular and diastolic pressure. Furthermore nitro derivates also bring about coronary vasodilatation which is present also in conditions of stenosis of epicardial arteries. In these conditions either coronary flow increases or its redistribution is more favorable. As the vasodilatory effect of nitro derivates does not involve sound arterioles, no "theft" of blood occurs. The dilatation of veins induced by nitrates explains also their effectiveness in patients suffering from heart failure with high left ventricular pressure. Mononitrates seem more effective than dinitrates since variability problems due to hepatic metabolism disappear. Nitrate plasters do not appear favourable since they produce constant blood levels and therefore could favour the development of tolerance.
CCB are a diverse group of drugs that bind to specific glycoprotein receptors associated with the cell membrane that are most likely identical to the voltage-sensitive calcium channel. By inhibiting the influx of calcium into myocardial, pacemaker, and conducting tissues and vascular smooth muscle, these agents modify excitation-contraction coupling in muscle and electrical impulse transmission in the heart. The vasodilating and electrophysiologic actions of these drugs have been harnessed for the treatment of coronary vasospasm, angina pectoris, and supraventricular arrhythmias. They also have great potential for the treatment of hypertension, cerebrovascular disorders, and Raynaud's phenomenon. Their utility in hypertrophic cardiomyopathy, congestive heart failure, myocardial preservation, and primary pulmonary hypertension has not been convincingly established. Future second-generation CCB may offer greater selectivity, improved side effect profiles, and an even wider range of actions.
A total of 130 anginal patients were examined within 3 months after the onset of anginal attacks. Angina was stable (SA) in 100 patients and unstable (UA) in 30. There were no differences between SA and UA patients in terms of the degree and spread of coronary arterial stenoses. Signs of coronary arterial spasm were detected in 27 (20.8%) of 130 patients, being more frequent in UA (53%), as compared to SA (11%; p less than 0.001). Acute myocardial ischemia produced groups of ventricular extrasystoles more frequently than it did isolated extrasystoles in patients with recent angina (78.6% vs. 16.7%; p less than 0.001). Groups of ventricular extrasystoles were recorded more frequently in UA patients, as compared to SA ones (23.3% vs. 7%; p less than 0.05).