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PubMed1995

The evolving role of calcium channel blockers in the treatment of angina pectoris: focus on felodipine.

Calcium channel blockers are used extensively in the treatment of the three major anginal syndromes. In the treatment of Prinzmetal's angina, their antivasospastic properties account for their therapeutic effectiveness. Calcium channel blockers are drugs of first choice in this syndrome. In chronic stable angina, calcium channel blockers may be used as monotherapy or in combination with beta-blockers and/or nitrates. In patients with unstable angina, reduction in the incidence of ischemic episodes produced by calcium channel blockers is well documented. Recent data suggest that calcium channel blockers should generally be used in combination with beta-blockers, nitrates and antithrombotic agents. Patients with ischemic heart disease often exhibit reduced ventricular function. All of the first generation calcium channel blockers exacerbate symptoms in patients with established heart failure and may precipitate heart failure, particularly when combined with beta-blockers. Second generation vascular-selective dihydropyridines have been introduced recently. Vascular selectivity determines the drug's degree of negative inotropic effect. Felodipine is one of the most vascular selective of the available dihydropyridines and has no negative inotropic effects at clinically administered doses. In a long term study, felodipine, 20 mg/day, abolished symptoms and chronic ischemic episodes in 81% of treated subjects with Prinzmetal's angina. In patients with stable angina, felodipine has been found to be effective either as monotherapy or in combination with beta-blockers. In patients with known or suspected ventricular dysfunction, vascular-selective dihydropyridines such as felodipine offer advantages over the nonselective calcium channel blockers, particularly in patients receiving beta-blockers.

Adrenergic beta-Antagonists↗
PubMed1995

[Long-term prognosis in unstable angina].

The expression unstable angina pectoris covers a wide range of clinical symptoms with different pathogenetic mechanisms and clinical outcome. Several forms of unstable angina pectoris, in particular progressive angina pectoris (crescendo angina) with chest pain at rest in a previously asymptomatic patient, progressive angina pectoris with chest pain at rest in a previously symptomatic patient, and chest pain at rest of at least 15 min duration without obvious trigger mechanisms have been distinguished. In simpler terms: one may also distinguish angina pectoris of recent onset, crescendo angina, and acute coronary insufficiency. Four risk factors appear to determine the prognosis in these patients: exercise-induced angina pectoris, multiple episodes of chest pain before hospitalization, electrocardiographic changes, and recurrent angina pectoris during hospitalization. Acute coronary insufficiency and nontransmural infarction have initially better prognosis than transmural infarction; however, recurrent cardiac events are more frequent in patients with nontransmural infarction, particularly in the elderly with persistent ECG changes, cardiac decompensation, and infarct extension. Unstable angina pectoris and myocardial ischemia after myocardial infarction are generally associated with a poorer prognosis. In contrast, recurrence of angina pectoris after PTCA (within the first six months) is most commonly due to restenosis and hence prognostically not of great importance. Unstable angina pectoris after coronary bypass surgery, however, is a prognostically unfavourable sign. Prognosis in patients with Prinzmetal angina is determined by the extent of coronary disease. In summary, long-term prognosis in patients with unstable angina pectoris depends heavily on the clinical presentation and the previous clinical history of the patient.

Angina Pectoris, Variant↗
PubMed1994

[Endothelin--an important factor in coronary heart disease].

The peptide hormone endothelin was initially discovered in endothelial cells. However, it has recently been shown that endothelin is produced by cardiomyocytes too. Endothelin is the most potent of all known vasoconstrictors. The coronary circulation is highly sensitive to endothelin, and intracoronary infusion may lead to lethal coronary spasm. Patients with variant angina pectoris have a higher plasma concentration of endothelin. Moreover, exposure to cold leads to a further increase in endothelin. Therefore increased production of endothelin may be an important mediator of vasospasm. Acute myocardial infarction is followed by an increase in circulating endothelin. Remaining high endothelin levels after myocardial infarction are associated with poor prognosis. Cardiomyocytes increase their production of endothelin during ischemia, and this increase may be harmful, either through an effect on the coronary circulation or by acting directly on the cardiomyocytes. Blockade of endothelin receptors has been shown to reduce the size of an infarction. Thus, intense research is directed towards discovering therapeutical agents that either inhibit production or block the effects of endothelin. Recently, an orally active endothelin receptor antagonist was discovered, and clinically useful therapeutical agents will most probably be available in the near future.

Coronary Circulation↗
PubMed1993

[Diagnosis of the dynamic lesion].

Rupture of atheromatous plaques, thrombosis and spastic contractions cause dynamic lesions in coronary arteries. This review focuses on the diagnostic approach to vasospastic lesions. Our current knowledge considers vasospastic angina as a--most likely--localized disease of the vascular smooth muscle, which occurs in nonatherosclerotic as well as in atherosclerotic segments. Currently the diagnosis can only be proven by functional tests under angiographical control. Since the pathophysiological mechanisms leading to vasospasm remain unclear, only empirically developed pharmacological tests are available. The use of ergonovine alkaloids is well established, the feasibility of acetylcholine is under investigation. The reproducibility regarding the course of the disease and the localization of the lesion has not yet been determined. The necessity to state the diagnosis is given by the improved prognosis of the disease under effective therapy with calcium channel blockers and nitrates.

Acetylcholine↗
PubMed1998

[Characteristics of spasm-induced vessels in patients with vasospastic angina and a history of syncope].

One hundred and eighty-seven consecutive patients with vasospastic angina and coronary spasm provoked by intracoronary injection of acetylcholine and/or ergonovine were treated from January 1991 to June 1997. Fifteen of these patients, 14 men and one woman (mean age of 63 years old), had a history of syncope. There were no significant differences in the distribution of induced spasm vessels, single spasm vs multiple spasms, variant angina pectoris and organic stenosis (< 75%) between patients with and without a history of syncope. There were no significant differences concerning the distribution of the sites of induced spasm in the circumflex artery and left anterior descending artery between the two groups. However, coronary spasm in the proximal portion of the right coronary artery (segment 1 or 2 according to the functional classification of American Heart Association) occurred more frequently in patients with a history of syncope [80.0% (12/15) vs 45.3% (78/172); p < 0.05]. Twelve of the 96 patients with coronary spasm in the proximal portion of the right coronary artery had a history of syncope, so these patients require careful management.

Acetylcholine↗
PubMed1991

Comparison of epicardial coronary artery tone and reactivity in Prinzmetal's variant angina and chronic stable angina pectoris.

It has been suggested that a generalized coronary vasomotion disorder is present in variant angina and that evaluation of baseline coronary artery tone may be useful for predicting the occurrence of coronary artery spasm. The vasomotor response of angiographically normal proximal and distal coronary artery segments was studied in 9 patients with atypical chest pain and normal coronary arteriograms (control group), 13 patients with active variant angina and 41 patients with chronic stable angina. Ergonovine (intravenous, 100 to 300 micrograms, or intracoronary, 8 to 20 micrograms, was administered to all 22 patients in the control and variant angina groups and to 11 of the 41 patients with chronic stable angina. All patients also received intracoronary isosorbide dinitrate (1 to 2 mg). Computerized coronary artery diameter measurement of angiographically normal segments was carried out before and after ergonovine and nitrate administration. Mean baseline intraluminal diameter of proximal and distal coronary segments was not significantly different in control patients and those with variant angina (nonspastic segments only) or coronary artery disease (proximal 2.89 +/- 0.15, 2.83 +/- 0.14 and 2.82 +/- 0.09 mm; distal 1.60 +/- 0.08, 1.63 +/- 0.07 and 1.62 +/- 0.06 mm, respectively). After ergonovine, proximal segments constricted by 10 +/- 2%, 15 +/- 3% and 11 +/- 4% and distal segments by 11 +/- 3%, 11 +/- 2% and 14 +/- 3% in control, variant angina and coronary artery disease groups, respectively (p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Clinical significance of coronary artery calcification.

Coronary artery calcification (CAC) was easily demonstrated by plain CT-scan. The aim of this study was to clarify the clinical significance of CAC in cardiovascular diseases. The subjects were 90 patients with ischemic heart disease (30 myocardial infarction, 50 exertional angina pectoris and 10 variant form of angina pectoris; 46 males and 44 females, 68 +/- 10 y/o) and 50 patients without ischemic heart diseases (30 hypertension, 10 arrhythmia, 3 valvular disease, 2 cardiomyopathy, 2 congenital heart disease and 3 others; 25 males and 25 females 65 +/- 9 y/o). CAC and calcification of thoracic aorta were evaluated by plain CT-scan (1 second scan time and 5 mm slice). The relationship between CAC and other clinical features (age, sex, hypertension, diabetes mellitus, hyperlipidemia, smoking, resting ECG, exercise stress ECG, aortic calcification and optic fundi) were studied. CAC were seen more frequently in patients with ischemic heart disease (63%), old age (67%), aortic calcification (70%) and positive exercise testing (64%). On the other hand, CAC were rare in variant angina (30%). In younger patients (under 70 y/o), CAC were seen more frequently in diabetic patients. But, in older patients, CAC were frequently in those with hyperlipidemia. These results suggested that CAC was associated with not only systemic arteriosclerosis, but also ischemic heart disease, except vasospastic angina. The prognostic value of CAC would be studied later.

Age Factors↗
PubMed1983

A case of variant angina and myocardial infarction 6 months after successful bypass surgery.

A 61-year-old man with variant angina underwent bypass surgery to the left anterior descending artery (LAD) which had a 90% narrowing in the proximal segment. The postoperative course was favorable, but 6 months after surgery, the calcium antagonist, diltiazem, with which the patient had been continuously treated since surgery, was stopped because of hepatitis. Immediately after discontinuation of the calcium antagonist, the patient had an acute anterior myocardial infarction. An angiogram demonstrated a patent graft and an anteroapical infarction. The infarction is thought to have been caused by a severe, prolonged spasm of the LAD distal to the graft or diffuse spasm of the LAD throughout its entire length. Thus, after bypass surgery calcium antagonists should be given continuously to patients with variant forms of angina pectoris.

Angina Pectoris, Variant↗