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Results for “Angina Pectoris, Variant”

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PubMed1986

Phasic contractions of canine and human coronary arteries induced by potassium channel blockers.

To gain insight into mechanisms underlying phasic coronary vasospasm in patients with variant angina pectoris, we studied whether phasic contractions could be induced in isolated canine and human coronary arteries by agents which block potassium channels. Phasic contractions of canine coronary arteries were always induced by 3,4-diaminopyridine (10(-2) M) and less frequently by 4-aminopyridine (10(-2) M). These agents also caused phasic contractions in human, swine and monkey coronary arteries and in canine basilar, carotid, renal and femoral arteries. The cycle length of phasic coronary contractions ranged from 30 sec to 1 hour, and the developed tension was 2.5 times greater than for potassium contractions. The contractions continued for more than 11 hours. Morphologically, perinuclear vacuolization, a characteristic change of vasospasm, appeared in the coronary smooth muscles. The phasic contractions were not eliminated by tetrodotoxin, atropine, phentolamine or yohimbine, but they were eliminated by nicorandil which activates potassium channels and nifedipine which blocks slow calcium channels. The results indicate that potassium channel blockers can induce phasic arterial contractions.

4-Aminopyridine↗

PubMed1992

[Noninvasive diagnosis of coronary spasm].

The objective of this work was to compare the sensitivity of non-invasive tests used for the diagnosis of variant angina pectoris (VAP). In a group of 38 patients with VAP the authors compare the sensitivity of the cold test (CT), hyperventilation test (HT), handgrip (HG), bicycle ergometry (BE) and a newly suggested combination of hyperventilation with HG and BE resp. The authors evaluated first the sensitivity of ST elevations which are an entirely specific sign and in particular denivelization of ST (by depression or elevation) which is a less specific sign. The sensitivity of different tests was as follows: CT 5% and 5% resp., HT 18% and 39% resp., HG 13% and 29% resp., BE 26% and 66% resp., HV+HG 37% and 63% resp., HV+BE 50% and 87% resp. Then the authors assessed the sensitivity of repeated examinations HV+HG 47% and evaluation during denivelization of ST 63%, HV+BE 66% and 89% resp. The authors evaluated moreover the sensitivity of ST elevations in patients according to the activity of the disease. Patients with at least five stenocardias per week had a higher sensitivity, as compared with patients with less frequent attacks: HV+HG 42% and 25% resp., HV+BE 60% and 33% resp. The highest sensitivity was found in a combination of HV+BE. Repetition of the test in case of a negative result increased markedly the sensitivity, a higher sensitivity was found also in patients with more frequent stenocardias.

Adult↗

PubMed1986

When are arrhythmias and conduction disturbances markers of myocardial ischemia at rest?

Myocardial ischemia, particularly when transmural as in variant angina pectoris, may be associated with ventricular tachycardia, ventricular fibrillation and paroxysmal atrioventricular block (15%). Syncope (7%) and sudden death (3%) due to these malignant arrhythmias are sometimes a unique marker of myocardial ischemia. Two-hundred fifty-four patients (220 males and 34 females), aged 5 +/- 9 years with transmural myocardial ischemia related to coronary artery spasm, were studied. Particular attention was paid to the role of syncopal attacks as unique clinical manifestation of silent ischemia. Patients examined were divided into 3 Groups. Group 1 includes 5/254 (2%) patients with atrial fibrillation during acute ischemia. Group 2 was divided into four subgroups: subgroup A includes 17/254 (7%) patients with syncopal attacks due to malignant arrhythmias (ventricular tachycardia and advanced A-V block); subgroup B, 15/254 (6%) patients with documented malignant arrhythmias, without syncopal attacks; subgroup C, 7/254 (3%) with ventricular fibrillation during acute ischemia and subgroup D, 18/254 (7%) patients with history of syncopal attacks without documented arrhythmias during hospital observation. Group 3 includes 17/254 (7%) patients with left anterior hemiblock in basal condition, 7/254 (3%) patients with left anterior hemiblock and one left posterior hemiblock during acute ischemia and one patient with right bundle branch block during acute ischemia. Syncopal symptoms are present in many of these cases of angina pectoris; paroxysmal A-V block is documented in nearly half of the cases with syncope (65%); ventricular tachycardia is frequently demonstrated during ischemia but leads to syncope in only a few cases; patients with syncope do not present specific clinical features.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris, Variant↗

PubMed1981

The role of coronary arterial spasm in ischemic heart disease.

With the arteriographic demonstration of coronary arterial spasm, fundamental questions have been raised concerning the role of spasm in myocardial ischemia and infarction. It is now clear that coronary arterial spasm is the cause of Prinzmetal's variant angina pectoris in patients with and without coronary atherosclerosis. In most patients with coronary heart disease, major ischemic events frequently result from increased myocardial oxygen demand or coronary thrombosis. However, recent evidence suggests that coronary arterial spasm may initiate or contribute to the development of unstable angina pectoris, acute myocardial infarction, and sudden death in these patients. Thus, episodes of myocardial ischemia and infarction are induced by factors, acting singly or in combination, that augment myocardial oxygen demand or diminish myocardial oxygen supply, and the latter alteration can result from thrombotic coronary occlusion or a dynamic increase in coronary arterial tone (that is, coronary arterial spasm).

Angina Pectoris↗

PubMed1991

A new strategy for the reduction of acute myocardial infarction in variant angina.

To study the effects of stepwise early treatment in variant angina pectoris, frequencies of cardiac events and complications were examined after three different types of treatment. The subjects of the study consisted of 159 consecutive patients with variant angina pectoris, who were in need of hospitalization. The three treatment modalities were the introduction of calcium antagonists, nicorandil and nitroglycerin infusion, and percutaneous transluminal coronary angioplasty (PTCA), respectively. The cardiac event rate for this series of patients was 16% (25 of 159). The cumulative cardiac event rate was 22% at 1 year and 23% at 3 years in the first treatment period; 11% at the same intervals in the second treatment period; and 6% at the same intervals in the third treatment period. Our results suggest that it is important in the treatment of variant angina pectoris not only to prevent anginal attacks by the use of fast-acting coronary vasodilators, but also to initiate early revascularization.

Adult↗

PubMed1979

Altered adrenergic activity in coronary arterial spasm: insight into mechanism based on study of coronary hemodynamics and the electrocardiogram.

To elucidate the pathophysiologic mechanism of coronary arterial spasm, the hypothesis was examined that underlying alterations in sympathetic activity may account for this syndrome in some patients. Observations were directed to alterations in coronary arterial hemodynamics and the electrocardiogram. Spasm of the left anterior descending coronary artery produced a mean increase in coronary vascular resistance of 107 percent (P less than 0.05) in four patients in whom coronary sinus blood flow was measured with the thermodilution technique. The alpha adrenergic blocking agent phentolamine, given intravenously, acutely reversed coronary spasm and its clinical manifestations in eight patients and reduced coronary resistance. In four patients, administration of the long-acting oral alpha blocking agent phenoxybenzamine (20 to 80 mg/day) caused disappearance of symptoms during a follow-up period of 3 to 12 months. Transient prolongation of the corrected Q-T interval preceded spontaneous or ergonovine maleate-provoked coronary spasm in 11 patients with variant angina pectoris, whereas no significant change in the Q-T interval followed ergonovine administration in 27 control patients with atypical chest pain who did not have coronary spasm. T wave inversions in the resting electrocardiogram were normalized by isoproterenol infusion in one patient and by long-term phenoxybenzamine treatment in four patients with variant angina pectoris. These Q-T and T wave changes are analogous to those described with unilateral or asymmetric stellate ganglion stimulation in animals. These observations suggest that alterations in the sympathetic nervous system that are consistent with asymmetric stellate ganglion activity and transient alpha adrenergic receptor stimulation can presage the development of coronary arterial spasm in some patients with variant angina pectoris.

Adult↗

PubMed1989

[Vasospastic angina pectoris].

The authors discuss the pathogenesis and treatment of variant angina pectoris, and illustrate the condition by describing nine cases. Alertness for the presence of coronary spasms is recommended, and also the more frequent use of provocative diagnostic tests.

Angina Pectoris, Variant↗

PubMed1979

Inhibition of constrictor responses of dog coronary artery by atropine. A possible effectiveness of atropine on variant form of angina pectoris.

A possible effectiveness of atropine on variant form of angina pectoris was investigated using the left circumflex coronary arterial strips of dogs. Acetylcholine 10(-5)--10(-3) Gm/ml dose-dependently constricted the isolated arterial strips during potassium-contracture in 6 cases, and repetitive applications of acetylcholine could produce the similar contractions to the control. In 18 strips atropine 10(-6) Gm/ml significantly depressed the contractions of coronary arteries induced by acetylcholine 10(-5)--10(-3) Gm/ml. In 5 arterial strips atropine 10(-6) Gm/ml significantly inhibited norepinephrine-induced responses of these arteries, and by 10(-5) Gm/ml further suppression of the responses was obtained. The results suggest that atropine may suppress the contractile responses of the coronary artery induce by acetylcholine and nonrepinephrine through a muscarinic-receptor blocking action and simultaneously partly through an adrenergic alpha-receptor blocking action.

Acetylcholine↗

PubMed2002

Denopamine, a selective beta1-receptor agonist and a new coronary vasodilator.

Up until now, it has been suggested that nitrate and/or calcium channel blockers were effective against variant angina pectoris. On the other hand, it is known that about 20% of variant angina pectoris was refractory to both nitrate and calcium channel blockers. In Japan, it has been reported that denopamine, which is an oral beta1-adrenoceptor selective agonist developed by the Japanese pharmaceutical industry (Tanabe Seiyaku), is effective in those refractory cases. To date, in Japan nine cases have been recognized of patients with vasospastic angina pectoris whose symptoms were relieved by taking denopamine, including one case in which the author has had personal experience. Eight of these nine cases were refractory, and were not relieved by combined therapy using both nitrate and a calcium channel blocker. It was also documented that denopamine was effective in cases where attacks were not relieved by prazosin or magnesium, which have been documented as effective in other refractory cases. In a study of canine coronary arteries, localization of beta-adrenoceptor subtypes was documented, with the beta1-adrenoceptor predominantly found in the conduit coronary artery. In recent years it has been emphasized that the principal role of sympathetic nerves was not associated with the constrictive action of alpha-adrenoceptors, but with the coronary dilative action of beta-adrenoceptors. It would therefore be worthwhile to determine whether denopamine is able to relieve vasospastic angina pectoris in many more cases.

Adrenergic beta-Agonists↗

PubMed1976

Prinzmetal's angina pectoris with normal coronary arteriograms.

Four cases of variant angina pectoris with normal findings on coronary arteriogram were experienced. The facts may show that the existence of serious arteriosclerotic lesions in a major branch of coronary artery as pointed out by Prinzmetal is at least not essential for the occurrence of anginal attack in the present disease. But the finding that age and sex distribution of variant angina was nearly the same as that of effort angina seems to still indicate the possibility that arteriosclerotic lesion somehow participates in the mechanism of occurrence of the present disease.

Adult↗

PubMed1959