Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Angina Pectoris, Variant”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 703 records · Page 39Linked to original sources
PubMed1990

[Variant (Prinzmetal's) angina with diffuse coronary spasm without coronary sclerosis].

A 49-year-old man developed, over a period of three years, progressively more frequent nocturnal attacks of angina and palpitations. Exercise electrocardiogram was negative. 24-hour Holter monitoring revealed ventricular extrasystoles and tachycardia with ST segment elevations. The dominant left coronary artery, which was free of atherotic changes, went into diffuse spasm after ergonovine administration, accompanied by angina and ventricular extrasystoles. Registration of spontaneous ischaemia confirmed the diagnosis of variant (Prinzmetal) angina. Administration of twice daily 90 mg diltiazem retard and once daily 120 mg isosorbide dinitrate retard at night ended the spasms and with it the attacks of angina and the arrhythmias. This case illustrates that typical angina and ventricular tachyarrhythmias can be caused by spontaneous coronary spasms, even in the presence of normal exercise ECGs and coronary angiograms. If coronary artery spasms are not detectable by ECG, the ergonovine test may further the diagnosis.

Angina Pectoris, Variant↗
PubMed1990

Behavior of right and left ventricles during episodes of variant angina in relation to the site of coronary vasospasm.

The effects of single-vessel coronary occlusion on simultaneously evaluated right (RV) and left ventricular (LV) performance were assessed and compared with LV perfusion patterns in 25 patients with variant angina. Coronary spasm involved the right coronary artery in 15 patients (group 1) and the left anterior descending coronary artery in 10 patients (group 2). Biventricular function was assessed by radionuclide angiography under basal conditions, during spontaneous or ergonovine-induced ischemia, and after resolution of the ischemic attack. Myocardial perfusion was assessed by thallium 201 scintigraphy in 21 patients of this series during superimposable ischemic episodes. In group 1, ischemia caused RV (14 of 15 patients) and LV (13 of 15 patients) regional dysfunction with significant reduction in RV and LV ejection fractions. The interventricular spetum was involved in six of 15 patients, causing a more pronounced LV impairment. In group 2, all patients showed septal dyssynergies associated with a reduction of LV ejection fraction; absent or trivial RV involvement was observed. In both groups, LV perfusion defects were present in all patients with LV wall motion abnormalities during ischemia, matching the site of regional dyssynergies. Thus, in a group of patients with variant angina and single-vessel disease, transient occlusion of the right coronary artery directly caused RV and LV impairment; in these patients, the extent of LV but not RV dysfunction appeared related to the presence of septal ischemia. Vasospasm of the left anterior descending coronary artery consistently caused LV dysfunction not associated with secondary effects on RV systolic function.

Angina Pectoris, Variant↗
PubMed1999

Circadian distribution of ischemic attacks and ischemia-related ventricular arrhythmias in patients with variant angina.

BACKGROUND: There are limited data about the circadian distribution of ischemic episodes in patients with variant angina. Furthermore, no previous study investigated whether ischemia-related ventricular arrhythmias follow a circadian variation in these patients. METHODS: The circadian variation of transient ischemia and ischemia-induced ventricular arrhythmias was assessed by cosinor methodology on 24-hour Holter recordings of 26 patients with variant angina. RESULTS: On the whole, 301 ischemic episodes were detected in the population, with premature ventricular complexes occurring in 49 of them (16%). Ischemic episodes followed a typical circadian variation (acrophase hr 02:36, p < 0.01) in the total sample. However, a significant circadian variation of ischemic episodes was detectable in the 14 patients without (n = 167, acrophase hr 04:00, p < 0.0001), but not in the 12 patients with (n = 134, p = 0.14) hemodynamically significant coronary stenoses, independently of the location (anterior/inferior) of ischemia. There was no significant circadian variation of ischemia-related ventricular arrhythmias. CONCLUSIONS: Among patients with variant angina, a clearcut circadian variation of ischemia is present in those without, but not in those with, hemodynamically significant coronary artery stenoses, thus suggesting that different pathophysiologic mechanisms may operate, at least in part, in triggering coronary spasm in these two subgroups of patients. There was no significant circadian variation of ischemia-related ventricular arrhythmias in these patients.

Angina Pectoris, Variant↗
PubMed1989

[Surgical treatment of variant angina. Apropos of a clinical case].

A case of a male 66 years-old patient who presented with a clinical picture of Prinzmetal's variant angina early in the evolution of an acute myocardial infarction is reported. Transient elevation of ST-segment was documented on Holter monitoring in association with angina at rest as well as asymptomatic episodes of ST-segment changes. Significant two-vessels obstructive lesions (left anterior descending and circumflex arteries) was present. As variant angina had several recurrences in spite of medical therapy with nitrates and calcium antagonists, the patient was submitted to coronary by-pass surgery associated to plexectomy. A Thallium myocardial scintigraphy suggests that a peroperative infarction had occurred. The patient was asymptomatic at six months follow-up.

Aged↗
PubMed1984

Transient predominant right ventricular ischemia caused by coronary vasospasm.

This study describes the clinical experience with four patients with variant angina caused by spasm of the right coronary artery who were assessed for evidence of right ventricular involvement. The patients were suspected of having predominant right ventricular ischemia on the basis of normal thallium-201 scans, left ventricular ejection fraction, regional wall motion assessed by equilibrium radionuclide angiography (RNA), two-dimensional echocardiographic findings, and left ventricular hemodynamics; all procedures were performed during transient ST segment elevation in the inferior leads. Right ventricular ischemia was documented in four patients by first-pass radionuclide studies and phase analysis of RNA, and in three patients by simultaneous right and left hemodynamic monitoring. The clinical findings from these four patients are compared with those from four other patients with similar electrocardiographic changes, coronary anatomic distribution, and documented right coronary spasm but with evidence of left ventricular involvement as documented by abnormal thallium-201 scintigraphy, RNA, two-dimensional echocardiography, and left hemodynamics during ischemic episodes. Although preliminary, these data indicate the existence of prevalent right ventricular ischemia during variant angina caused by right coronary vasospasm. This condition should be suspected whenever typical anginal symptoms and/or ischemic electrocardiographic changes are accompanied by normal thallium-201 scintigraphic findings and/or normal left ventricular function as assessed by RNA, echocardiography, and left hemodynamic monitoring. Among noninvasive procedures, first-pass radionuclide study and phase analysis of RNA represent suitable techniques for detecting transient right ventricular dysfunction.

Angina Pectoris, Variant↗
PubMed1986

Significance of the walk-through angina phenomenon during exercise testing.

Out of 3,900 patients who performed an exercise test at our clinic, 3 patients demonstrated a walk-through phenomenon (WTP), defined as the occurrence of mild angina during the first stages of exercise with disappearance of chest pain at higher workloads despite a greater pressure-rate product. 2 patients had variant angina, one with normal coronary arteries and the other with single vessel disease, while the third patient had stable exertional angina and a severe coronary artery disease with occlusion of two major vessels retrogradely filled by collateral channels. Repeat exercise tests failed to reproduce constantly the WTP in the 2 patients with variant angina, while in the third patient the phenomenon was repeatedly induced by exercise testing. Thus the WTP, although rarely found during exercise testing, can be observed in two subsets of patients. In variant angina the WTP is not reproducible and is probably due to coronary spasm, spontaneously subsiding during exercise. In patients with exertional angina and severe coronary artery disease, the WTP can be repeatedly observed during exercise and is likely to be secondary to a delayed vasodilation of collateral vessels. The clinical characteristics of the patients and the response to repeat exercise tests may be useful in identifying the different pathogenetic mechanisms.

Adult↗
PubMed1981

[Myocardial infarction in hyperthyroidism (author's transl)].

Three patients with untreated hyperthyroidism at the time of admission are reported. Two of them were young women with myocardial infarction and no significant lesions of the coronary arteries, and the third was a male with a prior history of Prinzmetal's variant angina with ventricular fibrillation. Emphasis is made on the fact that the association of hyperthyroidism and ischemic cardiomyopathy is well known but infrequent. Finally, a comment is made on the possible mechanisms of occlusion of a coronary artery in this situation, namely vasospasm, embolism with later recanalization, or the direct effect of thyroid hormones on the factors determining myocardial oxygen consumption.

Adult↗
PubMed1984

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications.

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)

Angina Pectoris, Variant↗
PubMed1994

Gianturco-Roubin stent placement for variant angina refractory to medical treatment.

A 43-yr-old man with mild, fixed obstruction of the left anterior descending (LAD) coronary artery and severe, uncontrolled variant angina underwent placement of an endovascular stent to preserve patency of the artery. The decision for stent placement was based on several factors, including refractoriness to medical treatment and standard balloon angioplasty, documented spasm localized to the proximal LAD lesion, and the morbidity, mortality, and costs associated with the surgical approach in this type of patient. At follow-up, there was moderate restenosis of the stented coronary segment; the vasospastic angina syndrome had totally resolved.

Adult↗
PubMed1982

Action of intracoronary nitroglycerin in refractory coronary artery spasm.

Coronary artery spasm usually responds to sublingual nitroglycerin. This report describes four patients with variant angina and one patient with rest angina who had coronary spasm that was refractory to sublingual or i.v. nitroglycerin. In four patients, spasm occurred spontaneous and in one patient after 0.05 mg of ergonovine. In each case, 25-100 micrograms of intracoronary nitroglycerin promptly (30-45 seconds) resulted in reopacification of the vessel involved in spasm and resolution of evidence for ischemia. Thus, intracoronary nitroglycerin can reverse coronary artery spasm that does not respond to systemic nitroglycerin administration.

Adult↗
PubMed1983

Clinical value of calcium antagonists in treatment of cardiovascular disorders.

All calcium antagonists have the ability to decrease the symptoms and signs in some patients with ischemic heart disease and help lower the blood pressure in hypertensive persons, but in clinical doses nifedipine does not exhibit antiarrhythmic properties, although these are an important part of the action of verapamil, diltiazem and some substances with a similar chemical structure. In certain disorders beta-adrenergic blocking drugs are useful adjuncts, and under some circumstances, particularly variant angina and supraventricular arrhythmias, specific calcium antagonists are the drugs of choice. More data are needed to define the role of calcium antagonists during cardiopulmonary bypass, in the protection of the ischemic myocardium, in the management of hypertrophic cardiomyopathy and in specific cases of primary pulmonary hypertension. When used with an appropriate sense of perspective and careful observation, calcium antagonists provide useful additional means of helping selected patients suffering from particular cardiovascular diseases.

Adrenergic beta-Antagonists↗
PubMed1977

Onset of Prinzmetal's angina two years following sudden death syndrome survival.

A patient who was resuscitated after an episode of ventricular fibrillation without myocardial infarction outside the hospital developed angina for the first time two years later. Although the clinical pattern did not fulfill all of the criteria of Prinzmetal's variant angina and was found to correspond with episodes of ventricular tachycardia, we feel that Prinzmetal's angina can be implicated as the mechanism of previos ventricular fibrillation. During the patient's second hospitalization, angiography demonstrated a single, moderately stenotic, right coronary lesion which was bypassed. Immediately postoperatively, the patient developed ventricular fibrillation requiring more than two hours of cardiopulmonary resuscitation. Six months after bypass surgery, she experienced an inferior wall myocardial infarction. She is presently asymptomatic with normal heart size.

Angina Pectoris↗
PubMed1982

Limitations of ergonovine testing in patients with variant angina.

Fourteen patients with variant angina underwent ergonovine testing during diagnostic coronary angiography. The clinical electrocardiographic or angiographic manifestations of coronary artery spasm could not be reproduced in six of these patients. Five patients had chest pain and transient ST-segment elevation within 4 days of the ergonovine study, including three who developed coronary spasm in the catheterization laboratory. It appears that the sensitivity of ergonovine testing in the diagnosis of coronary spasm is lower than previously emphasized.

Adult↗
PubMed1986

Increasing pre-excitation ("concertina effect") during vasospastic angina.

A patient with Wolff-Parkinson-White syndrome and variant angina developed progressive ST-segment elevation in the inferior leads after hyperventilation-induced right coronary artery spasm. At the same time, increasing pre-excitation ("concertina effect") developed with gradual prolongation of the AH interval on His bundle ECG. The ECG changes promptly disappeared after sublingual nitroglycerin, with termination of the chest pain. Transient ischemia induced by coronary artery spasm can be an etiology of increasing pre-excitation.

Angina Pectoris, Variant↗
PubMed1980

Refractory variant angina controlled with combined drug therapy in a patient with a single coronary artery.

A young man with a single left coronary artery and refractory variant angina is described. Spontaneous coronary artery spasm developed during coronary arteriography at the site of a 50% fixed left anterior descending coronary artery stenosis. Frequent episodes of rest angina with transient ST segment elevation persisted in hospital in spite of treatment with three different calcium antagonist drugs. Symptoms disappeared only when the combination of nifedipine, diltiazem, isosorbide dinitrate, and nitroglycerin ointment were given. Ergonovine testing was used to objectively assess the response to treatment.

Adult↗
PubMed2002

Coronary vasospasm and aborted sudden death treated with an implantable defibrillator and stenting.

In selected patients suffering from variant angina, an implantable cardioverter-defibrillator (ICD) and coronary stenting can be helpful to prevent sudden death and treat coronary artery spasm. We report a case of a 47-year-old woman suffering from variant angina, who experienced an episode of ventricular fibrillation promptly cardioverted. After coronary angiography documentation of a mild atherosclerosis, an ICD was implanted and oral nitrates and calcium antagonists were prescribed. The recurrence of chest pain and palpitations prompted us to perform a second coronary angiography that documented a focal coronary artery spasm successfully treated with stent implantation. No other episodes of angina or ventricular arrhythmia were documented during the following 6 months of follow-up.

Angina Pectoris, Variant↗
PubMed1982

[Surgical treatment of Prinzmetal variant angina. Coronary artery by pass and plexectomy (author's transl)].

Aorto-coronary by pass, widely accepted in the treatment of patients with coronary artery disease is still controversial in the treatment of Prinzmetal variant angina. Recurrence of attacks, occlusion of grafts and post-operative infarction were frequent by described and seem to be related with the persistence of coronary spasm. Authors propose the association of myocardial revascularization and coronary denervation by resection of periaortic plexi. Results of 50 surgical plexectomies associated with coronary by pass appear far better than by pass alone (mortality 4%, myocardial necrosis 4%, persistence of attacks 4%).

Adult↗
PubMed1980

Increase in R-wave amplitude during transient epicardial injury (Prinzmetal type).

An increase in QRS amplitude with S-T elevation occurs during the acute phase of myocardial infarction, coronary ligation and variant angina. Ischemic conduction delay, postulated as the cause, has not been well characterized. Six patients with transient chest pain, S-T elevation and increase in R-wave voltage also displayed concomitant shift of the frontal QRS axis toward the locus of injury. Electrocardiographic considerations suggest that regional ischemic block, not true hemiblock as has been suggested, offers the most inclusive explanation, providing previously neglected clinical confirmation of experimental observations.

Adult↗