PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Angina Pectoris, Variant”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 1,603 records · Page 89Linked to original sources
PubMed1980

[Mid-systolic click syndrome, coronary spasm and sudden death. General review apropos of a tracing from terminal Prinzmetal's angina, recorded by the Holter method].

The authors review the literature on arrhythmias and ST changes, the principal causes of sudden death in the mid systolic click-late systolic murmur (SC-SM) syndrome, having recorded the ECG during sudden death of a patient with this syndrome by Holter monitoring. This would also appear to be the first reported case of sudden death recorded by this technique. It showed that death was caused by ventricular fibrillation which was preceded by a clinical and electrical episode of Prinzmetal angina. Hypotheses explaining the abnormalities of ventricular repolarisation and rhythm in so-called "idiopathic" SC-SM syndrome are reviewed. Special attention is paid to studies suggesting the participation of coronary spasm and autonomic nervous system disturbances. In conclusion, the authors underline: - the value of ambulatory electrocardiography in patients with the SC-SM syndrome and especially in a defined high risk group; - the value of testing for coronary spasm when coronary angiography is envisaged; - the need for better management with antiarrhythmic therapy. The indications of betablockade are discussed as these drugs are thought to favourise coronary spasm.

Angina Pectoris↗
PubMed1980

[Induced coronary spasm: immediate revascularization by the opposite coronary artery. Use of myocardial scintigraphy].

The case reported analyses the instantaneous revascularisation distal to a coronary spasm by electrocardiography and thallium scintigraphy. The patient, a 48 year old man, had an 18 months history of spontaneous anginal chest pain sensitive to trinitrin. No electrocardiogrammes had been recorded during an attack. Coronary angiography was normal apart from a slight reduction in calibre of a dominant right coronary artery. Injection of 0.4 mg methylergometrine provoked an occlusive spasm of this artery after 4 minutes. At the same time the patient experienced angina and 4,5 mm depression of the ST segment, without ST changes in D3 and AVF, was observed. Opacification of the left coronary artery during spasme of the right showed retrograde revascularisation of the posterior interventricular artery which was reversed when the coronary spasm was terminated with trinitrin. Thallium scintigraphy was performed during another spasm provocation test four days later which gave identical clinical and electrical changes. A zone of hypofixation with blurred limits over the inferior myocardial wall was demonstrated. In the absence of ST elevation and of lacuna on myocardial scanning, the myocardial ischaemia induced by this occlusive spasm could not be considered to be total. Therefore the immediate revascularisation of the coronary artery in spasm seemed to have played the role of an effective collateral circulation.

Angina Pectoris↗
PubMed1981

[Apropos of a case of idiopathic cryoagglutininemia with cryoglobulinemia and bone marrow lymphoplasmacytoid infiltration].

A case of idiopathic cryoagglutininaemia, with cryoglobulinaemia and lymphoplasmacytoid infiltration of the bone marrow is reported. The case is not held to be an independent clinical entity but an aspect of immunoproliferative disease, similar to Waldenstrom's disease. An association of steroids in high doses and cyclophosphamide led to a definite improvement in the clinical and haematological picture and this has continued for the past 4 years with little or no treatment.

Anemia, Hemolytic, Autoimmune↗
PubMed1982

Coronary arterial spasm.

Coronary arterial spasm has been postulated to be a cause of myocardial ischemia for over 100 years. It was not until the work of Prinzmetal et al in 1959, however, that major clinical attention and research began to be addressed to the role of vasospasm in the manifestations of ischemic heart disease. It is now known that spasm may be clinically important in patients with significant underlying atherosclerotic coronary artery disease as well as in patients with anatomically normal or subcritically stenosed coronary vessels. Research has suggested that spasm may be associated with symptoms of stable resting and/or exertional angina pectoris and that it almost certainly plays a role in the pathogenesis of unstable angina pectoris and acute myocardial infarction. Symptomatic arrhythmias, including sinus bradycardia, heart block, and ventricular tachyarrhythmias, have been documented to complicate coronary vasospasm. Given the potential importance of coronary arterial spasm in so many different ischemic heart disease syndromes, the development of therapeutic agents that may prevent spasm has obvious clinical importance.

Adult↗
PubMed1982

Management of unstable angina pectoris.

The diagnosis of unstable angina may be confirmed if an ECG taken during an episode of pain demonstrates ST-segment changes that resolve when the pain is relieved. An intra-aortic balloon device should be used in the rare patient who has recurrent episodes of ischemia despite maximum drug therapy. Coronary angiography should be performed as soon as possible after the device is inserted.

Administration, Oral↗
PubMed1982

[Disappearance of coronary collateral circulation during a crisis of spontaneous angina. The role of spasm].

Disappearance of the collateral coronary circulation was observed during an attack of spontaneous angina. During coronary angiography, the patient developed precordial pain, ST depression in Leads I, II, III, AVL, AVF, and V2 to V6. The two coronary arteries were opacified: there was no change in the left coronary tree but the collateral circulation arising from the right coronary artery and revascularising the obstructed left anterior descending artery the ECG reverted to its previous state and the collateral circulation reappeared. This case suggests that coronary artery spasm may lead to disappearance of the collateral circulation. It raises problems of methodology in the demonstration of spastic phenomena and emphasises the role of the collateral circulation in the genesis of ischaemia. It is another illustration of coronary artery spasm accompanied by ST depression.

Angina Pectoris, Variant↗
PubMed1982

Benefits from adding nifedipine to the treatment of unstable angina when beta-blockade and isosorbide dinitrate have proved inadequate.

Nifedipine (10 mg orally six times daily) was given to patients with unstable angina persisting despite adequate beta-blockade (group I, 35 patients) or despite the association of adequate beta-blockade and sublingual isosorbide dinitrate (group II, 47 patients). Stabilization of anginal symptoms was achieved in 31/35 patients of group I and in 39/47 patients of group II. Aorto-coronary bypass grafting was carried out in 19 patients because of persisting unstable angina (five patients) or because of the severity of residual angina (14 patients). Tolerance to these drug combinations was excellent, with side-effects consisting mainly of transient headache (eight patients) and noncardiac ankle edema (eight patients). Nifedipine was found to be valuable in stabilizing unstable angina persisting despite beta-blockade and nitrates.

Aged↗
PubMed1982

[Surgical treatment of Prinzmetal's angina pectoris by plexectomy associated with aortocoronary bypass. Apropos of 56 cases].

The results of coronary bypass surgery are generally not as good in Prinzmetal angina as in classical angina pectoris. The percentage of myocardial infarction, recurrent angina and death is much higher. One reason for these failures could be the persistence of coronary spasm. In order to prevent this, denervation of the pre-supra and retro aortic nerve plexuses was carried out in 56 patients (54 male, 2 female) with Prinzmetal angina and operable coronary arterial lesions. Forty patients had documented coronary spasm mainly of the left anterior descending (20 cases) or the right coronary artery (13 cases). Surgery consisted of cardiac denervation associated with direct myocardial revascularisation by implantation of I (37 cases), 2 (13 cases) or 3 (6 cases) aorto coronary bypass grafts. Two deaths were observed in the perioperative period (one low output syndrome and one severe arrhythmia) and one myocardial infarction in the postoperative period. Of the 54 survivors, 49 are asymptomatic and 2 have recurrent spontaneous angina. Exercise electrocardiography in 44 patients was negative in 40 cases. Continuous electrocardiographic recordings (Holter method) in 33 patients was negative for ischemia and of 25 bypass grafts controlled, 24 were patent. Seventy five methylergometrine provocation tests were performed: only 2 were positive, both in patients with recurrent attacks. Therefore, with respect to the total numbers of recurrent angina (2), post operative infarction (I), peri and post operative deaths (3), the percentage of poor results was only 10,7 p. 100, almost three times lower than in previously reported series. In conclusion, we can say that the association of cardiac denervation with coronary bypass surgery significantly improves the percentage of good results (89,3 p. 100 of patients presenting with Prinzmetal angina).

Adult↗
PubMed1982

[Treatment of a severe coronary artery spasm, refractory to complete denervation of the heart (autotransplantation)].

The case reported is that of a 49 year old man with very severe Prinzmetal angina due to spasm of the left circumflex artery. Despite intensive medical treatment he continued to suffer frequent attacks with atrioventricular block. As plexectomy was not possible in this case, complete cardiac denervation was performed. After surgery, he had no further attacks and continuous ECG monitoring showed no ischemic phenomena. Nevertheless, a stress test was still able to induce spasm of the same artery which was painless but associated with ECG changes. Eighteen months postoperatively, resting angina recurred with positive stress tests giving painful attacks. Four hypotheses are discussed: 1) the local factor was very important, with a zone of hyperactivity on the left circumflex artery, 2) one of the mechanisms of coronary artery spasm could be the nervous stimulation of this zone, 3) this zone was insensitive to nervous stimulation after autotransplantation but remained sensitive to methylergometrine, 4) the recurrence of resting angina and painful symptoms on stress testing suggests the possibility of reinnervation of the heart, as has been shown after cardiac transplantation, the autonomic nervous system does not play the role generally attributed to it in the genesis of spasm.

Aged↗