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 1,261 records · Page 70Linked to original sources
PubMed2003

Limitations of medical therapy in patients with pure coronary spastic angina.

OBJECTIVES: To assess the efficacy of medication for the treatment of pure coronary spastic angina, 71 consecutive patients with this diagnosis who had undergone coronary arteriography in a hospital with a follow-up of at least 2 years were studied. METHODS AND RESULTS: All 71 patients without significant organic stenosis were treated with long-acting calcium antagonists. The disappearance of chest pain attacks while receiving medical therapy was observed in 27 patients (38%), whereas the remaining 44 patients (62%) had chest pain attacks. Of special interest, 30 patients had more than one attack per month irrespective of the administration of calcium antagonists or isosorbide dinitrate. Medical treatment showed a good response in female patients (63% vs 31%, respectively; p < 0.05) and those with ST-segment elevation during selective spasm provocation tests (63% vs 30%, respectively; p < 0.05). In contrast, patients with a longer history of chest pain attacks before hospital admission and those with diffuse spasms (77% vs 34%, respectively; p < 0.01) had poor responses to medical treatment. In this study, neither sudden death nor acute myocardial infarction was observed during the follow-up periods. CONCLUSION: The limitations of medical therapy, including the administration of long-acting calcium antagonists, were observed in 30 of 71 patients (42%) with pure coronary spastic angina. Medical treatment was effective in only 38% of patients with pure coronary spastic angina in Japan.

Acetylcholine↗
PubMed1982

Immediate appearance of coronary collaterals during ergonovine-induced arterial spasm.

Angiographically demonstrable collateral flow occurred immediately when coronary arterial spasm was induced by ergonovine in two patients with angina who had organic stenosis of less than 40 percent. These findings suggest that coronary collaterals may develop in response to intermittent brief myocardial ischemia in man, and that collaterals may be preserved even if they are closed at rest and can immediately function when a coronary artery is acutely occluded.

Angina Pectoris↗
PubMed1986

Age-related changes of clinical features and prevalences of coronary risk factors in Japanese patients with vasospastic angina.

From among 899 consecutive patients who underwent their first coronary arteriography, we selected 147 pts with vasospastic angina (VA) and 356 pts with classic angina (CA) and divided them into three different age groups: -49 years old, 50 to 59, and 60-. In these 899 pts, incidences of VA showed no increase with aging. Prevalence of coronary risk factors in CA, such as diabetes, hypercholesterolemia, hypertension, and obesity, was higher than in VA, although prevalence of smoking in CA was lower than in VA. In VA, we found an age-related increase in the incidence of smoking only, in contrast to the other four risk factors. The VA showed no age-related increase in the incidence of complication of fixed coronary stenosis. These findings suggest that aging and atherosclerosis might not play a major role in pathogenesis of VA, although the mere presence of atherosclerosis irrespective of its severity could interact with local susceptibility to spasm, leading to coronary vasospasm.

Adult↗
PubMed1988

Nifedipine and angina pectoris. Short-term changes in quantitative coronary angiography with nifedipine and clinical response to treatment in effort-induced, mixed, and spontaneous angina pectoris.

Changes induced by nifedipine (10 mg sublingually) in the residual luminal diameter of significant (greater than 50 percent) coronary lesions were assessed angiographically in 69 patients with effort-induced angina (group 1), in 22 patients with mixed angina (group 2), and in 14 patients with Prinzmetal's angina (group 3). These changes were related to the clinical response to treatment with the same drug, as evaluated through diary records and Holter monitoring in the mixed (spontaneous component) and Prinzmetal forms and through exercise testing in effort-induced and mixed (effort-associated component) angina. In groups 1 and 2, segments of stenotic vessels showed either an increase or decrease or no change in diameter with the calcium antagonist; in group 3, the majority of the lesions had compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (20 percent [14/69] unchanged; 19 percent [13/69] worsened) and mixed (41 percent [9/22] exacerbated) forms; 100 percent of the 14 patients with the Prinzmetal form had relief of the anginal episodes. In group 1, the response to exercise tests was dissociated from the short-term vasomotor pattern, and the pressure-rate product failed to explain the clinical results. Forty-five percent (ten) of the patients in group 2 showed significant short-term widening of critical stenoses, as well as obvious improvement; patients who did worse with treatment in this group had reacted to nifedipine with narrowing of critical stenoses. These data suggest that the response to nifedipine of classic effort-induced angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina, and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmetal form are quite sensitive to the relaxant action of calcium blockade, and this probably represents a background to the highly positive clinical response to treatment.

Angina Pectoris↗
PubMed1988

Current management of severe exercise-related cardiac events.

Severe cardiac events during either exercise testing or cardiac rehabilitation are described in five patients. The three events related to exercise testing involved patients with atypical chest pain which, in retrospect, probably reflected unstable angina pectoris or coronary vasospasm (or both). Prompt coronary angiography with subsequent percutaneous transluminal coronary angioplasty was performed. Two cardiac arrests (one fatal) occurred during participation in cardiac rehabilitation programs. One was caused by primary ventricular fibrillation. Electrophysiologic testing was used in determining the efficacy of the drug. The fatality was due to an acute myocardial infarction. On-site intravenous thrombolytic therapy might prove useful in similar events in the future. Comparisons of surveys published in the 1970s with those in the 1980s show that the mortality and morbidity during exercise testing remain low and that similar rates during cardiac rehabilitation are even lower; however, these cases exemplify that emergency situations can and do arise, necessitating prompt intervention and aggressive subsequent management.

Adult↗
PubMed1978

Electrographic changes associated with cyclical reduction of coronary blood flow.

Electrographic changes associated with cyclical reduction of blood flow in partially constricted one or two coronary arteries of anesthetized dogs were examined. In the preparations with single vessel constriction, cyclical ST elevation occurred along with cyclical reduction of coronary blood flow below 25% of the control value. The ST elevation was associated with reciprocal ST depression in the contralateral ventricular surface. In the preparations with double vessel constriction, cyclical reduction of flow frequently occurred in both vessels. The reduction of flow in one vessel occurred not synchronously with that in another vessel in the majority of preparations. The reduction of flow in both vessels was associated with ST elevation in the corresponding areas of the left ventricle. Premature ventricular contractions frequently occurred at the beginning of or immediately after disappearance of ST elevation, or when ST elevation persisted for more than 10 min. Ventricular fibrillation frequently occurred in the preparations with double vessel constriction.

Angina Pectoris↗
PubMed1982

Angiographic evidence of left main trunk spasm as a possible cause of syndrome X.

The present case is a 49-year-old female who began to feel a chest pain during exercise 2 years ago. Recently, the chest pain occurred during light exercise as well as at rest. The electrocardiogram during the attack showed remarkable ischemic ST segment depression. No abnormality was found in the coronary cineangiography. She was diagnosed as Syndrome X. However, coronary cineangiography during an attack on another day showed a severe spasm in the left main trunk. Thus, a spasm must be considered as one of the causes of "Syndrome X".

Angina Pectoris, Variant↗
PubMed1987

The role of parasympathetic nerve activity in the pathogenesis of coronary vasospasm.

To evaluate the role of the autonomic nervous system, especially the parasympathetic nervous system, in the initiation mechanism of vasospastic angina pectoris (AP), the coefficient of R-R interval variation (CV) on the electrocardiogram (ECG) and plasma catecholamine concentration were measured in 25 patients with vasospastic AP, 10 patients with effort AP and 12 control subjects. CV which has been recognized as reflecting parasympathetic nervous system activity was calculated from 100 consecutive heart beats on the ECG and represented as the percentage of standard deviation of the R-R interval per mean R-R interval. Repeated measurements of plasma catecholamine concentration revealed higher values at any sampling point throughout a day in patients with vasospastic AP than those in control subjects. A distinctly higher CV was observed at night in the vasospastic AP group. This elevated CV was abolished by atropine sulfate (1.5 mg/day per os). Pilocarpine injection (1.3 mg/10 kg B.W. subcutaneously) induced a marked increase in CV that preceded the occurrence of chest pain and/or ischemic ECG changes in 5 patients with vasospastic AP. The increment in CV at 10 min after pilocarpine administration was greater in vasospastic AP than in control subjects (p less than 0.05). It is concluded that enhanced parasympathetic activity may play a role in the initiation of coronary vasospasm associated with sympathetic hyperactivity.

Angina Pectoris, Variant↗
PubMed1987

Long-term prognosis of vasospastic angina without significant atherosclerotic coronary artery disease.

Long-term prognosis of 90 patients with vasospastic angina without significant coronary artery disease (less than 50% reduction in luminal diameter) was examined for a mean follow-up period of 4 years. All patients had episodes of angina at rest and were treated with calcium antagonists. One patient developed myocardial infarction and 2 died suddenly during the follow-up period. In the patient with myocardial infarction, there was an abrupt worsening of angina prior to the infarction despite therapy with a calcium antagonist. One of the sudden death patients discontinued his calcium antagonist before his death. Of the sudden death patients, one had ventricular tachycardia and the other had a complete atrioventricular block during an anginal attack. The incidence of such serious arrhythmias was higher (p less than 0.01) in sudden death patients (2/2) than that in survivors (6/88). The treatment with calcium antagonists reduced the severity and frequency of angina in all patients. These results suggest that long-term prognosis of vasospastic angina without significant coronary artery disease is good as characterized by the low incidence of myocardial infarction and death and the favorable response to treatment with calcium antagonists.

Adult↗
PubMed2000

Differences between coronary hyperresponsiveness to ergonovine and vasospastic angina.

The objective of the present study was to investigate the differences between coronary hyperresponsiveness without ischemia and vasospastic angina in an ergonovine provocation test using multivariate analysis. We have sometimes experienced a more than 50% narrowing response of vascular diameter without ischemia in a coronary response to ergonovine. We studied 107 patients with less than 50% stenosis in a coronary arteriogram. Their vascular responses to ergonovine were measured and the patients were divided into three groups, as follows: Group 1 had 50% or less vascular narrowing response without ischemia; Group 2 had a vascular hyperresponsiveness of more than 50% narrowing response without ischemia; and Group 3 experienced a hyperresponsiveness with ischemia. The degree of coronary response was found to be related to smoking, inpaired glucose tolerance (IGT) and the Gensini score by multiple regression analysis. A multiple logistic analysis revealed that the Gensini score and smoking were significant predictive factors for Group 3 (odds ratio: 1.20 and 8.97). The only factor different between Group 2 and Group 1 was gender. The coronary hyperresponsiveness to ergonovine without ischemia differs from vasospastic angina in the degree of coronary atherosclerosis and smoking habits. The patients with hyperresponsiveness had similar characteristics to those with atypical chest pain rather than vasospastic angina, except for a gender difference.

Aged↗
PubMed2004

A case of vasospastic angina resulting from coronary emboli in a patient with prosthetic valves.

In addition to coronary atherosclerotic disease, coronary thromboembolism can also lead to acute coronary syndromes. However, coronary thromboembolism due to prosthetic heart valves is very rare and not very well-known. It have been reported only a few cases. In this paper, we present a rare case with vasospastic angina pectoris secondary to coronary thromboembolism in a patient with prosthetic heart valves.

Adult↗