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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha-adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST- and T-wave changes were studied. Cocaine administered intravenously (maximum 32 mg) produced subjective sensation of central nervous stimulation (the "high") in all patients. However there was no significant change in coronary artery diameter (assessed by computer-assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two-dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (thermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p less than 0.007). Despite a significant elevation in heart rate (average 56%, p less than 0.007), mean systemic arterial pressure (average 12%, p less than 0.05) and rate-pressure product (average 69%, p less than 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does cocaine cause coronary vasospasm in chronic cocaine abusers? A study of coronary and systemic hemodynamics. 156 28

A case of a 57-year-old man with hypertension and stable angina, on aspirin therapy, who was treated for epistaxis with intranasal cocaine, and who subsequently suffered a non-Q wave myocardial infarction is reported. Of note, the cocaine was administered in a manner which differs from that advocated in standard references. Specifically, intranasal packing soaked with 4% cocaine was left in place with continuous nasal mucous membrane contact over 5 to 6 hours. The authors speculate that myocardial infarction occurred on the basis of coronary artery spasm. This case should alert practitioners to myocardial ischemia occurring as a complication of the therapeutic use of intranasal cocaine for the treatment of epistaxis.
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PMID:Myocardial infarction associated with inappropriate use of topical cocaine as treatment for epistaxis. 158 32

While angina is not uncommonly seen in association with hyperthyroidism, only rare case reports have suggested that myocardial ischemia in this state may be due to coronary artery spasm. The authors review the literature and describe a case in which the repetitive occurrence of episodes of myocardial ischemia due to coronary spasm correlated with repeated transient elevations in thyroid hormone levels, thus clarifying this relationship. The importance of defining thyroid status in patients presenting with coronary vasospasm is emphasized and the effects of thyroid hormone on the heart are reviewed.
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PMID:Case report: coronary vasospasm--relation to the hyperthyroid state. 164 52

The present study investigates the prognostic significance of silent myocardial ischemia in variant angina. Forty-eight-hour Holter monitoring and coronary angiography were performed in 54 patients with transient ST elevation and no history of myocardial infarction admitted to the coronary care unit for worsening of symptoms. Coronary artery spasm was documented in most of these patients. Over the subsequent month, 20 patients (group 1) had a major coronary event (2 died, 6 had nonfatal myocardial infarction and 12 had urgent coronary revascularization), and the remaining 34 patients (group 2) had a good clinical outcome. From 2,578 hours of recording, 547 ischemic episodes were identified of which only 9% were associated with angina. The mean daily number of ST elevation in group 1 was similar to that in group 2 (4.8 +/- 5.1 vs 4.1 +/- 4.6; p = not significant). Conversely, the mean daily duration of such ischemic episodes was consistently greater in group 1 than in 2 (79 +/- 36 vs 37 +/- 25 minutes; p less than 0.005). The occurrence of greater than or equal to 1 long-lasting (greater than or equal to 10 minutes) episode of ST elevation was observed in 18 of 20 patients in group 1 (sensitivity 90%), but only in 4 of 34 in group 2 (specificity 88%). Significant coronary atherosclerosis (greater than 50% stenoses) was found at angiography in 18 of 20 patients in group 1, and in 18 of 34 in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prognostic significance of silent myocardial ischemia in variant angina pectoris. 174 57

Cardiac arrests, excluding those associated with cardiac surgery, occurred in eleven out of 13,278 patients who had general anesthesia in our hospital for seven years from 1983 to 1989. Four of them were successfully resuscitated, while the remaining seven patients were lost. The causes of these cardiac arrests were as follows: massive bleeding in four; cardiac compression by surgeons in two; possible coronary artery spasm in one; hyperpotassemia in one; severe metabolic acidosis in one; myocardial ischemia in one; and unknown cardiogenic origin in one. There is no case in which anesthesia was the primary cause of cardiac arrest. Although we can not be absolutely free from cardiac arrest during anesthesia and surgery, we should do our best to detect and correct any factors leading to perioperative cardiac arrests.
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PMID:[Survey of cardiac arrests during and following anesthesia and surgery for the past seven years]. 176 5

A 57-year-old man without any history of coronary artery disease underwent total hip replacement for which a continuous lumbar epidural analgesia combined with general anesthesia was used. During the recovery from anesthesia, the patient developed sudden hypotension and ventricular fibrillation (Vf), followed by ST elevation (I, II, III, aVF and V2-V6) on ECG. A coronary angiography, which was performed 30 min after the onset of Vf, revealed both the total occlusion of proximal left anterior descending artery (LAD) and 25% stenosis of proximal right coronary artery. It seemed that coronary artery spasm had occurred during the emergence from anesthesia, and then the coronary spasm ceased in a minute or two, while thrombus was produced in proximal LAD. The patient recovered from the episode of myocardial ischemia after percutaneous transluminal coronary recanalization and intraaortic balloon pumping. This patient was operated again on 4th and 8th postoperative days uneventfully under general anesthesia (enflurane and nitrous oxide in oxygen).
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PMID:[Subendocardial infarction on recovery from anesthesia]. 177 May 80

Coronary artery spasm is undoubtedly one of the causative factors of ischemic heart disease, particularly variant-type angina pectoris and myocardial infarction, but the disease mechanisms involved are still unclear. The present review describes the clinical background of coronary artery spasm in relation to ischemic heart disease, including a brief history of studies in this field, and also suggests future guidelines for experimental investigations based on the characteristics of coronary artery spasm, focusing particularly on data we have obtained in our laboratory from studies of cholinergic constriction. The pig may be a suitable animal in which coronary artery spasm could be provoked with cholinergic agents following endothelial denudation. The use of such large animals would allow the study of spastic arterial segments by various methods with angiographic confirmation. After endothelial denudation it is possible that phenotypic changes in cholinergic receptors might occur in smooth muscle cells, and that such changes might remain even after endothelial repair.
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PMID:Coronary artery spasm and vascular biology. Cholinergic constriction. 178 45

Coronary spasm is an important etiologic mechanism in the pathogenesis of myocardial ischemia. Provocative test of coronary spasm during coronary arteriography is clinically useful. The ergonovine test has gained widespread use, and we have examined the efficacy and safety of intracoronary ergonovine application with a fixed dose of 16 micrograms. We studied 119 patients undergoing coronary arteriography. Coronary spasm was induced in 34 cases by intracoronary administration of 16 micrograms of ergonovine maleate. Coronary spasm was readily resolved by intracoronary administration of isosorbide dinitrate. None of the cases negative to the intracoronary ergonovine applications could be induced by additional systemic administration of 0.4 mg of ergonovine. Side effects of ergonovine such as elevation of blood pressure, headache and chest symptoms were infrequent in the intracoronary ergonovine test. We conclude that our method of intracoronary ergonovine application is sensitive and safe for the diagnosis of coronary spasm.
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PMID:[Intracoronary administration of ergonovine maleate for detecting vasospastic angina; one dose method]. 189 59

A 57-year-old man was admitted to our hospital because he had had attacks of chest pain at rest for more than a year, in spite of daily oral diltiazem (90 mg/day) and isosorbide dinitrate (15 m/day). The diagnosis of variant angina was made for him based on ST elevation in chest leads of the electrocardiogram during his first attack. However, one year later, the electrocardiograms during attacks showed only ST depression or T wave inversion in chest leads. The coronary arteriogram during spontaneous chest pain revealed that the left anterior descending artery was totally occluded at its middle portion, and that its peripheral portion was perfused by collateral circulation from the right coronary artery. The coronary arteriograms after administration of nitroglycerin were apparently normal, and no signs of collateral circulation were observed. These findings indicated that the transient collateral circulation could develop after repetitive coronary artery spasms even in the absence of significant coronary stenosis, and that it could lessen the degree of myocardial ischemia during coronary artery spasm.
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PMID:[A case of vasospastic angina: development of transient collateral circulation lessen the degree of myocardial ischemia during coronary artery spasm]. 201 2

Coronary vasospasm has been implicated as a cause of myocardial ischemia and sudden cardiac death in cocaine abusers. However, the mechanism or mechanisms remain unknown. Autopsy records (n = 5,871) from the medical examiner's files at Baltimore, Maryland and northern Virginia were examined and 495 persons (8.4%) were identified with positive toxicologic findings for cocaine. Of these, six subjects (1.2%) had total thrombotic occlusion, involving primarily the left anterior descending coronary artery. The mean number of adventitial mast cells per coronary segment and the degree of atherosclerosis were determined. These observations were compared with findings in age- and gender-matched subjects who died from cocaine overdose and in patients who had sudden cardiac death (acute thrombosis) without a history of illicit drug abuse. There were significantly more mast cells in subjects with cocaine-associated thrombosis than in the other groups. The number of mast cells showed a significant correlation with the degree of cross-sectional luminal narrowing (r = 0.68) in subjects with cocaine-associated thrombosis but not in subjects with sudden death due to thrombosis (r = 0.34, p less than 0.03). Subjects with cocaine-associated thrombosis also had significant coronary atherosclerosis without plaque hemorrhage (five had one or more vessels with greater than 75% cross-sectional area luminal narrowing) despite a mean age of 29 +/- 2 years. These findings suggest that adventitial mast cells may potentiate atherosclerosis and vasospasm, thrombosis and premature sudden death in long-term cocaine abusers.
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PMID:Increase in atherosclerosis and adventitial mast cells in cocaine abusers: an alternative mechanism of cocaine-associated coronary vasospasm and thrombosis. 203 85


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