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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aspects of myocardial oxidative phosphorylation and Ca2+ metabolism were studied in a swine model in which coronary atherosclerosis was induced by a combination of denudation of the endothelium of the coronary arteries plus 7--11 months of feeding a high fat--high cholesterol diet. By microscopy, a moderate amount of coronary atherosclerosis was present at the time of sacrifice, and 2 of the 14 swine hearts had old myocardial infarcts. Myocardial mitochondria from grossly normal areas showed partial uncoupling and decreased state 3 O2 uptake with 3 of 4 substrates tested. In addition, Ca2+ stimulated mitochondrial respiration was decreased in the atherosclerotic swine. In the sarcoplasmic reticulum Ca2+ uptake under conditions of heavy loading was greater in the atherosclerotic swine than in control animals. The degree of atherosclerosis was not great enough to suggest that persistent myocardial ischaemia was present. Possibly coronary artery spasm induced an intermittent ischaemia resulting in the metabolic abnormalities observed, or the changes may have been brought about by the effects of the high fat--high cholesterol diet on subcellular membranes.
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PMID:Oxidative phosphorylation and aspects of calcium metabolism in myocardia of hypercholesterolaemic swine with moderate coronary atherosclerosis. 20 97

Thirty-five patients with atypical chest pain were given ergonovine maleate as a provocative test for coronary spasm. None of the patients had significant coronary atherosclerosis. The patients were divided into two groups based on clinical information available before ergonovine testing. Group 1 patients (n=13) had objective evidence of cardiac disease manifested by episodes of syncope, ventricular tachyarrhythmias, myocardial infarction, or transient ST segment shifts with chest pain. Group 2 patients had chest pain but no objective evidence of cardiac disease. The ergonovine test was positive in 11 of 13 patients in group 1. None of the 22 group 2 patients had a positive response to ergonovine. These data suggest that ergonovine testing does not allow for any more precise recognition of patients with atypical chest pain who have coronary artery spasm than do clinical data alone.
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PMID:Predictability of the response to the ergonovine test. Value in the diagnosis of coronary spasm. 51 54

Two cases of coronary spasm in cardiac transplant recipients in which the presenting symptom was syncope without chest pain are reported. Diagnosing coronary spasm in transplant patients appears to be important because, based upon the few cases in the literature, prognosis is very poor. Coronary spasm may be related to accelerated atherosclerosis occurring in the transplanted heart.
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PMID:Syncope: a symptom of coronary artery spasm after cardiac transplantation. 157 64

Coronary artery spasm plays an important role in acute ischemic events, and it has a close relationship with coronary atherosclerosis. Thus we attempted to determine the most significant risk factor for coronary artery spasm. Among 3000 consecutive patients who underwent coronary cineangiography with ergonovine maleate testing, 330 with typical angina pectoris (group 1) and 294 with old myocardial infarction (group 2) were studied. We divided each group into three or four subgroups according to the presence of fixed organic stenosis (FOS+) or a positive reaction to ergonovine maleate (coronary artery spasm [CAS]+). We examined the relationship between coronary artery spasm and eight coronary risk factors: age, sex, hypertension, diabetes mellitus, smoking, and serum cholesterol, uric acid, and high-density lipoprotein cholesterol levels. The proportion of smokers in the subgroups with CAS(+) was significantly higher than in the subgroups with CAS(-)(p less than 0.01). There was no correlation between smoking and fixed organic stenosis. According to the results of multiple regression analysis, there was a positive correlation between smoking and CAS(+) and between serum high-density lipoprotein cholesterol levels and CAS(+)(p less than 0.01). Thus we concluded that smoking is the most significant risk factor in discriminating between patients with and without coronary artery spasm.
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PMID:Statistical analysis of clinical risk factors for coronary artery spasm: identification of the most important determinant. 161 25

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

It has been suggested that histamine is involved in the pathogenesis of coronary spasm but its exact role remains unclear. H1 receptor stimulation of the coronary artery was performed with a selective intracoronary infusion of histamine (2 micrograms/min) in 21 patients with variant angina after blockade of the H2 receptor with cimetidine (25 mg/kg) and its effect on the coronary artery diameter was examined. Intracoronary injection of acetylcholine was also performed in 19 of the 21 patients. Ergonovine (0.2 mg) was intravenously administered in one patient. The coronary artery diameter was measured with cinevideodensitometric analysis. A mean plasma histamine concentration in the coronary sinus increased from 4 x 10(-9) to 7 x 10(-8) M 5 min after histamine infusion into the left coronary artery (n = 18). Coronary spasm was induced in 6 patients (29%) with histamine, in 18 (95%) with acetylcholine and in 1 with ergonovine. The effect of histamine on the luminal diameter was analyzed at the site of spasm in the 26 coronary arteries in which spasm was induced by acetylcholine or ergonovine. Of the 20 coronary arteries with a normal arteriogram or a fixed stenosis less than or equal to 50% of luminal diameter, histamine decreased the diameter in 4, increased it in 14 (70%) and caused no change in 2; of the 6 coronary arteries with a fixed stenosis greater than or equal to 75%, histamine decreased the diameter in 5 and increased it in 1. In the coronary arteries in which spasm was not induced by either acetylcholine or ergonovine, histamine increased the diameter, especially in those without advanced atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of H1 receptor stimulation on coronary artery diameter in patients with variant angina: comparison with effect of acetylcholine. 167 98

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

From the studies and observations reviewed in this chapter, it can be appreciated that there is considerable direct and circumstantial evidence to implicate coronary artery spasm as a primary phenomenon in some patients with myocardial infarction. Although currently available data indicate that the number of acute myocardial infarctions due primarily to "pure" coronary artery spasm is relatively small, it should be emphasized that essentially very little if any data exist at "time zero" or at the actual onset of infarction. Most myocardial infarctions are probably multifactorial in etiology. To what extent coronary artery spasm, atherosclerosis, platelets, in situ thrombosis, endothelial mediators, and passive influences on vascular caliber interact in the pathogenesis of acute myocardial infarction remains incompletely understood.
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PMID:Coronary artery spasm and acute myocardial infarction. 249 19

Nitrates are old drugs, introduced into medical treatment more than 100 years ago, initially as a homeopathic remedy against headache (1850), and only later against angina pectoris (1867). Their typical hemodynamic, antiischemic effects were described in man in the 1950s and 1960s. They include: a reduction in venous return, lowering of the abnormally increased left ventricular enddiastolic pressure during ischemia, a decrease in left ventricular systolic wall stress, and changes in left ventricular geometry resulting in a decrease of myocardial oxygen consumption. The vasodilatory effect on large epicardial coronary arteries, especially on eccentric stenoses through relaxation of vascular smooth muscle tone was described even more recently (1980). This effect proved to be of considerable clinical importance both in angina at rest, that is during a primary increase in vasomotor tone (coronary artery spasm) as well as in angina provoked by exercise, where the increase in vasomotor tone and in the degree of stenosis is often due to a rise in alpha-sympathetic tone. The relaxing effect on the large coronary arteries is regarded as additive to the one on venous tone. The real clinical importance of nitrates became, however, evident only in the last decade with the discovery of EDRF, the so-called endothelial-derived relaxing factor, an endogenous compound of endothelial origin at least partly consisting of nitrous oxide and therefore, like nitrates, it exerts its effect through the stimulation of cGMP. The tendency for coronary arteries to constrict in presence of atherosclerosis is explained by the lack of EDRF, especially in the region of atherosclerotic plaques where the endothelium is often absent or has lost its endocrine function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The mechanism of action of nitrates, 1988 status]. 251 90

A case of a postpartum myocardial infarction in a 27-year-old black multiparous woman is presented. The patient had postpartum pregnancy-induced hypertension in a previous pregnancy. Her most recent pregnancy and immediate postpartum period had been uncomplicated, and she had been sent home with bromocriptine to suppress lactation. Ten days postpartum, she presented with severe hypertension followed by cardiac arrest. Subsequent coronary catheterization revealed no evidence of coronary atherosclerosis but showed a 60-70% stenotic plaque in the left anterior descending artery, possibly secondary to coronary artery spasm. A review of all previously reported cases of postpartum myocardial infarction is presented in an effort to identify the possible etiology of this event and to consider the role of bromocriptine. The most common associated finding in all cases was a history of pregnancy-induced hypertension, which may have been associated with a predisposition to coronary vasospasm. The compounding role of ergot derivatives on vasospasm is considered.
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PMID:Postpartum myocardial infarction in a patient receiving bromocriptine. 266 21


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