Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the importance of usual risk factors of coronary artery disease (CAD) in patients with coronary artery spasm, 40 patients with vasospastic angina (VA), normal or nearly normal coronary arteries and without previous myocardial infarction were compared with 2 control groups of 40 patients each, matched for age and sex: 1 group with CAD and 1 without heart disease. Ninety percent of patients with VA were cigarette smokers and 70% were heavy smokers (more than 20 cigarettes daily), compared with 53% and 33% in patients with CAD (p less than 0.001) and 30% and 15% in those without heart disease (p less than 0.001). Except for cigarette smoking, the risk factor profile of patients with VA appeared more like the profile of patients without heart disease than that of patients with CAD. The results suggest that cigarette smoking may play a role in CAD independent of atherosclerosis and possibly favoring coronary artery spasm.
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PMID:Comparison of risk factors in vasospastic angina without significant fixed coronary narrowing to significant fixed coronary narrowing and no vasospastic angina. 394 8

We studied the effects of prostacyclin on the frequency, duration and severity of ischemic attacks in spontaneous angina. Twenty-seven patients who did not respond to 48 hours infusion of placebo, received after a two-day observation period, 48 hours infusion of prostacyclin at an average rate of 4.0 ng/kg/min. Prostacyclin decreased number of ischemic attacks in only one of four patients with Prinzmetal angina, and was without any effect in five other patients whose attacks were associated with increase in blood pressure and heart rate. However, in 12 of 18 patients with coronary atherosclerosis, whose attacks were characterized by ST-segment depression without increase in heart rate or blood pressure, and often occurred at night, prostacyclin consistently diminished both frequency of anginal attacks and nitroglycerin consumption. This improvement lasted from 10 days to 3 months. Healing of endothelial damage by prostacyclin could explain the favorable therapeutic response in this subset of patients with spontaneous angina.
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PMID:Treatment with prostacyclin of various forms of spontaneous angina pectoris not responding to placebo. 639 38

With the arteriographic demonstration of coronary arterial spasm, fundamental questions have been raised concerning the role of spasm in myocardial ischemia and infarction. It is now clear that coronary arterial spasm is the cause of Prinzmetal's variant angina pectoris in patients with and without coronary atherosclerosis. In most patients with coronary heart disease, major ischemic events frequently result from increased myocardial oxygen demand or coronary thrombosis. However, recent evidence suggests that coronary arterial spasm may initiate or contribute to the development of unstable angina pectoris, acute myocardial infarction, and sudden death in these patients. Thus, episodes of myocardial ischemia and infarction are induced by factors, acting singly or in combination, that augment myocardial oxygen demand or diminish myocardial oxygen supply, and the latter alteration can result from thrombotic coronary occlusion or a dynamic increase in coronary arterial tone (that is, coronary arterial spasm).
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PMID:The role of coronary arterial spasm in ischemic heart disease. 689 63

A patient with classic effort and high-grade, fixed proximal coronary atherosclerosis underwent a single saphenous vein graft to a large, dominant right coronary artery (RCA). After being asymptomatic for 1 1/2 years, she had several episodes of rest angina culminating in Prinzmetal angina and ventricular fibrillation. Electrocardiographic changes occurred in the RCA distribution. Symptoms subsided with oral nifedipine therapy. Angiography revealed intact vein graft and coronary circulation. The patient has done well for a follow-up period of 7 months.
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PMID:Coronary artery spasm occurring late after vein graft surgery. 698 10

In this paper we have tried to explain the natural history of atherosclerosis as a condition marked by intimal vessel expansion tending to the endoluminal proliferation until to the obliteration of the lumen because of the presence of atheroma with fixed stenosis. During the course of the life, the various histologic alterations are responsible of the different ischaemic syndromes, ranging from instable vasospastic angina, to chronic ischaemia caused by fixed stenosis, until to myocardial infarction. Besides, we have outlined that in the young (< 40 years old), the most frequent and important event is the vasospasm owed by the fibromuscular proliferation that could cause an infarction with "intact" coronary arteries. On the other side, in the elderly, are observed specially degenerative atherosclerotic lesions with fixed stenosis and consequent thrombosis, cracking of the plaque as cause of acute myocardial infarction.
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PMID:[Coronary atherosclerosis: a long natural history]. 807 68

In subjects with coronary artery diseases (obstructive and vasospastic angina pectoris (AP)) who have no diabetes, hypertension, obesity and physical inactivity, insulin sensitivity was significantly reduced with compensated hyperinsulinemia on OGTT. Insulin resistance significantly correlated with coronary atherosclerosis score. In vasospastic AP (VAP), those who fulfilled more than 3 risk factors out of 5 (hyperinsulinemia, obesity, glucose intolerance, hypertension, dyslipidemia) consist of 70 and 40% for smokers and nonsmokers respectively. Insulin resistance syndrome who fulfilled all the criteria was 9-10% for VAP. In atherothrombotic brain infarction (ATTI) with the same exclusion criteria, the similar insulin resistance and hyperinsulinemia have been observed, but not in embolic (cardiac origin) or lacunar infarction. In ATTI, high TG and apo B with low HDL-chol were noted in blood. In essential hypertension without diabetes and obesity, hyperinsulinemia was noted in 25-35% and insulin resistance in 56-88%. Reduction of blood pressure with alpha blocker (bunazosin), ACE inhibitor (cilazapril), long-acting Ca++ blocker (amlodipine) significantly improved lowered insulin sensitivity. Insulin resistance rather than hyperinsulinemia is more closely associated with blood pressure. Cardiovascular diseases (vasospastic and obstructive AP, brain cortical artery diseases) are prone to develop diabetes because of insulin resistance and also promote the generation of cumulative risk factors resulting in a vicious cycle. Efforts to alleviate insulin resistance is crucial for the primary and secondary prevention of cardiovascular diseases.
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PMID:Clinical impact of insulin resistance syndrome in cardiovascular diseases and its therapeutic approach. 924 Jul 71

Fluctuations of spasmodicity have been reported in affected vessels in patients with vasospastic angina, but the incidence of spasmodicity induced by pharmacologic agents on both vessels with spasm and vessels without induced spasm has not been investigated. Repeated spasm provocation tests by acetylcholine or ergonovine were performed at 13.1 +/- 9.9 month intervals (3-50 months) in 111 vessels of 50 patients with ischemic heart disease, consisting of 19 old myocardial infarction and 31 angina pectoris, who did not undergo angioplasty or have signs of advancing atherosclerosis. Spasm was defined as present when more than 90 percent stenosis was accompanied by the appearance of usual chest pain or significant electrocardiographic changes. Ninety-six vessels (86.5%), 65 without spasm and 31 with spasm, revealed coincident responses and the remaining 15 vessels contrary reacted. The coincidence rate of spasmodicity in patients at intervals of within 24 months (90.2%) was significantly higher (p < 0.05) than that at intervals of over 24 months apart (70.4%). The spasm coincidence rate was 67.3% in the vessels with provoked spasm by either the first or second tests. Only one (0.9%) out of the 111 vessels showed obvious progressive atherosclerosis during this study. The majority of vessels showed identical spasmodicity within 2 years. In conclusion, coronary spasmodicity might remain unchanged for at least 2 years despite medication with calcium channel blockers and isosorbide dinitrate.
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PMID:[Is coronary spasmodicity unchangeable?: a study with acetylcholine or ergonovine in patients with ischemic heart disease]. 936 54

Studies have shown the presence of insulin resistance together with compensatory hyperinsulinemia in vasospastic angina as well as obstructive coronary artery disease. There is growing evidence that the development of coronary atherosclerosis may be closely related to systemic atherosclerosis as well as coronary spasm. However, no information is available about the possible relationship between insulin resistance and the existence of carotid atherosclerosis in vasospastic angina without segmental stenosis or luminal irregularities in coronary angiograms. To evaluate the independent effect of insulin resistance on carotid intima media thickening, we performed insulin sensitivity tests (steady-state plasma glucose method) on 40 patients with vasospastic angina and 24 control subjects with angiographically intact coronary arteries. Both oral glucose tolerance tests and lipid analyses were performed. Using B-mode ultrasonography, we assessed intima media thickness and plaque formation of common carotid arteries in these subjects. The steady-state plasma glucose level in the vasospastic angina group was about twofold higher than that of the control group, confirming the presence of insulin resistance in patients with vasospastic angina. The patients with vasospastic angina showed a significant increase in the average intima media thickness of the carotid wall and frequency of plaque formation, although they were comparable to the control subjects in risk factors other than insulin resistance. The intima media thickness was correlated with age (r = .62, P < .001), 2-hour insulin area (r = .45, P < .01), and steady-state plasma glucose level (r = .68, P < .0001) in patients with vasospastic angina. Similar correlations were observed in the control subjects. Multiple regression analyses of data indicated that 67% of the variation in the intima media thickness could be accounted for by age, steady-state plasma glucose level, and cigarette-years in vasospastic angina. In addition, differences in IMT were independently related to vasospastic angina. These results suggest that insulin resistance in association with compensatory hyperinsulinemia may be an important pathogenic factor for the development of coronary artery spasms and systemic early atherosclerosis.
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PMID:Insulin resistance as an independent risk factor for carotid artery wall intima media thickening in vasospastic angina. 940 26

We investigated the association of remnant-like particle cholesterol (RLP-C), with vasospastic angina (VSA). We selected 66 subjects with nearly normal coronary artery as a control group, and 74 VSA with nearly normal coronary artery, of whom 19 had prior myocardial infarction (MI). Coronary risk factors, triglyceride, lipoproteins and apolipoproteins were evaluated using stepwise discriminant analysis, smoking was the only discriminator of the control group from VSA and RLP-C was the only discriminator of VSA with MI from VSA without MI. In comparison between VSA with and without MI, using stepwise logistic regression analysis, the only significant variable was RLP-C, and odds ratio of RLP-C for MI was 1.59. Thus, RLP-C is a major discriminator of VSA with MI and appears to be a major risk factor for MI in VSA.
Atherosclerosis 1998 Feb
PMID:Remnant-like particle cholesterol is a major risk factor for myocardial infarction in vasospastic angina with nearly normal coronary artery. 954 92

To test the hypothesis that coronary spasm could be a coronary manifestation of systemic endothelial dysfunction and that the activity of coronary spasm could influence systemic endothelial function, we examined brachial flow-mediated, endothelium-dependent vasodilation and nitroglycerin-induced endothelium-independent vasodilation with high-resolution ultrasound in 11 men with variant angina pectoris (6 active and 5 inactive) without established coronary atherosclerosis. Endothelium-dependent vasodilation in peripheral circulation was preserved in men with active and inactive variant angina pectoris, suggesting that systemic endothelial dysfunction is not involved in either the pathogenesis or the activity of coronary spasm.
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PMID:Systemic endothelial function is preserved in men with both active and inactive variant angina pectoris. 1061 4


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