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

The coronary collateral circulation of 162 patients suffering from atherosclerosis and coronary insufficiency (coronary artery disease) was studied. It was found to be present in 44 patients, or 27.1%; homocoronary in 9%, intercoronary in 90.9%. As other Authors have previously reported, anastomotic circulation is more developed when the coronary occlusion exceeds 75%. Not one of the 44 cases with normal coronary arteries or occlusion inferior to 75% presented collateral circulation. In addition, it was found to be present more frequently in cases with three branch lesions. The time of insurgence of coronary insufficiency seems to condition the development of anastomotic circulation which appears more frequently when the symptoms have been present for more than 5 years (43.9%). Anastomotic circulation is also found more frequently (48.4%) in patients who have suffered myocardial infarction and who have angina. Collateral circulation was not found in any of the 46 patients with unstable isolated angina; this seems to show the importance, in its pathogenesis, of the functional factor (spasm). In conclusion, we may say that anastomotic circulation is more developed: 1) in cases of severe occlusive lesions (in severe coronary occlusive disease/atherosclerosis) (85%);2) in three branch lesions; 3) in cases of long standing symptomatology; 4) in stable angina and in angina t infarction.
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PMID:[Coronary collateral circulation in coronary atherosclerosis (author's transl)]. 73 69

A 35-year-old man suffered transmural diaphragmatic wall infarction immediately after receiving a nonpenetrating trauma to his chest. During subsequent months crippling angina pectoris developed and coronary arteriography was performed. A complete obstruction of the left circumflex coronary artery was demonstrated 2 cm. distal to its origin. In contrast to most cases previously published, in this case no signs of atherosclerosis were observed in the other coronary arteries. It must be assumed, therefore, that blunt trauma can induce complete coronary occlusion with infarction, even in subjects with normal coronary arteries.
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PMID:Acute coronary occlusion following blunt injury to the chest in the absence of coronary atherosclerosis. 96 90

This study of 24 women under age 40 years with myocardial infarction demonstrates that even in young women myocardial infarction is most commonly due to coronary atherosclerotic heart disease. Other causes of coronary occlusion were documented in 17% of these patients, indicating that these lesser causes of myocardial infarction are more common in young women than in older persons or in young men. In those patients with coronary atherosclerosis one or more significant risk factors could usually, but not always, be documented. The clinical manifestation of the coronary occlusion in the study group was not unlike its manifestation in groups of different ages or sex, or both.
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PMID:Myocardial infarction in young women. 96 5

The prevalence of complicated and calcified lesions and coronary stenosis, the mean heart weight, and the extent of atherosclerosis in the aorta and coronary arteries were greater in the "sudden heart death" group than in the high atherosclerosis group. In the "other sudden death" group, which included sudden deaths without myocardial infarction or coronary occlusion, all the above variables, except heart weight, were found to be lower than in the low atherosclerosis group and were close to those in the standardized average atherosclerosis group. The mean heart weight in the "other sudden death" group was lower than in the "sudden heart death" group but significantly higher than in the three reference atherosclerosis groups.
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PMID:Atherosclerosis and sudden death. 108 91

Since the seventies, and in particular the eighties of this century, findings on pathogenetic mechanisms of ischaemic heart disease are expanding markedly and are becoming more accurate. This makes it possible to know and understand better factors which influence the genesis and development of myocardial ischaemia including the most serious clinical forms (unstable angina pectoris, acute myocardial infarction and sudden cardiac death). Diminution of the cardiac flow and/or increased oxygen demands of the heart muscle are not the only determinants of myocardial ischaemia which is influenced markedly also by neurohumoral, metabolic, prothrombotic (proaggregation and procoagulation) factors as well as antithrombotic and haemodynamic factors. Acute coronary syndromes have as a rule, in particular in patients with out severe atherosclerotic stenosis of the coronary arteries, a common pathophysiological mechanism of fissuration of the atherosclerotic plaque followed by different grades of dynamic coronary occlusion depending on vasoconstriction--spasm of the coronary arteries and thrombus formation. The coronary arteries, usually affected with atherosclerosis, may be due to the comprehensive action of various factors temporarily, intermittently or permanently occluded. In case of the development of acute coronary syndromes thrombosis plays a key role. Better knowledge of pathogenetic mechanism of IHD markedly changes views on treatment and management of patients with IHD in particular patients with acute coronary syndromes. The authors emphasize strategies focused (also preventively) on preventing progression of the disease with the aim to improve survival and the short-term and long-term prognosis.
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PMID:[Pathogenesis of myocardial ischemia and acute coronary syndromes]. 129 43

Spontaneous acute occlusion of the coronary artery produces regional myocardial ischemia and infarction. This coronary occlusion could be due to rapid progression of atherosclerosis or vasospasm. The factors that can precipitate an acute attack of myocardial infarction or coronary spasm are not known. It is proposed that a stress-induced rise of unesterified arachidonic acid could trigger a leukocyte respiratory burst with the release of free radicals such as superoxide anion (O2-), hydrogen peroxide, hydroxyl radical, and singlet oxygen. These free radicals have the ability to inhibit prostacyclin (PGI2) formation and enhance the breakdown of endothelium-derived vascular relaxing factor (EDRF) which are potent vasodilators and platelet anti-aggregators. This may lead to rapid progression of atherosclerosis or coronary vasospasm leading to acute myocardial infarction. If this is true, free radical quenchers and inhibitors of leukocyte oxidative burst may be useful in the prevention of progression of atherosclerosis and coronary vasospasm.
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PMID:Can free radicals induce coronary vasospasm and acute myocardial infarction? 143

We studied myocardial injury during acute coronary occlusion-reperfusion and atherosclerosis in rabbits fed a high cholesterol diet with or without fish oil supplementation. New Zealand white male rabbits were divided into 3 groups. Eight control rabbits fed with laboratory standard rabbit chow were group I. In addition to the standard chow, 15 rabbits fed with a 1% cholesterol-enriched diet for 6 weeks were group II, and 10 rabbits fed with a 1% cholesterol-enriched and 10% fish oil supplemented diet for 6 weeks were group III. Acute coronary occlusion was induced by ligating the marginal branch of the left circumflex coronary artery for 1 h, followed by reperfusion for 4 h. Myocardial injury was assessed by tissue creatine kinase activities and amino-nitrogen concentrations from the ischemic (infarct) and nonischemic (normal) myocardium, and the infarct area/risk area ratios of the left ventricle. The surface area of the atherosclerotic lesions of the aorta and pulmonary artery was measured by planimeter. There was significantly more myocardial loss of creatine kinase and amino-nitrogen in the cholesterol-fed rabbits than the controls (p less than 0.01 and 0.02, respectively). The cholesterol and fish oil-treated rabbits had a nonsignificant reduction in myocardial loss of both agents as compared to their corresponding cholesterol-fed ones. The same trend was also found in the infarct area/risk area ratio. Fish oil treated rabbits had a good effect on the reduction of atherosclerotic lesions and tissue cholesterol levels in the aorta and pulmonary artery, but not in the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of dietary supplementation with fish oil on atherosclerosis and myocardial injury during acute coronary occlusion-reperfusion in diet-induced hypercholesterolemic rabbits. 161 95

The causes of unstable angina are still largely unknown. However, some facts deriving from angiographic, postmortem, and pathophysiologic studies are well established. Angiographic findings: coronary thrombi and complicated stenoses are more frequent in unstable than in stable angina. Conversely, the severity of coronary atherosclerosis and the development of collateral circulation is similar in both coronary syndromes. Postmortem findings: the following features are more frequent in unstable than in stable angina: (1) mural thrombi, which often represent out-growth from the inside of a fissured plaque; (2) inflammatory cells at the site of plaques and in perivascular nerves; and (3) contraction bands in smooth muscle cells of the media surrounding plaques. However, fissured plaques can be found in 10% of individuals dying of noncardiac causes, and fissured plaque may occasionally be missing under the coronary thrombus in unstable angina. Pathophysiologic findings: patients with unstable angina compared with those with stable angina exhibit: (1) higher levels of serotonin in the coronary sinus; (2) higher systemic levels of fibrino-peptide A; (3) higher urinary levels of thromboxane A2 metabolites; and (4) a greater coronary reactivity to constrictor stimuli. A critical analysis of these established facts is required to set the stage for a better comprehension of the causes which can cause a coronary segment to progress in a stuttering way toward acute persistent coronary occlusion and myocardial infarction. Plaque fissure is likely to be an important background thrombogenic stimulus in many cases.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The elusive cause of instability in unstable angina. 189 62

Studies of the association between type A behavior and coronary heart disease have yielded inconsistent findings. A possible explanation for these inconsistent findings is that type A behavior is simply a marker for other behaviors that are truly related to coronary heart disease. Hostility is one such behavior that has been found in several recent studies to predict coronary heart disease and coronary atherosclerosis; however, several other studies have found null results. In the present study, the predictive power of hostility was tested in a study population of hospitalized men (n = 118) and women (n = 40) scheduled for coronary angiography. Potential coronary risk behaviors were assessed in the angiography patients and they were given the type A Structured Interview. Hostility was measured with the Cook-Medley Hostility Inventory and the Behavior Pattern Hostility Index, a measure of hostility derived from the type A Structured Interview. No significant positive associations were found for either Cook-Medley hostility or behavior pattern hostility and coronary occlusion. This was true whether hostility or coronary occlusion was treated as a dichotomous variable or as a continuous variable. In fact, most of the observed associations were opposite to the predicted direction, although none was statistically significant. Replicating cutpoints of the Cook-Medley Hostility Inventory used in other studies that have reported positive associations with coronary heart disease also yielded null findings. The association between hostility and coronary occlusion was slightly modified by age and sex, but the interaction coefficients were not significant. The sample size yielded adequate statistical power to detect the hypothesized associations, and there was no evidence that selection bias, measurement error, or unexamined confounding accounted for the null findings. These results failed to confirm some earlier reports showing a positive association between hostility and coronary artery disease.
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PMID:Hostility and coronary artery disease. 198 42

The very first presentation of ischemic heart disease--acute infarction, sudden death, or unstable angina--most often occurs abruptly. The first approximation that it occurs as a random event only when a certain "threshold severity" of coronary atherosclerosis has gradually developed, although widely accepted, should perhaps be reconsidered and expanded on the basis of the following considerations. Acute coronary occlusion leading to myocardial infarction often occurs at the site of mild or noncritical coronary stenoses. Conversely, in patients with chronic angina severe coronary stenoses can remain unchanged for years with no detectable progression. When a coronary artery occludes, the size of infarction can vary greatly, and when ischemia and infarction occur, malignant arrhythmias occur in some patients but not in others. Thus, in a second approximation, ischemic heart disease should be considered as the result of the variable combination of three major components: a) A very variable chronic atherosclerotic background, which can result from a variety of pathologic processes; b) A number of acute ischemic stimuli, which can unpredictably impair myocardial blood flow as a result of coronary thrombosis and/or vasoconstriction; c) A variable response of the heart to a sudden reduction of coronary blood flow in terms of collateral perfusion and malignant arrhythmias. Therefore, at one extreme end of the spectrum in any individual, ischemic syndromes may present predominantly as a result of an extremely large chronic background component. At the other extreme, powerful acute ischemic stimuli can unexpectedly impair blood supply by coronary thrombosis, constriction, or their combination, in the presence of a mild chronic atherosclerotic background.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of myocardial ischemia. 209 77


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