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

Pathogenesis of the so-called "heart attack" still remains to be elucidated. The links between stable effort angina and unstable or acute myocardial infarction, and between asymptomatic and spontaneous angina are all missing. In medicine presently, pathophysiology of ischemic heart disease is considered a consequence of i) the progression of atherosclerotic narrowing of the coronary artery, and ii) dynamic and transient obstruction (coronary spasm), but these mechanisms are traditionally believed to be unrelated. This article demonstrates various experimental evidence indicating that these two mechanisms are related. And, this review article describes how to produce experimental coronary spasm in the presence of atherosclerosis, similar to that seen in patients with variant angina, and that coronary spasm can produce sudden progression of coronary atherosclerotic obstruction due to intramural hemorrhage. Establishment of various animal models to elucidate mechanisms related to various stages of ischemic heart disease are needed.
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PMID:Experimental induction of spasm, sudden progression of organic stenosis and intramural hemorrhage in the epicardial coronary arteries. 195 7

Atherosclerotic plaque rupture with superimposed thrombosis is recognized as the lesion causing greater than 90% of acute myocardial infarctions. To determine the severity of atherosclerosis at the site of plaque rupture, 184 coronary arteries from autopsies of 162 patients who died of acute myocardial infarction were studied. There were 102 men, 72 +/- 10 years old (mean +/- SD), and 60 women, 75 +/- 8 years old. All arteries were dissected from the heart, fixed, decalcified, cut at 2 to 3 mm intervals and processed routinely for histologic examination. A planimeter was used to measure artery, plaque, thrombus and luminal cross-sectional area at the site of plaque rupture with thrombosis in sections projected at x13.8 magnification. At the site of atherosclerotic plaque rupture with superimposed thrombosis, the degree of stenosis due to plaque was: 90 +/- 7% for the right (n = 67), 91 +/- 6% for the left anterior descending (n = 79) and 91 +/- 6% for the left circumflex (n = 38) coronary arteries. Plaque rupture in fatal acute myocardial infarction occurs at sites of severe narrowing (mean 91%, range 67% to 99%). Thus, plaque rupture with thrombosis is unlikely to cause the fatal acute myocardial infarction in patients with mild to moderate coronary stenosis.
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PMID:The severity of coronary atherosclerosis at sites of plaque rupture with occlusive thrombosis. 200 14

A clinicopathological synthesis is presented of the relationship of ischemic heart disease to sudden cardiac death. The immediate pathophysiological process responsible for sudden cardiac death is a lethal arrhythmia, usually ventricular fibrillation. Although significant coronary atherosclerosis is present in most cases of naturally occurring sudden death, available evidence indicates that several mechanisms can be operative in the pathogenesis of the fatal event. These are (1) acute myocardial infarction in a minority of cases; (2) myocardial ischemia, without infarction, which is initiated either by (a) an exertion-induced increase in myocardial oxygen demand or (b) an acute coronary event often involving plaque degeneration and platelet aggregation; and (3) a primary arrhythmia, usually resulting from altered electrical conduction in the setting of a previous myocardial infarction.
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PMID:Relationship of ischemic heart disease to sudden death. 195 28

From October 1984 up to February 1989, 40 patients had "redo" myocardial revascularizations using one or both internal mammary arteries (IMA) in over 1000 cases operated upon in our Department for coronary bypass grafts. Thirty-one patients had a further operation for unstable angina difficult to control with drugs. Mean interval of recurrence of angina after previous surgery was 48.5 months for all the cases, but the mean interval before the second bypass operation was 68 months. Severe disease of previous vein grafts was the reason for surgery in 25 patients and progressive atherosclerosis in native coronary arteries in 15 patients. Twenty-one patients had a single mammary artery; both mammary arteries were used in 19. Two cases had endarterectomy on left anterior descending (LAD). Four patients had peroperative acute myocardial infarction (AMI), 3 a low cardiac output syndrome, postoperative bleeding occurred in 3 cases and wound infection in one case. An intraaortic balloon pump was used preoperatively in one case and coming off bypass in two others. One patient died on the second day postoperatively from cardiac arrest following bilateral pneumothorax. There were no late deaths. At a mean follow-up of 20.5 months, 28 patients are free of symptoms but 11 are complaining of angina, 5 during exercise and 6 at rest. An exercise test was positive in 8 patients.
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PMID:Reoperation for myocardial revascularization using the internal mammary artery. 201 Apr 57

By summing up a series of epidemiological evidence a continuous elevation of total serum cholesterol, especially LDL-cholesterol, leads atherosclerosis and causes the narrowing or occlusion of coronary artery which introduces acute myocardial infarction or angina pectoris in the heart. In the brain, it is a risk factor for cerebral thrombosis. On the other hand, a lower level, 160 mg/dl or less of total serum cholesterol relates with the higher incidence of cerebral hemorrhage or subarachnoid hemorrhage, but still with the lower incidence of ischemic heart disease. It is concluded that the higher the total serum cholesterol level and the longer the period of continuous elevation is, the higher the incidence of ischemic heart disease. And there is a U-shape relationship between the level of serum cholesterol and cerebrovascular disease as a whole with a nadir around 160 to 200 mg/dl which means an optimal range of total serum cholesterol. A subject with total serum cholesterol over the optimal level may need some sort of modification in his daily life, in eating or physical exercise but not necessarily requires any pharmacological therapy.
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PMID:[Serum cholesterol levels as a risk factor of cardiovascular disease]. 207 72

ELISA using the test systems and a complex of equipment manufactured by Flow Company was employed to study over time the content of fibronectin, fibrinogen, products of its degradation and myoglobin in 178 patients suffering from coronary heart disease (stable and progressive angina pectoris, acute myocardial infarction). The concentration of myoglobin, fibronectin, fibrinogen and products of its degradation was established to depend on the gravity of coronary heart disease and the tame elapsed since the disease onset. In patients with progressive disease, there was an increased consumption of fibronectin which may be due both to its expenditure during blood coagulation and fulfillment of angioprotective function because of exacerbation of systemic atherosclerosis.
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PMID:[The content of fibronectin, fibrinogen, its degradation products and myoglobin in patients with ischemic heart disease]. 209

The results of several major trials of i.v. thrombolysis in patients with acute myocardial infarction have demonstrated the efficacy of the treatment in reducing mortality. Streptokinase and rt-PA have been shown to be effective (APSAC = anisoylated plasminogen streptokinase activator complex; GISSI = Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto miocardico, ASSET = Anglo Scandinavian study of early thrombolysis, rt-PA). This treatment is associated with the potential for cerebral and major bleeding, especially in elderly patients. The benefit of this treatment in patients with cardiogenic shock or hypotension (ISIS-2) is discussed. There is no convincing evidence that patients with ST-segment depression or those with an equivocal electrocardiogram had been benefited from i.v. thrombolysis. Further studies with i.v. thrombolysis and/or other strategies need to be explored. Overall the use of i.v. thrombolytic agents in combination with PTCA in patients with acute myocardial infarction have resulted in improvement in ventricular function and survival in patients eligible for this therapy. However, new techniques and therapeutic approaches to prevent reocclusion, to prevent reperfusion injury, to prevent restenosis after PTCA, to prevent atherosclerosis in the infarct and non-infarct related arteries, and to reduce the potential for ventricular arrhythmias and sudden death as well as the potential for mural thrombi and embolization after infarction are needed. The 1990's will see attempts to determine the optimum adjunctive therapy or "cocktail" of agents to be used with i.v. thrombolysis.
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PMID:Thrombolysis in acute myocardial infarction: need for a change in strategy and future directions. 212 41

Calcium antagonists are now widely used for the treatment of clinical hypertension and angina pectoris. They are efficacious for the treatment of vasospastic, fixed atherosclerotic and mixed angina; they reduce the incidence of silent ischemia; and they have been shown to reduce postmyocardial infarct angina. Experimental data suggest that they may have certain cardioprotective properties in cases of acute myocardial ischemia and infarction, stunned myocardium, diastolic dysfunction, left ventricular hypertrophy and atherosclerosis. Moreover, they have been shown to improve exercise performance, as well as the diastolic abnormalities in patients with hypertrophic cardiomyopathy. In animals, they may delay or reduce the extent of myocardial necrosis after coronary occlusion or coronary occlusion followed by reperfusion, and in low doses that do not alter the hemodynamic profile, they have been shown to enhance the return of ventricular function in animals with stunned myocardium. However, the early first-generation calcium antagonists (nifedipine, verapamil, diltiazem) have not been shown to reduce myocardial infarct size or to enhance survival in patients with acute myocardial infarction. There now are clinical studies that suggest that, unlike beta blockers or nitrates, nifedipine may slow the development of atherosclerotic progression in humans over a 2-year period, and it seems likely that in the 1990s there will be further expansion of the use of calcium antagonists for not only angina and hypertension but also for aspects of cardioprotection. That calcium antagonists may delay, prevent or possibly regress atherosclerotic lesions is an exciting possibility.
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PMID:Progress in cardioprotection: the role of calcium antagonists. 214 58

Post-mortem examinations were performed on 89 Chinese with fatal acute myocardial infarction, who represented an unselected 45.6% of a series comprising 195 consecutive hospital deaths from acute myocardial infarction in Hong Kong. In 83 patients (93.3%), the acute infarcts were correctly identified, and old infarct scars or patchy fibrosis were found in 21 patients (23.6%). Of the 85 sudden deaths, 33 patients (38.8%) had no definite mechanical complication and therefore could have died of primary arrhythmias, ten patients (11.8%) had rupture in the free ventricular wall with cardiac tamponade. Two other patients had rupture of the interventricular septum and one more patient had rupture of papillary muscle. Evidence of significant coronary atherosclerosis was identified in 94.7% of patients, with one-vessel disease in 18.7%, two-vessel disease in 33.3% and three-vessel disease in 42.7% of patients respectively. Critical lesions were present in left main stem in 8%, left anterior descending artery in 45.3%, circumflex artery in 8% and right coronary artery in 17.3% respectively. Occlusive coronary thrombi were identified in 18.7% of patients. These pathological findings were compared with reports on fatal myocardial infarctions from the western countries.
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PMID:Pathology of fatal acute myocardial infarction in the Chinese. 203 86

Rupture of an atherosclerotic plaque associated with partial or complete thrombotic vessel occlusion is fundamental to the development of ischemic coronary syndromes. Plaques that produce only mild-to-moderate angiographic luminal stenosis are frequently those that undergo abrupt disruption, leading to unstable angina or acute myocardial infarction. Plaques with increased lipid content appear more prone to rupture, particularly when the lipid pool is localized eccentrically within the intima. Macrophages appear to play an important role in atherogenesis, perhaps by participating in the uptake and metabolism of lipoproteins, secretion of growth factors, and production of enzymes and toxic metabolites that may facilitate plaque rupture. In addition, the particular composition or configuration of a plaque and the hemodynamic forces to which it is exposed may determine its susceptibility to disruption. Exposure of collagen, lipids, and smooth muscle cells after plaque rupture leads to the activation of platelets and the coagulation cascade system. The resulting thrombus may lead to marked reduction in myocardial perfusion and the development of an unstable coronary syndrome, or it may become organized and incorporated into the diseased vessel, thus contributing to the progression of atherosclerosis. In unstable angina, plaque disruption leads to thrombosis, which is usually labile and results in only a transient reduction in myocardial perfusion. Release of vasoactive substances, arterial spasm, or increases in myocardial oxygen demand may contribute to ischemia. In acute myocardial infarction, plaque disruption results in a more persistent thrombotic vessel occlusion; the extent of necrosis depends on the size of the artery, the duration of occlusion, the presence of collateral flow, and the integrity of the fibrinolytic system. Thrombi that undergo lysis expose a highly thrombogenic surface to the circulating blood, which has the capacity of activating platelets and the coagulation cascade system and may lead to thrombotic reocclusion. Measurements aimed at reversing the process of atherosclerosis via cholesterol reduction and enhanced high density lipoprotein activity are encouraging. Active research is being focused on the development of new antithrombotic tools, such as inhibitors of thrombin, thromboxane, and serotonin receptor antagonists, and monoclonal antibodies aimed at blocking platelet membrane receptors or adhesive proteins. These compounds may prove useful when immediate and potent inhibition of the hemostatic system is desired. Intensive research is still needed in the areas of pathogenesis and therapeutic intervention in atherosclerosis.
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PMID:Atherosclerotic plaque rupture and thrombosis. Evolving concepts. 220 64


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