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

The natural history of coronary artery disease has to be studied by comparing coronary angiograms of the same patient taken at different times. However, conclusions from repeated angiographic studies are fraught with substantial errors mainly because of: 1. patients selection, 2. variable time interval and 3. technical pitfalls. Despite this bias published interval studies demonstrate that coronary atherosclerosis predominantly is a progressive disease: after 2-3 years 50% to 60%, after 3-4 years 60% to 70% and after 5 years more than 80% of patients demonstrate progressive coronary artery disease at angiography. In addition, quantitative evaluation of coronary angiograms reveals that progression of coronary artery disease: 1. has a variable pattern and pace in each coronary artery and 2. predominantly involves initially normal coronary artery segments. From all clinical and angiographic parameters under scrutiny progressive coronary artery disease is significantly correlated to: abnormal lipid levels at the time of the first angiogram, a period of unstable angina pectoris, interval myocardial infarction and initial severity of coronary artery obstruction. It has to be emphasized, however, that in the individual patient the speed of progression is highly variably supporting the concept of different underlying pathophysiological mechanisms (primary/secondary progression). Regression or coronary stenosis is a rare phenomenon which may occur spontaneously and is anecdotally reported in patients after vigorous treatment of severe hyperlipoproteinemia.
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PMID:[Progression and regression of coronary sclerosis in the angiographic image]. 652 2

Coronary atherosclerosis is the major health problem of the twentieth century. Although there has been a recent decrease in mortality from this condition in many Western countries, the incidence has remained the same, and coronary atherosclerosis continues to be the leading cause of death. Our understanding of the disease process has been steadily increasing; however, much still needs to be clarified. The clinical presentations of coronary artery disease are diverse and not clearly linked to the severity or extent of the disease. Patients with similar coronary lesions present variously with stable and unstable angina or myocardial infarction, and all too many have sudden death as the initial clinical presentation. Recently, much attention has focused on the initial events leading to the development of atherosclerotic plaques. Current concepts unite formerly opposed views on the roles of intimal injury, platelets, lipids, and monoclonal smooth muscle cell proliferation in initiating atherogenesis. Progress has been made in understanding the early structural and functional alterations caused by myocardial ischemia. This understanding is leading to the development of interventions such as intracoronary thrombolysis to prevent or limit permanent myocardial injury. Measures to prevent serious complications of ischemic heart disease such as infarct rupture, aneurysm formation, and ischemic cardiomyopathy are still needed.
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PMID:Pathophysiology of atherosclerotic heart disease. 654 47

A surgical experience with 2,445 consecutive women who underwent isolated bypass grafting was analyzed for comparison with 18,079 consecutive men. Severe or unstable angina occurred preoperatively in 60% of women and 45% of men (p less than 0.001). Despite less three vessel disease (44 versus 56%, p less than 0.001) and better left ventricular contraction (normal in 60% of women and 53% of men [p less than 0.001]), women had a higher operative mortality rate (2.9 versus 1.3%). When matched for age, severity of angina and extent of coronary atherosclerosis, women still had twice the operative mortality of men. In matched patients, body surface area was the strongest predictor of operative risk, even when the model was adjusted for gender. When the model was adjusted for body surface area, gender was not an important predictor of operative death. The smaller size of women, rather than their sex, appears to explain the difference in operative mortality. After a mean interval of 2 years, women had a lower overall graft patency rate (76.4%) than men (82.1%) (p less than 0.001). At 5 and 10 years postoperatively, a higher percent of men were angina-free. Yet, survival for women (90.6%) and for men (93.0%) at 5 years, and at 10 years (78.6 and 78.2%, respectively) was not dissimilar.
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PMID:Coronary artery surgery in women compared with men: analyses of risks and long-term results. 660 Jul 58

Patterns of changes in blood plasma lipids and apolipoproteins were examined in 16 patients with acute large-focal myocardial infarction. Six of those were investigated during unstable angina pectoris. Lipoproteins responsible for cholesterol transport to tissues (apo-beta-containing lipoproteins) and its outflow (apo-A-I-containing lipoproteins) were shown to undergo a variety of metabolic changes in the course of myocardial infarction. Possible prognostic implications of patterns of post-infarction changes in lipoprotein and apolipoprotein spectrum are discussed with respect to predicting further development of atherosclerosis.
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PMID:[Changes in blood plasma lipid and apolipoprotein content in the course of acute myocardial infarction]. 664 76

To characterize the clinical and angiographic factors associated with progression of coronary atherosclerosis, 313 consecutive medically treated patients who had had two coronary arteriograms 3 to 119 months (mean 39 +/- 25) apart were studied. One hundred eighty-one patients underwent recatheterization for stable angina, 52 for unstable angina and 80 for various other reasons. In addition to the conventional angiographic features present at the first angiographic study (number of diseased vessels 1.5 +/- 0.8, ejection fraction 59 +/- 11%), an extent score was defined based on the number of coronary segments with 5 to 75% narrowings from a 15 segment coding system. Multivariate logistic regression identified four independent predictors of progression of coronary artery disease: the interval between studies (p less than 0.0001), unstable angina (p less than 0.0001), a high extent score (p = 0.0001) and young age (p = 0.0026). In a subset of 74 patients aged 50 years or younger with, at the time of the first evaluation, an extent score of 4 or more, the probability of progression between 2 and 4 years and after 4 years was, respectively, 80 and 90% compared with 50% for the other patients. Risk stratification for progression of coronary artery disease can thus be obtained.
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PMID:Clinical and angiographic factors associated with progression of coronary artery disease. 669 37

We studied the progression of atherosclerotic coronary lesions in 38 patients who had previously undergone angiography and were later hospitalized for an episode of unstable angina pectoris, and in 38 matched patients with stable angina who had also undergone prior catheterization. Patients with unstable angina and those with stable angina were similar in terms of age (mean, 49 and 50 years, respectively), number of risk factors (1.5 per patient in both groups), interval between studies (mean +/- S.D., 44 +/- 31 and 35 +/- 31 months, respectively), number of diseased vessels on the first angiogram (1.52 in both groups), and initial ejection fraction (65 and 63 per cent, respectively). Progression of coronary lesions was demonstrated in 29 of the 38 patients with unstable angina, as compared with 12 of the 38 with stable angina (P less than 0.0005). Progression to 70 per cent or more stenosis was recorded in 21 of the patients with unstable angina but in only 5 of those with stable angina (P less than 0.0005). Also more frequent in the patients with unstable angina were multifocal progression (11 vs. 2, P less than 0.01) and progression of the left main or preseptal left anterior descending artery or both (9 vs. 1, P less than 0.01). Thus, we have demonstrated by angiography that unstable angina is associated with progression in the extent and severity of coronary atherosclerosis.
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PMID:Unstable angina and progression of coronary atherosclerosis. 688 39

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

The formation of platelet aggregates has been suggested to be the initial step in coronary occlusion and the subsequent myocardial infarction (AMI). By scanning electron microscopy we followed: the platelet morphology and aggregation, the macrophage (M) morphology and the lymphocyte (T, B) count and structure in 11 patients with AMI and in 18 patients with unstable angina (UA). Generally, in the patients with AMI, most of the platelets presented relatively frequent (42.5%) or very frequent pseudopodia (35.27%) and the network of surface extensions was associated with several huge platelet aggregates in 6 patients. The mean lymphocyte count was: T = 40.36 +/- 23.95%; B = 28.09 +/- 7.38%; M = 31.54 +/- 21.25%. In the patients with unstable angina the proportion of platelets with pseudopodia was more reduced, namely, that of platelets with relatively frequent pseudopodia was 33.8% and with very frequent pseudopodia was 27.8%. The mean lymphocyte count was: T = 40.30 +/- 20.24%; B = 34.6 +/- 14.39%; M = 25 +/- 10.50%. These data indicate that platelet changes and the formation of aggregates can be an important factor in the occurrence of AMI. The change of immunocompetent cell count in both groups of coronary patients suggests the association of an immunologic process in coronary atherosclerosis.
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PMID:Changes of human platelets studied by scanning electron microscopy in acute myocardial infarction. 698 94

There is an abundance of information suggesting that prostaglandins are involved in the development and clinical expression of atherosclerosis. Many studies demonstrate a relationship between prostaglandins and the risk factors for peripheral and coronary artery disease. Thus, part of the mechanism by which hyperlipidemia, diabetes mellitus, smoking, hypertension, sex hormones, age, heredity, emotional stress and diet contribute to the development and progression of atherosclerosis may be through an imbalance between thromboxane A2 and prostaglandin I2. Recent studies show a temporal relationship between acute ischemic events (specifically, unstable angina) and a transcardiac increase in thromboxane B2, while others demonstrate a salutary effect of disaggregatory and vasodilatory prostaglandins in such patients. If prostaglandins and thromboxane prove important in ischemic vascular disease, attention will be directed at the correction of their pathologic imbalance. This may be accomplished by dietary manipulation as well as by the development of prostaglandin receptor antagonists or inhibitors of specific prostaglandin pathways.
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PMID:Prostaglandins and ischemic heart disease. 703 86

In the last decade, increasing information has become available to the effect that an increase in coronary artery tone and coronary artery spasm play an important role in patients with various ischemic heart disease syndromes. Coronary spasm may be superimposed on a coronary vessel already severely obstructed by atherosclerosis. Conversely, spasm may occur in an artery that is only minimally involved with atherosclerosis. The majority of patients studied in the United States with both stable and unstable angina pectoris have underlying severe organic obstructive coronary artery disease. There has now emerged a considerable amount of information from several centers showing that the calcium-channel blockers or calcium-flux antagonists are highly effective in the treatment of stable and unstable angina pectoris. This report focuses on the uses and limitations of one of these agents, nifedipine, in patients with unstable angina and provides a sequential approach to their management.
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PMID:Inpatient treatment of unstable angina: clinical perspective and sequential management. 711 12


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