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

A 59-year-old white male accidentally ingested a mouthful of a plant growth chemical, Cycocel, containing 11.8% of the active ingredient (2-chloroethyl)trimethylammonium chloride (chlormequat). He was seen by a family physician and then transferred to a hospital where he died as a result of ventricular fibrillation, which progressed to asystole. Postingestion symptoms were typical of cholinergic crisis and included salivation, diaphoresis, bradycardia, visual disturbances, and seizure. Autopsy findings showed marked pulmonary edema, coronary atherosclerosis, atheromata of aorta, and localized adenocarcinoma of the prostate. Toxicological analyses of biological samples showed the presence of chlormequat in the stomach contents and urine.
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PMID:Sudden death following accidental ingestion of chlormequat. 239 50

The relationship between diuretic therapy and possible increased risk of coronary heart disease (CHD), especially sudden death, is controversial. The initial report from the Multiple Risk Factor Intervention Trial (MRFIT) raised the possibility that the increased CHD mortality observed in a subset of special intervention men with hypertension and certain electrocardiographic abnormalities on their baseline examination might be an unexpected adverse effect of diuretic therapy. Subsequent reports from the MRFIT have revealed a stronger association of CHD mortality to hydrochlorothiazide than to chlorthalidone. There was no consistent relationship of CHD mortality to the dose of either drug, to the most recent serum potassium level, or to the presence of ventricular premature beats. Unfavorable trends of the same magnitude were also seen among similar white men in the Hypertension Detection and Follow-up Program and in the Oslo hypertension trial, although the sample sizes in these two studies were too small to yield clearcut conclusions. Clinical studies have shown an increased risk of CHD death among hypertensive men with left ventricular hypertrophy. Such men are also noted to have a higher frequency of ventricular premature beats, even in the absence of diuretic therapy. Other studies have shown that diuretic-induced hypokalemia is accentuated in the presence of epinephrine and that low potassium levels decrease the threshold for ventricular fibrillation. Thus, although the evidence is still incomplete, it is possible that the excess CHD mortality among MRFIT special intervention men with electrocardiographic abnormalities may have been caused by a combination of increased left ventricular mass in the presence of coronary atherosclerosis, and hypokalemia caused by good compliance with diuretic therapy and accentuated by stress-induced increases in circulating catecholamines. Given the very large population of patients receiving diuretic therapy, further evaluation of this possibility is important.
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PMID:Unexpected effects of treating hypertension in men with electrocardiographic abnormalities: a critical analysis. 241 86

In the medical part of this review the devastating role of the "modern plague" smoking is exposed. The numerous and variable diseases of this habit or dependence are depicted. The most serious consequences of smoking concern--next to pulmonary diseases--the vascular system. Smokers are at risk for ischemic heart disease, cerebrovascular insults, peripheral arterial occlusive disease and thoracic and abdominal aortic aneurysms. The pathogenic mechanisms promoting atherosclerosis and thrombosis are reviewed: smoking promotes atherogenesis on one hand, on the other hand it initiates thrombotic and spastic vascular occlusion. Sympathico-adrenergic and hemostatic mechanisms thus affect the coronary system, partly in a reversible manner. This view is supported by the high incidence of mainly acute coronary events (infarction, instable angina, ventricular fibrillation) in smokers with rapidly improved prognosis after tobacco withdrawal. In the psychologic part of the review smoking is viewed as self-medication, and the attempt is made to depict the various types of smokers and their psychologic profiles.
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PMID:[Medical and psychological problems of smoking]. 264 27

Injury to the endothelial lining of arteries is an important mechanism in both the early and late stages of the development of atherosclerosis. Platelets can contribute to the early lesions by releasing factors that cause smooth muscle cell migration and proliferation. In the later stages, the formation of large platelet-fibrin thrombi that become organized into the vessel wall contributes to the development of focal atherosclerotic narrowing of arteries. Injury to the vessel wall can also be a factor in causing spasm of coronary arteries, particularly at sites of stenosis. The spasm may cause ischemia, anginal pain, and, in some individuals, ventricular fibrillation and death. In other individuals, the spasm may not cause death but may persist long enough for an occlusive thrombus to form and cause myocardial infarction. The events leading to thrombosis involve not only the release of arachidonic acid and the formation of TXA2, but other pathways that are independent of the arachidonate pathway. In some circumstances thrombin (which causes platelet aggregation and release that are largely independent of the arachidonate pathway and TXA2 formation) is the primary stimulus causing the initiation and growth of the thrombus. The role of products of the arachidonate pathway in causing spasm is not understood. PGI2 produced by the vessel wall could be important in preventing or minimizing coronary artery spasm. The best way to prevent the development of atherosclerosis and its clinical complications is to prevent or minimize injury of the endothelium.
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PMID:Platelets, endothelium, and vessel injury. 315 7

In sudden death of ventricular fibrillation occurring in coronary patients a new method of postmortem thermographic macroscopic diagnosis of ischemic stage myocardial infarction was found helpful in identifying areas of myocardial ischemia topographically close to stenosing atherosclerosis and considered due to thrombosis of the major and intramural branches of coronary arteries. Radionuclide and histochemical investigations confirmed relevant thermographic findings.
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PMID:[A new method of postmortem macroscopic diagnosis of the ischemic stage of myocardial infarction]. 336 43

Coronary artery occlusion and reperfusion in the anesthetized rat was used as a whole animal model of arrhythmia and sudden cardiac death to examine the influence of long-term dietary lipid modulation of myocardial membrane fatty acids on the development of cardiac arrhythmias. Feeding rats a diet supplemented with tuna fish oil significantly reduced the incidence and severity of arrhythmias, preventing ventricular fibrillation during both occlusion and reperfusion. Dietary sunflower seed oil reduced arrhythmias during occlusion but not in reperfusion. Dietary fat can modify the vulnerability of the myocardium to arrhythmic stimuli. The efficacy of tuna fish oil in reducing vulnerability to both ischemic and reperfusion arrhythmias suggests a potential beneficial effect of dietary n-3 fatty acids in addition to their influence on hemostasis, plasma lipids, and atherosclerosis that may contribute to their proposed role in lowering cardiovascular disease mortality and morbidity.
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PMID:Dietary fish oil prevents ventricular fibrillation following coronary artery occlusion and reperfusion. 341 86

This is the second of a two-part series on the effects of cognitive stress on cardiovascular disease. This paper reviews the relationship between cognitive stress and cardiovascular reactivity as it relates to the development of atherosclerosis and arrhythmias. In addition, the moderation of cardiovascular reactivity by the opportunity to exercise control over the stressor is discussed. The findings may be summarized as follows. First, recent animal work has suggested that the magnitude of heart rate change in the presence of a conditioned aversive stimulus is positively correlated with the extent of coronary atherosclerosis under diets high and low in atherogenic potential. Second, cardiovascular reactivity in humans may be related to several factors that could have an influence on the pathogenesis of atherosclerosis. These factors include: increased beta-adrenergic driving, increased shearing force on the intimal lining of the vessels, changes in pulsatile flow and the subsequent smooth muscle reparatory process. Cognitive (psychological) stress has also been related to ST segment depression, rate-pressure product changes, and changes in cardiac contractility. Animal studies have shown that the susceptibility to ventricular fibrillation may be enhanced by the presence of a conditioned aversive stimulus and may be reduced through adaptation to the aversive environment. The balance between sympathetic and parasympathetic influences on the myocardium may also play a critical role in the susceptibility of an already diseased heart to succumb to fatal arrhythmias during a behavioral stressor. Finally, studies in which subjects may exercise some control over an aversive stimulus suggest that cardiovascular reactivity may be pronounced and sustained in situations requiring frequent adjustment to changes in the criteria for successful performance, and/or the presence of positive incentives.
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PMID:Cognitive stress and cardiovascular reactivity. II. Relationship to atherosclerosis, arrhythmias, and cognitive control. 353 65

The leading cause of mortality in industrialized societies is sudden cardiac death. Almost half a million people die each year in the United States from myocardial ischemia and infarction leading to ventricular fibrillation. These phenomena result from severe coronary artery disease due to atherosclerosis with acute mural thrombosis causing occlusion, which serves as the terminal event. Various studies have found evidence of fresh coronary artery mural thrombosis in 74 to 94 percent of patients undergoing autopsies shortly after death due to acute myocardial infarction. Not all thrombi are occlusive, but vasospasm associated with fresh injury to the diseased vessel may be sufficient with developing new thrombus to block blood flow. Because platelets are a major constituent of newly formed thrombi and contribute significantly to vaso-occlusive disease, it is important to understand basic aspects of their function. Such studies may lead to measures that prevent vascular disease and thrombosis. This chapter has described ultrastructural features of platelet-vessel wall interaction. Adhesion, spreading, secretion, and aggregate or thrombus formation have been emphasized. The findings of current studies indicate strong similarities between platelet-vessel wall interactions and the response of platelets to other surfaces. Also, platelet transformations observed during aggregate formation in suspension are identical to physical changes in thrombi on damaged vessels. The similarities are much more impressive than the differences. Therefore, the role of platelets in arterial thrombosis can be understood best as an extension of their hemostatic function. An advantage of this observation is that understanding basic mechanisms of platelet function in hemostasis can lead to solution of the problems presented by platelet involvement in thrombosis. The disadvantage is that agents used to prevent thrombosis can place the hemostatic mechanism in jeopardy. Finding the answer to this paradox will occupy our attention for years to come.
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PMID:Platelet structural physiology: the ultrastructure of adhesion, secretion, and aggregation in arterial thrombosis. 360 10

In the United States, more than 300,000 sudden cardiac deaths (SCD) occur each year, the most common underlying etiology of which is coronary heart disease (CHD). With increasing age, the proportion of cardiovascular causes among all natural sudden deaths increases, and the fraction of CHD deaths that are sudden decreases. The lower incidence of coronary atherosclerosis in women is reflected in their proportionately lower risk of SCD. There are no data suggesting specific hereditary factors in risk for SCD due to CHD. On an individual basis, the known risk factors for CHD cannot distinguish those at risk for SCD from those at risk for other manifestations of CHD. Pathologic studies of SCD victims have shown that extensive coronary atherosclerosis is a major marker; healed myocardial infarction is a common finding, as is myocardial hypertrophy. Nonatherosclerotic coronary artery abnormalities may be associated with SCD. Chronic congestive heart failure is a common cause of SCD. Other etiologies include inflammatory, infiltrative, neoplastic and degenerative processes, diseases of the cardiac valves, and primary electrophysiologic abnormalities. The largest group of prehospital cardiac arrest victims have ventricular fibrillation identified on initial contact, with their survival outcome being intermediate between patients with ventricular tachycardia (best outcome) and those with bradyarrhythmia or asystole (worst outcome) on initial contact.
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PMID:Sudden cardiac death: epidemiology, causes, and mechanisms. 362 Dec 77

Sudden death, a major cause of mortality in the Western world, usually results from electrophysiologic phenomena in chronically damaged hearts with advanced coronary atherosclerosis. The exact pathophysiologic mechanisms are not known, but there is reasonable circumstantial evidence to implicate myocardial ischemia--clinically manifest or silent--as one of probably multiple factors of pathogenetic significance. This may be on the basis of coronary artery spasm, platelet aggregation, left ventricular dysfunction perpetuating a vicious circle of hypoperfusion and ventricular vulnerability to electrical instability. The increasing use and quality of continuous ambulatory electrocardiographic (Holter) monitoring have allowed improved detection of ST-segment changes and arrhythmias. The majority of sudden deaths result from ventricular tachyarrhythmias degenerating into ventricular fibrillation, and a more significant proportion of these than had been previously thought may be ischemically mediated. Importantly, as many as 20 to 25 per cent of the approximately 450,000 yearly terminal events represent bradyarrhythmias that may be preceded or accompanied by silent myocardial ischemia. Research is still required to determine the incidence, role, and mechanisms of silent myocardial ischemia in sudden death, with the hope that this common catastrophic event can be better prevented.
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PMID:Silent myocardial ischemia as a mechanism of sudden cardiac death. 377 20


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