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

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.
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PMID:Cardiovascular disease and trace metals. 4 Feb 34

Clinical studies have long suggested the presence of a specific cardiomyopathy in sickle cell anemia secondary to intracoronary thrombosis and subsequent infarction. Fifty-two autopsy patients were studied (48 with SS hemoglobin, 4 with S-C or S-Thal hemoglobin) to ascertain the range of cardiac pathologic abnormalities associated with this disease. The average age was 17 years (range 1 month to 48 years). Renal failure and infection were the most common causes of death; the former was a more common cause in adults than in children. Right and left ventricular hypertrophy and dilatation were the most common abnormal pathologic findings. No evidence of recent or remote myocardial infarction, coronary thrombosis or arteritis was noted in any patient. Eight patients who were studied with postmortem coronary arteriograms exhibited markedly increased coronary arterial caliber with no evidence of atherosclerosis. Seventeen of the 52 patients studied had clinical evidence of congestive heart failure before death. Of these 17 patients, 7 had moderate to severe left ventricular hypertrophy associated with chronic renal failure and hypertension, 2 had right ventricular hypertrophy with organized pulmonary thrombosis, 2 had rheumatic mitral valve disease and 2 died during the second trimester of pregnancy. Two of the 17 patients thought to have pulmonary edema before death in fact had aspiration pneumonia and hemorrhagic pneumonitis, respectively. The data suggest that cardiac dysfunction in sickle cell anemia can usually be explained by the adverse effect of coexisting disease on the diminished cardiac reserve of chronic anemia. The data do not support the concept of a specific "sickle cell cardiomyopathy".
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PMID:Clinicopathologic analysis of cardiac dysfunction in 52 patients with sickle cell anemia. 15 Jul 86

Stroke is increasingly becoming a major cause of death and morbidity in African population among most of which the frequencies of hypertension are considerable, although hard data based on community surveys are lacking and most of the information available is from hospital data. The epidemiology of stroke in the Africans is reviewed. The frequencies in hospital populations varied from 0.9% to 4.0% and stroke accounted for 0.5% to 45% of neurological admissions. There is male predominance in published series. The main risk factors are hypertension, diabetes mellitus and homozygous sickle cell disease (in children only). Ischaemic stroke is by far the commonest clinical type encountered. These conclusions are further supported by experience at Ibadan, of over 1100 Africans seen over 18 years reported briefly in this communication. The results of the first community study over a 2-year period on the incidence of stroke in an African Urban (Ibadan) Community are presented. The study was carried out as part of a multinational multicentric study initiated and sponsored by the World Health Organization. The male to female ratio was five to two. Incidence rates reached peaks in the eighth decade in males and in seventh decade in females and were higher in males in all age groups, and the rates are comparable with those recorded in European populations, except in those under the age of 40 in Ibadan, in which age-specific incidence rates are considerably lower than in European and Japanese populations. Hypertension, diabetes mellitus constituted the main risk factors. Mortality and recurrence rates are described and are similar to experience in the Caucasians. Hypertension in the Nigerians predispose to a high frequency of cerebrovascular disease other than through mainly cerebral atherosclerosis. With increasing longevity of Nigerians and other Africans, the mortality and morbidity caused by cerebrovascular disease would probably become of enormous dimensions and adequate control of high blood pressure on a community basis may be the only way of preventing this: this would be desirable as myocardial infarction in contradistinction to hypertensive heart disease is an uncommon complication of high blood pressure in the Africans and prevention of hypertensive heart disease as shown by experience elsewhere can be achieved by control of high blood pressure, which does not seem to prevent ischaemic myocardial disease.
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PMID:Stroke in the Africans. 41 66

Sudden cardiac death can usually be resolved by the pathologist into ischaemic heart disease, non-vascular cardiac disease such as aortic stenosis or hypertrophic obstructive cardiomyopathy and infrequently a morphologically normal heart on naked eye examination. When ischaemic heart disease is present one third of cases have a recent occlusive coronary artery thrombosis. Two thirds of patients have coronary stenosis only; the minimum degree of disease reasonably associated with sudden death is one area of 85% stenosis. The majority of patients, however, have multiple areas of stenosis. The predominant causes of non-ischaemic sudden death are severe LV hypertrophy, hypertrophic obstructive cardiomyopathy and the prolapsing mitral valve syndrome. Where the heart and coronary arteries are morphologically normal, review of any previous ECG's, a family history and histological examination of the myocardium and conduction system may reveal a cause or at least allow a reasonable assumption of cardiac arrhythmia to be made. Sudden unexpected death where the circumstances strongly suggest a cardiac cause may pose problems for the pathologist. Ischaemic heart disease (coronary atherosclerosis) is undoubtedly the most frequent cause but even when this is so the detailed pathology is controversial. It is when coronary artery disease is conspicuously absent, often in young individuals previously in good health, that a problem exists. Sudden death in infancy (cot death) is a different entity with its own problems and is not here discussed further.
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PMID:Sudden unexpected cardiac death--a practical approach to the forensic problem. 46 29

Although coronary artery embolism is a recognized entity, there is little morphologic information indicating it is a cause of myocardial infarction. We studied patients with coronary artery embolic infarcts, which comprised 13% of our autopsy-studied infarcts. Underlying diseases predisposing to coronary emboli included valvular heart disease (40%), myocardiopathy (29%), coronary atherosclerosis (16%), and chronic atrial fibrillation (24%). Mural thrombi were present in 18 (33%). Myocardial infaction, clinically diagnosed in 15 (27%) patients, caused death in 11 (20%). Most emboli involved the left coronary artery and lodged distally, causing infarcts that were usually transmural. Because of their distal location and recanalization, coronary emboli may be a cause of infarcts with angiographically normal coronaries. Thus, coronary emboli are not rare, may produce signs and symptoms indistinguishable from altherosclerotic coronary disease, and by lodging distally in coronary arteries that are usually previously normal, they most often cause small but transmural myocardial infarction.
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PMID:Coronary artery embolism and myocardial infarction. 62 43

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

The most serious complication of diabetes mellitus is clinical nephropathy. The development of persistent proteinuria (urinary excretion of more than 300 mg albumin/24 hours) implies an extremely high risk of early death. Renal failure is the most frequent cause of death but the mortality of cardiovascular diseases is also increased. Besides the link between albuminuria (nephropathy) and atherosclerosis in coronary arteries, albuminuria is also a predictor of microangiopathy in other organs than the kidneys. The annual incidence of proliferative retinopathy in early nephropathy is 10-15% compared to only 1% in patients without nephropathy. Also signs of cardiomyopathy have been demonstrated in early nephropathy. Further we have described markers of universal endothelial damage in these patients, and we hypothesize that albuminuria not only is a predictor of renal disease but also of widespread vascular disease. Long-term improvement of metabolic control by use of insulin infusion pumps and early antihypertensive treatment seem to stop the further progression of early diabetic nephropathy and to significantly improve the prognosis of clinical nephropathy.
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PMID:Diabetic retinopathy, nephropathy and neuropathy. Generalized vascular damage in insulin-dependent diabetic patients. 149 Jun 95

Findings from 44 autopsy examinations of cardiac transplant patients during a 10-year period were reviewed. The autopsy rate was 85%. One half of the autopsy patients underwent original transplantation for ischemic heart disease and 34% for cardiomyopathy. Survival after transplantation ranged from 0 (intraoperative) to 91 months. Rejection (including hyperacute rejection) was responsible for 41% of deaths, followed by infection (25%), and intraoperative deaths at first transplantation (9%). Most of the remaining complications were related to surgery or artificial heart support, accelerated allograft atherosclerosis, and lymphoma. Infections were not only responsible for a substantial percentage of deaths but were also a co-morbid finding in a number of patients who died primarily of other causes. Pulmonary infections represented the most common anatomic site. Twenty-five percent of the autopsy patients had gastrointestinal and/or pancreatic abnormalities, principally mucosal inflammation, erosions or hemorrhage, and pancreatitis. Review of premortem rejection history indicated that 64% of patients who died of or with rejection at autopsy had had an episode of rejection 3 weeks after transplantation and/or at least one episode of severe rejection.
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PMID:Autopsy findings in cardiac transplant patients. A 10-year experience. 154 52

Diabetes mellitus is associated with excessive cardiovascular morbidity and mortality. Patients with diabetes mellitus suffer premature and severe atherosclerosis, and the relative impact is greater in women than in men. Clinical, experimental and pathological studies support the existence of a specific cardiomyopathy associated with diabetes mellitus. The cardiomyopathy plays an essential role in the pathogenesis of primary myocardial involvement, resulting in ventricular dysfunction, diminished cardiac pump performance and eventually overt heart failure. The authors discuss coronary heart disease and diabetic cardiomyopathy and indicate relevant treatment regimens.
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PMID:[Myocardial disease in diabetes mellitus]. 155 23

The hypothesis that diabetes mellitus provokes a specific cardiomyopathy is supported by numerous clinical, epidemiological and anatomopathological studies. However, the frequent association of diabetes mellitus with other conditions, such as hypertension and coronary atherosclerosis, both capable of causing the dysfunction of the cardiac muscle, makes it difficult to interpret many of the data reported in the literature and contributes to the continuing debate regarding the effective existence of diabetic cardiomyopathy and its possible pathogenetic mechanisms. In clinical terms, diabetic cardiomyopathy is manifested both as an altered diastolic and/or systolic phase, assessed using various non-invasive techniques, or as congested cardiac decompensation. The pathogenesis of diabetic cardiomyopathy is still not altogether clear. The alteration of the smallest coronary vessels might be responsible for the increased interstitial fibrosis found in the heart of diabetic patients. In this paper numerous data from the literature on this argument are reported and the authors advance the hypothesis that endothelial dysfunction may play a pathogenetic role in the development of cardiopathy.
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PMID:[Diabetic cardiomyopathy: possible pathogenetic role of coronary microcirculation]. 163 Jun 65


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