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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors involved in the development of coronary atherosclerosis and the possible role of estrogens in its development are discussed. Risk factors in the development of atherosclerosis include hyperlipemia, hypertension, cigarette smoking, and diabetes. However, the incidence of heart disease and presence of risk factors are also related to heredity, geography, and socioeconomic conditions, and to diet, exercise, and emotional stress. Contrary to previous belief, high doses of estrogens aggravate the condition of men and menopausal women at risk of heart attack. Although estrogens do not markedly alter cholesterol levels, they do tend to elevate triglyceride levels and contribute to hyperlipemia. They are also associated with diabotegenic sequelae and hypertension. Pregnancy and estrogens increase blood clotting Factors VII and X, accelerate prothrombin time, shorten clotting time, and incre ase platelef aggregation. Further research into the role of estrogens in the development of atherosclerosis is recommended.
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PMID:Estrogens and atherosclerosis. 99 76

In order to evaluate the sensibility and specificity of the maximal treadmill exercise-stress test, a correlation was made, in fifty patients, of the resus of the test and the findings at selective coronary arteriography. None of the patients had received cardioactive drugs previous to the study. Among twenty-nine patients with proven coronary disease, three had false negative exercise tests. The remaining twenty-six cases had positive tests. The sensitivity of the method (reliability in identifying the presence of disease) was 89.7%. Twelve of twenty-one subjects with normal coronary arteries had negative exercise tests. In eight patients without coronary artery lesions, the exercise test was positive (false positive tests). An additional patient had an equivocal response and is included among the false positive responses. These nine-patients form a special group since they had severe heart disease, even though it was not due to atherosclerosis of the major coronary vessels. The specificity of the test (reliability in identifying the absence of disease) was 57.1%. However, in the absence of other heart disease, none of the subjects with normal coronary arteries had a false positive response. An analysis is made of the possible causes of these false negative and false positive responses. It was also shown in this study that the patients with coronary artery disease and positive treadmill tests had a definite functional aerobic impairment as well as a significant reduction in such indices of myocardial oxygen consumption as the heart rate and the double product (pressure-pulse), when compared to the subjects with normal coronary vessels and negative tests. In the group of patients with false positive responses, these parameters were not significantly different from the normals. The exercise-stress test protocol used in this study appears to have an adequate sensibility and an acceptable specificity.
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PMID:[Correlation between exercise test and coronariography]. 102 29

At present we have no data to assure us that physical activity changes or prevents the development of coronary atherosclerosis or that it changes the progression of the disease which is already present. The data are excellent that in about 85% of patients with coronary disease, exercise training has beneficial personal and societal effects. However, even this opinion must be subjected to critical scrutiny. Several (controlled and randomized) studies of the effects of exercise training on arteriosclerotic heart disease subjects are in progress, in the United States, in Canada, and in Europe. The National Exercise and Heart Disease Project in the U.S.A has already accessed 600 arteriosclerotic heart disease subjects and expects to attain the target study population of 800 subjects by 1 June 1976. We msut be prepared and willing to accept the results of such rigorously controlled studies. In another four to five years of follow-up, the basis for our present views will be either confirmed or rejected -- although most of us anticipate a validation of our present opinion, viz., exercise training enhances the quality of life, and coping capacity, even though the direct effects on the course of coronary atherosclerosis have not been demonstrated.
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PMID:Exercise training as a therapeutic modality. 102 57

The known risk factors for atherosclerosis do not possess the same significance in young people as in the elderly. Hypercholesterolemia, diabetes and cigarette smoking appear to have a greater bearing below the age of 50 than later, particularly in myocardial infarction but also in apoplexy. On the other hand, hypertension is an important factor in the young and, especially in the case of apoplexy, even more so in advanced age. There is marked difference with regard to preexisting heart disease, which scarcely plays a role in myocardial infarction of the younger patient but is a factor in some 50% of hemiplegia cases. Only one fifth of elderly patients with this disease have no preexisting carcdiopathy. The similarity of the risk factors in elderly patients either with or without apoplexy is due to the fact that arteriosclerosis is already established in both groups and the risk factors which give rise to ischemia, thrombosis or embolism assume prominence. The therapeutic implications are briefly discussed.
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PMID:[Risk factors and age]. 113 58

The severity of coronary atherosclerosis at autopsy was studied in two series comprising 169 cases of coronary death and 231 people who died of violent causes. In the former the fatal attack lasted less than 24 hours from the onset of symptoms in 70% of cases. In only three men did the terminal attack last more than 24 hours, while in the remaining 28% of cases, although death was not witnessed these were also likely to have been sudden deaths. A recent infarct with or without an old myocardial infarct was found at autopsy in 47% of cases and an old infarct alone in 34%. In 19% of coronary deaths no recent or old infarct was detected. The surface areas of the atherosclerotic lesions were assessed in arterial specimens by pointcounting. The degree of stenosis was estimated visually. The mean extent of raised lesions and clacification and the median value of stenosis score, which expressed the degree of stensosi in the coronary arterial tree, were significantly higher in all age groups in persons who died of coronary heart disease than in those who died violently. A marked overlapping between the individuals in the two series was, however, found in both for the exent of raised lesions and the severity of stenosis score. Raised lesions in coronary patients were calcified to about the same extent as those in persons ten years older in the series of violent deaths. Coronary atherosclerosis was most severe in coronary patients who had had symptomatic heart disease and had an old myocardial infarct and least severe in those in whome sudden death was the first manifestation of coronary heart disease from violent deaths as regards the extent of the raised lesions or prevalence of occlusion. The degree of coronary stenosis in coronary patients was closely related to the total extent of advanced coronary atherosclerosis.
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PMID:Coronary atherosclerosis in cases of coronary death as compared with that occurring in the populatiom. A study of a medico-legal autopsy series of coronary deaths and violent deaths. 121 56

Coronary- and LV-angiography in coronary heart disease are indicated I) to clarify whether or not surgery is required (e.g. aorto-coronary-bypass operation, aneurysmectomy) in 1) drug resistent angina pectoris, 2) myocardial aneurysms (or the suspicion of), 3) VSD following myocardial infarction and/or 4) as preoperative investigations in mitral regurgitation or 5) other valve lesions. II) These investigations are furthermore indicated in the under-50-yr.-old considering their prognosis and diagnosis 1) following myocardial infarction 2) to clarify a pathological exercise test with or without angina pectoris 3) in the differential diagnosis of myocardial diseases and 4) occasionally in patients with a number of risk factors or exposed to particular occupational hazards or from families with a high incidence of early deaths from heart disease. Coronary- and LV-angiography are contraindicated in 1) generalized stenosing atherosclerosis, 2) acute myocardial infarction, 3) failure from other organ-systems (e.g. kidney), 4) drug resistent endogenous risk factors and/or relevant obesity, 5) biological age over 60-65.6) continued nicotine dependence. In many cases the specific diagnostic investigations will include the assessment of coronary flow at rest and during maximal drug induced coronary dilatation. This enables us to estimate the coronary reserve and to diagnose coronary insufficiency in patients with normal coronary angiograms.- Instructive morphological and/or functional results illustrate this presentation.
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PMID:[Indications for coronary arteriography and left ventriculography in coronary heart disease (author's transl)]. 125 Nov 19

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

Women, like men, are susceptible to coronary atherosclerosis. Like men, more women die of heart disease than all forms of cancer combined. Coronary atherosclerosis is the result of the interplay of a number of factors, the most important of which are abnormal levels of circulating lipoproteins. As more has become known about the mechanisms by which abnormal levels of circulating lipoproteins promote atherosclerosis, certain risk factors have emerged as concerns for women, including: (1) diabetes mellitus as a risk factor, perhaps through its more profound effects on circulating lipoproteins; (2) serum triglyceride levels, and (3) changes in high-density lipoprotein cholesterol. The widespread use of exogenous hormones in women as both oral contraceptives and postmenopausal hormone replacement may also play a role in developing atherosclerosis. In general, estrogen affects circulating lipoprotein levels favorably, whereas progestins have the opposite effect. The effects of estrogen/progestin combinations in either oral contraceptives or postmenopausal hormone replacement will depend on the relative dose and potency of each of these constituents. Epidemiologic studies indicate that the use of oral contraceptives has no profound effect on the long-term risk of heart disease, whereas unopposed estrogen (without progestin) in postmenopausal hormone replacement therapy may lower that risk considerably. Recent U.S. and European guidelines for the detection, evaluation, and treatment of hypercholesterolemia in adults make it imperative that obstetrician-gynecologists, in their dual role as primary-care physicians and prescribers of exogenous hormones, be aware of and informed about the relationship between circulating lipids and lipoproteins and coronary heart disease in women.
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PMID:Women, lipoproteins, and cardiovascular disease risk. 135 61

The renin-angiotensin system (RAS) plays a major role in the control of blood pressure and cardiovascular homeostasis and is involved in the pathogenesis of a number of cardiovascular disorders. The efficacy of angiotensin-converting enzyme (ACE) inhibitors in the treatment of hypertension and congestive heart failure has led to the widespread clinical use of ACE inhibitors in primary or secondary prevention of heart disease. The demonstration of the expression of the components of the RAS in several extrarenal tissues, as well as local generation of angiotensin II, has confirmed the existence of a tissue RAS that may serve organ-specific functions and act independently from the plasma RAS. The concept of paracrine/autocrine functions of the local RAS has changed our understanding of the functions of the RAS and suggests that tissue ACE inhibition may be of greater importance than inhibition of circulating ACE in the treatment of congestive heart failure and other cardiovascular disorders. Whereas the circulating endocrine RAS appears to be responsible for mediation of acute effects, the tissue RAS seems to be involved in more chronic situations, such as secondary structural changes of the cardiovascular system, and therefore could contribute to the pathogenesis of hypertension as well as other cardiovascular disorders, such as cardiac hypertrophy, coronary artery disease, and atherosclerosis. Several experimental and clinical findings suggest that reversal of cardiovascular structural changes secondary to cardiovascular disease and enhancement of renal sodium excretion by ACE inhibitors are important long-term antihypertensive actions possibly mediated by inhibition of the tissue RAS.
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PMID:Effects of angiotensin-converting enzyme inhibitors on tissue renin-angiotensin systems. 141 88

The prevalence of abnormal lipid and lipoprotein values was determined in 125 consecutive patients with lower-extremity arteriosclerosis obliterans, and the lipid and lipoprotein abnormalities in these patients were characterized. Only 13% of the patients had normal lipid/lipoprotein profiles. Forty-eight percent of patients had low levels of high-density lipoprotein cholesterol. High-density lipoprotein cholesterol values were lower in patients with concomitant coronary heart disease compared with those without heart disease. High-density lipoprotein cholesterol values were inversely related to weight, to triglyceride values, and to diabetes mellitus. Twenty-eight percent of patients had "desirable" total cholesterol levels (< 200 mg/dL), and 32% had low-density lipoprotein cholesterol values less than 130 mg/dL. Following National Cholesterol Education Program guidelines may be misleading in patients with documented lower-extremity atherosclerosis; therefore, complete lipid/lipoprotein profiles should be performed in these patients.
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PMID:Lipid and lipoprotein abnormalities in lower-extremity arteriosclerosis obliterans. 146 32


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