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

We evaluated left ventricular function in 10 scleroderma patients with signs and symptoms suggestive of congestive heart failure. M-mode and two-dimensional echocardiography demonstrated normal to increased systolic function in all patients. The presence of pulmonary venous congestion on the chest radiograph was not useful in assessing left ventricular systolic function. Five of nine patients with normal to increased left ventricular ejection fraction (LVEF) had increased cardiothoracic ratios and increased pulmonary vascular markings. Left ventricular hypertrophy was associated with a worse New York Heart Association functional class, more pulmonary vascular congestion, and greater left atrial size. In the presence of normal systolic function and ventricular hypertrophy, diminished left ventricular diastolic compliance may account for the cardiac dysfunction in these patients. Cold pressor testing induced peripheral Raynaud's phenomenon in nine of nine patients; however, no ST segment changes or chest pain was provoked. In seven of nine patients there was no abnormal fall in LVEF. The mechanism for the fall in ejection fraction seen in two patients may be related to an increase in afterload or myocardial ischemia secondary to coronary atherosclerosis. We found little to suggest that a myocardial Raynaud's phenomenon affects left ventricular perfusion or systolic function. Clinical signs and symptoms of congestive failure as well as chest radiographs are poor indicators of impaired systolic function in scleroderma patients. Based on these findings, it appears that evaluation of left ventricular systolic function should include echocardiographic or angiographic study before such patients are treated for heart failure with inotropic agents.
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PMID:Left ventricular function at rest and during Raynaud's phenomenon in patients with scleroderma. 650 43

Out of 9015 necropsies of patients, over the age of 14, performed between January 1, 1967 and March 1, 1979 at a general hospital in Sofia, 729 of them (8,07%) proved to have diabetes as well. Renal complications were found in 315 of them (43,2%)--chronic pyelonephritis being most frequent (21,2% of all diabetics) followed by diabetic glomerulosclerosis (DG)--18,5 per cent of the diabetics and in 7,9 per cent--a combination of both complications. The authors studied only the patients with DG. They lived about 5,2 years, on the average, less than the other diabetics and 91,1 per cent of them had arterial hypertension versus 61,3 per cent among the rest of the diabetics. A total of 90 per cent of the hypertonics with DG had left ventricular hypertrophy--I--III stage. Atheromatosis of aorta and coronary arteries were found, in those deceased from hypertonic disease, to be more frequent and more severely manifested, than those decreased from chronic pyelonephritis with hypertension and than those deceased from chronic glomerulonephritis with hypertension in all age groups. Regardless of that, the morbidity rate among the deceased with DG from cardiac complications is a little less than that among the deceased from hypertonic disease and the causes for brain vascular complications among diabetics, in spite of the more frequent and more severe atherogenesis has been three times less rare than among the deceased from hypertonic disease. Very likely, the involvement of the kidneys contributes to those discrepancies.
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PMID:[Cardiovascular changes among deceased patients with diabetes mellitus and diabetic nephropathy among 9015 autopsied over the age of 14]. 667 84

The causes of sudden, unexpected death in highly-conditioned competitive athletes are summarized. In the vast majority of young athletes (less than 35 years of age) sudden death is due to underlying structural cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths and may account for about one-half of the sudden deaths in a youthful athletic population. Cardiovascular abnormalities that appear to be less frequent important causes of sudden death include anomalous origin of the left coronary artery from the anterior sinus of Valsalva, ruptured aorta (due to cystic medial necrosis), idiopathic concentric left ventricular hypertrophy and coronary artery atherosclerosis. Other diseases which are probably particularly uncommon causes of sudden death in the young athlete include mitral valve prolapse, aortic valvular stenosis, acute myocarditis, QT interval prolongation syndromes, hypoplasia of the coronary arteries or sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life. In only about 25% of those competitive athletes who die suddenly is underlying disease identified prior to participation and rarely is the correct clinical diagnosis made. In contrast, when sudden death occurs in older competitive or recreational athletes (over 35 years of age) it is usually due to coronary artery disease.
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PMID:Hypertrophic cardiomyopathy: a common cause of sudden death in the young competitive athlete. 668 29

This study of 14 cases, found in 130 autopsies of people died in a Department of Cardio-vascular diseases, emphasizes the frequency of this lesion (10 p. 100) often ignored. Elderly people over 75 years are affected and twice more female than male. Grossly, this abnormality, responsible of a constant mitral insufficiency, is in the posterior cusp attachment at the junction with the ventricular wall. The atrial surface and the line of cusp apposition, commissures and chordae are respected. The main lesions associated with it are left ventricular hypertrophy, coronary and systemic atherosclerosis and most often aortic degenerative calcification, described by Monckeberg, in 50 p. 100 cases. Microscopically, calcifications are surrounded by fibrosis with non specific moderate inflammatory changes. Clinically mitral ring calcification must be searched in case of conduction disturbances of systolic murmurs by left anterior oblique radiography and above all by echocardiography. Except conduction disturbances, complications are infrequent and only seen in advanced lesions. No abnormality of calcium or lipid metabolisms is noted. In agreement with other studies, this one emphasizes the usefulness of echocardiographic diagnosis and the necessity to separate this geriatric entity from advanced post rheumatoid type lesions.
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PMID:[Calcifications of the mitral valve ring. A clinico-pathological study of 14 cases (author's transl)]. 730 71

From pharmacologic investigations and clinical studies it is known that angiotensin-converting enzyme (ACE) inhibitors exhibit additional local actions, which are not related to hemodynamic changes and which cannot be explained simply by interference with the renin-angiotensin system with subsequent inhibition of angiotensin II formation. Because ACE is identical to kininase II, which inactivates the nonapeptide bradykinin (BK), potentiation of BK might be responsible for these additional effects of ACE inhibitors. To prove the specificity of BK-mediated effects by ACE inhibition, we used the specific B2 kinin receptor antagonist HOE 140 in different models: endothelial cell cultures; atherosclerosis in high-cholesterol-fed rabbits; neointima formation with smooth cell proliferation and migration after endothelial denudation in rats; myocardial ischemia in rats, rabbits, and dogs; and left ventricular hypertrophy in rats. The beneficial effects of ramipril or BK given in non-blood pressure-lowering doses in these models were abolished by HOE 140 (icatibant). Ramipril exerts cardioprotective effects in different experimental models. The formation of the endothelial autacoids nitric oxide and prostacyclin, enhanced when BK degradation is inhibited by ACE inhibition, may contribute to the observed beneficial effects.
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PMID:Contribution of bradykinin to the cardiovascular effects of ramipril. 751 34

The epidemiological approach to investigation of cardiovascular disease was innovated in 1948 by Ancel Keys' Seven Countries Study and T.R. Dawber's Framingham Heart Study. Conducted in representative samples of the general population, these investigations provided an undistorted perception of the clinical spectrum of cardiovascular disease, its incidence and prognosis, the lifestyles and personal attributes that predispose to cardiovascular disease, and clues to pathogenesis. The many insights gained corrected numerous widely held misconceptions derived from clinical studies. It was learned, for example, that the adverse consequences of hypertension do not derive chiefly from the diastolic pressure, left ventricular hypertrophy was not an incidental compensatory phenomenon, and small amounts of proteinuria were more than orthostatic trivia. Exercise was considered dangerous for cardiovascular disease candidates; smoking, cholesterol, and a fatty diet were regarded as questionable promoters of atherosclerosis. The entities of sudden death and unrecognized myocardial infarction were not widely appreciated as prominent features of coronary disease, and the disabling and lethal nature of cardiac failure and atrial fibrillation was underestimated. It took epidemiological research to coin the term "risk factor" and dispel the notion that cardiovascular disease must have a single origin. Epidemiological investigation provided health professionals with multifactorial risk profiles to more efficiently target candidates for cardiovascular disease for preventive measures. Clinicians now look to epidemiological research to provide definitive information about possible predisposing factors for cardiovascular disease and preventive measures that are justified. As a result, clinicians are less inclined to regard usual or average values as acceptable and are more inclined to regard optimal values as "normal." Cardiovascular events are coming to be regarded as a medical failure rather than the first indication of treatment.
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PMID:Clinical misconceptions dispelled by epidemiological research. 758 24

Persistent inappropriate blood pressure elevation leads to the development of left ventricular hypertrophy, progressive atherosclerosis, and structural changes in the arterial tree. These changes result in clinical manifestations such as ischemic cardiac and cerebral events, congestive heart failure, renal failure, and peripheral vascular insufficiency. This article reviews the 5-year course of 439 patients with primary hypertension who were seen at a time (1946-1953) when potent antihypertensive therapy was not widely used. At the end of 5 years, 55% of the men (78 of 143) and 28% of the women (83 of 296) were dead. The principal causes of death were coronary insufficiency, congestive heart failure, cerebral infarction and hemorrhage, accelerated hypertension, renal failure, and dissecting aneurysm of the aorta. Coronary insufficiency and accelerated hypertension predominated in men, whereas women died principally of cerebral events and congestive heart failure. The 439 patients were stratified according to the level of their office blood pressure on the first visit, the severity of the changes in the optic fundi, the degree of left ventricular hypertrophy determined by electrocardiogram, cardiac enlargement determined by roentgenogram and their renal function, as measures of end-organ damage. Patients who had higher initial blood pressures showed more evidence of end-organ damage than patients with lower initial pressures. The higher the initial blood pressure or the more advanced the evidence of end-organ damage, the greater was the 5-year mortality. The mortality was particularly high in patients who had already sustained a clinical cardiovascular event before entry into the study and in those with malignant hypertension or gross cardiomegaly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Retrospective and prospective research on hypertension-related end-organ damage. 760 71

Hypertension is a complex disease, the treatment of which should not only lower systolic and diastolic blood pressure but also attenuate the secondary consequences of the disease. These include vascular injury (including atherosclerosis), stroke, left ventricular hypertrophy, and renal damage. To establish whether the long-acting, vascular-selective calcium antagonist amlodipine attenuates some of these secondary consequences of hypertension, 5-week-old stroke-prone hypertensive and 8-week-old spontaneously hypertensive rats were treated (orally) with 5 mg/kg/day and 10 mg/kg/day amlodipine, respectively, for 30 weeks. The treatment resulted in a significant lowering of systolic blood pressure, accompanied by reduced cardiac hypertrophy and prolonged survival. Evidence for a protective effect of amlodipine on the vasculature was obtained by treating cholesterol-fed rabbits with 1-5 mg/kg/body weight/day. This resulted in a reduction in vascular Ca2+ overloading and a reduced incidence of sudanophilic lesion formation. Protection against ischemia-induced changes in the myocardium included a reduction in the ischemia-induced externalization of endothelin-1 binding sites.
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PMID:End-organ involvement and calcium antagonist therapy: animal studies. 760 72

Patients with morbid obesity have high rates of sudden, unexpected cardiac death. The mechanism of death in these patients is uncertain. Twenty-eight patients with morbid obesity (22 sudden cardiac deaths, 6 unnatural deaths) were compared to 11 age-matched nonobese patients with traumatic deaths. Heart weight, left ventricular cavity diameter, left and right ventricular wall thickness, ventricular septal thickness, epicardial fat thickness, and extent of coronary artery atherosclerosis were determined; myocyte size, nuclear size, and degree of interstitial fibrosis were calculated morphometrically. Mean heart weights in the patients with morbid obesity were increased but remained constant as a percentage of body weight. Of the gross parameters, only heart weight and left ventricular cavity size were independent predictors of obesity. Of microscopic parameters, only nuclear area was an independent predictor of obesity. Of 22 patients with morbid obesity, dilated cardiomyopathy was the most frequent cause of sudden cardiac death in (10 patients), followed by severe coronary atherosclerosis (6), concentric left ventricular hypertrophy without left ventricular dilatation (4), pulmonary embolism (1), and hypoplastic coronary arteries (1). The cardiomyopathy of morbid obesity is characterized by cardiomegaly, left ventricular dilatation, and myocyte hypertrophy in the absence of interstitial fibrosis. It is the most common cause of sudden cardiac death in these patients.
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PMID:Sudden death as a result of heart disease in morbid obesity. 763 12

Cardiovascular complications are the main cause of mortality in patients with chronic renal failure. Hypertension and lipid abnormalities which often lead to left ventricular hypertrophy and accelerated atherosclerosis as well as coronary artery disease are a common cause of death. On the other hand uremia often causes pericarditis and thereby may lead to cardiac tamponade and constrictive pericarditis. Renal failure can also cause secondary hyperparathyroidism, amyloidosis, hemosiderosis and oxalosis which can produce visceral infiltrations and lead to a variety of disturbances of cardiovascular functions. Life-threatening arrhythmias are one of the major cardiovascular complications during maintenance dialysis as their occurrence might result in sudden death. The aim of cardiologic management which includes the complex of preventive and therapeutic measures is to reduce the morbidity and mortality and to improve the quality of life.
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PMID:[Cardiologic management in patients on a long-term dialysis program]. 763 9


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