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

By lowering blood pressure, a number of hypertensive complications can be prevented, including congestive heart failure and such consequences of hypertensive arteriolar disease as nephropathy, intracerebral hemorrhage, and lacunar stroke. Whether atherosclerotic complications such as myocardial infarction can be prevented is more problematic and may depend on effects of the antihypertensive drugs other than the reduction of blood pressure, such as effects on plasma lipids and possibly hemodynamic effects. The following discussion summarizes a series of studies that suggest that the hemodynamic effects of antihypertensive drugs may be an important aspect of this problem. In studies in rhesus monkeys and hypertensive patients, antihypertensive drugs were shown to have differing effects on blood velocity and heart rate, important parameters in the genesis of arterial flow disturbances. In patients with carotid stenosis, hydralazine increased, whereas propranolol reduced, the occurrence of abnormal high-velocity flow patterns associated with turbulence and vortex formation. In a hypertensive (one kidney, one-clip) cholesterol-fed rabbit model, propranolol was significantly more effective than hydralazine in preventing the occurrence of aortic atherosclerosis. These observations suggest that the cardioprotective effect of beta blockers may extend to an antiatherosclerotic effect by hemodynamic mechanisms. This hypothesis is being further tested in patients with carotid stenosis.
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PMID:Hemodynamic effects of antihypertensive drugs. Possible implications for the prevention of atherosclerosis. 651 56

We studied 48 autopsy patients younger than 30 years who had severe coronary atherosclerosis. Twenty-one patients (44%) died suddenly, 26 (54%) had a history of chest pain, and one had chronic congestive heart failure. Twenty-one patients (44%) had single-vessel disease, 19 (40%) had two-vessel disease, and only nine (16%) had three or four major coronary arteries severely narrowed (greater than 75% cross-sectional area luminal narrowing) by atherosclerotic plaques. Thrombi in coronary arteries were noted in 27 patients (56%) and the left anterior descending coronary artery was the most frequently involved. The severity of coronary atherosclerosis was much less in patients younger than 30 years, and the atherosclerotic plaque consisted largely of foam cells, fibrous tissue, and pultaceous debris, with minimal calcific deposits. Thus, it is this population that is most likely to be susceptible to regression of the atherosclerotic plaque.
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PMID:Coronary heart disease in 48 autopsy patients 30 years old and younger. 668 16

16 patients with advanced carcinoma of the prostate were studied in a prospective trial during treatment with oestrogens. Changes in plasma levels of gonadotropins (LH and FSH) and testosterone as well as salt-water balance, antithrombin III, fibrinolytic activity, plasma lipoproteins known to influence the risk of cardiovascular complications, were recorded during the initial 2 months. The plasma testosterone, LH and FSH concentrations were suppressed. The plasma volume was increased and the plasma albumin concentration was decreased. The antithrombin III concentration and the tissue fibrinolytic activity were decreased. The low density lipoprotein (LDL) level decreased and the high density lipoprotein (HDL) level increased. The recorded changes of cardiovascular risk factors indicate that the risk of water retention and thereby congestive heart failure and the risk for thromboembolic disease are increased during oestrogen treatment. The changes in lipoproteins with a marked elevation of the HDL/LDL ratio are thought to retard the development of atherosclerosis.
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PMID:[Effects of oestrogens on cardiovascular risk factors in patients with carcinoma of the prostate (author's transl)]. 680 22

We reviewed a consecutive series of 90 patients undergoing concomitant resection of ascending aortic anerysm and aortic valve replacement (AVR) utilizing noncomposite "conventional" techniques in order to assess the early and late results, to define limitations of this operative approach, and thereby to clarify the indications for composite reconstruction of the aortic root. Mean age was 55 years. Twenty percent had Marfan's syndrome, and 13% had aortic dissections. The cause of the aneurysm was dissection in 13% of cases, syphilis in 11%, atherosclerosis in 9%, and degeneration (with or without cystic medionecrosis) in 67%. Follow-up averaged 3.8 years and extended to 11.5 years maximum. AVR and complete excision of the aneurysm (preserving small tongues of aortic wall circumscribing the coronary artery ostia) coupled with tubular graft replacement of the ascending aorta were performed. Nineteen percent of patients required individual technical modifications relating to the coronary arteries. Operative mortality rate was 13%, with the majority of deaths being due to cardiac causes. Contemporary (1975 to 1978) operative mortality rate was 4.3%. Seven percent required re-exploration for hemorrhage and 2.4% had perioperative myocardial infarctions. Late functional results were generally good (average N.Y.H.A. Class 1.4). Late thromboembolism, angina, myocardial infarction, and congestive heart failure occurred at linearized rates of 3.4% per patient-year, 4.9% per patient-year, 1.1% per patient-year, and 5.2% per patient-year, respectively. No prosthetic valve endocarditis, graft infection, or recurrent aneurysms of the aortic root were observed. Late reoperation was necessary in eight patients (3% per patient-year), but reoperation for disease confined to the ascending aorta accounted for only three of these cases (1.1% per patient-year). Overall actuarial survival rates were 67% +/- 5% at 5 years and 50% +/- 9% at 10 years; survival rates for the 78 operative survivors were 77% +/- 5% and 57% +/- 10% at the same time intervals, respectively. Only one late death could be attributed to complications arising in the reconstructed aortic root. These results confirm that such simple, noncomposite techniques are safe, portend minimal risk of late complications and the attendant necessity for reoperation, and provide satisfactory long-term survival. We believe that composite techniques should be primarily reserved for selected cases of advanced necrotizing prosthetic or natural endocarditis.
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PMID:Concomitant resection of ascending aortic aneurysm and replacement of the aortic valve: operative and long-term results with "conventional" techniques in ninety patients. 698 12

Classical writings suggest that the Roman emperor Hadrian died from congestive heart failure resulting from hypertension and coronary atherosclerosis. This diagnosis is supported by the identification of bilateral diagonal ear creases on sculptures of several busts of Hadrian as well as literary evidence of behavior pattern A.
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PMID:Diagonal earlobe creases, type A behavior and the death of Emperor Hadrian. 699 Jun 26

The clinical characteristics, electrocardiographic changes, and long-term prognosis were studied in 50 patients suffering nontransmural myocardial infarctions. It is concluded that nontransmural myocardial infarcts tend to occur in older patients with known coronary atherosclerosis and these infarctions are frequently preceded by a period of unstable angina. The clinical course is often complicated with congestive heart failure and other major management problems. Three different groups of electrocardiographic changes were noted and all four in-hospital deaths showed the same pattern of electrocardiographic changes. The prognosis of patients suffering nontransmural myocardial infarctions is not good, as evidenced by a death rate similar to reported patients suffering transmural myocardial infarction and a significant incidence of cardiovascular disability in those who survive.
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PMID:Clinical characteristics, electrocardiographic and enzyme correlations, and long-term prognosis of patients with chest pain associated with ST depression and/or T wave inversion. 735 99

Morphologic changes in the subendocardial myocardium that appeared to be caused by severe, chronic subendocardial ischemia were studied in patients with fatal ischemic heart disease admitted to the Specialized Center of Research for Ischemic Heart Disease at the University of Alabama in Birmingham in the period 1970--1977. Thirteen patients were selected for this report on the basis that they had the lesions in the subendocardial myocardium we believe to have been caused by subendocardial ischemia and had no evidence of acute or remote myocardial infarction or other conditions that may have contributed to their terminal illness or death. Clinical findings were unstable angina, congestive heart failure, usually no increase in plasma enzymes indicative of myocardial damage, and electrocardiographic changes consistent with subendocardial ischemia. All 13 patients had 75% or greater stenosis of the three major coronary arteries; none had acute thrombotic or embolic coronary artery occlusion. The left ventricle in all cases was hypertrophied. The subendocardial myocardium showed circumferential pallor, hyperemia, or focal fibrosis without perceptible loss of volume in papillary muscles or trabeculae carneae. Microscopically, acute lesions showed one to two layers of preserved myofibers adjacent to the endocardium, vacuolar change in the deeper fibers, and focal areas of coagulation necrosis of variable size in the myocardium external to the fibers with vacuolar change. Coagulation necrosis was extensive in some cases and usually was not associated with infiltration of neutrophils. The repair reaction involved removal of necrotic sarcoplasm by mononuclear phagocytes, resulting in a reticular-appearing tissue without evidence of stromal collapse. Granulation tissue was not seen. Collagen fibers appeared to be deposited within the area of previous sarcolemmal sheaths. The distribution and morphology of subendocardial myocardial lesions associated with severe coronary atherosclerosis are distinctive and can be distinguished from myocardial necrosis or fibrosis associated with acute total occlusion of a coronary artery.
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PMID:Subendocardial ischemic myocardial lesions associated with severe coronary atherosclerosis. 736 50

Congestive heart failure is the end product of a progressive series of events resulting from acute myocardial damage. Circulatory neurohormonal systems are activated during the acute phase of left ventricular dysfunction resulting from initial myocardial damage and again in the latter phase of decompensated heart failure. However, these neurohormonal mechanisms return to normal during the compensated stage of heart failure. Recent studies have suggested that autocrine/paracrine modulators of cardiovascular function are activated in the preclinical phase preceding the development of overt heart failure. The renin-angiotensin system in particular has been shown to modulate many of the chronic processes involved in the pathophysiology of cardiovascular disorders. Recent studies suggest that locally generated angiotensin II may contribute to the secondary structural changes seen in cardiovascular disorders, such as cardiac hypertrophy and remodelling, coronary artery disease, and atherosclerosis. Thus, inhibition of angiotensin formation with angiotensin converting enzyme (ACE) inhibitors, particularly at the tissue level, may provide valuable cardioprotective effects. Additional evidence points to the efficacy of ACE inhibitors in preventing the progression of asymptomatic left ventricular dysfunction to overt heart failure.
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PMID:Angiotensin as local modulating factor in ventricular dysfunction and failure due to coronary artery disease. 752 57

The coexistence of different clinical syndromes due to atherosclerosis in different organs is not rare and emphasizes the diffuse nature of this vascular process. Although renovascular disease may cause hypertension and/or renal insufficiency, it may also occur in the absence of the usual clinical markers that suggest renovascular hypertension. We report a patient with stable coronary anatomy who presented with crescendo angina pectoris. Diagnosis of renovascular hypertension was made by screening renal angiography at the time of the cardiac catheterization. Renal artery stenting resulted in stabilization of the coronary syndrome and obviated the need for further coronary intervention. To our knowledge, this is the first case of renovascular hypertension precipitating an unstable coronary syndrome in a patient with documented stable coronary anatomy. Review of the literature supports that patients undergoing cardiac catheterization are a high risk population for renovascular disease, particularly in the presence of other predictive factors such as documented coronary artery disease, older age, female gender, congestive heart failure, peripheral vascular disease, renal insufficiency, and smoking. Firm recommendations for routine screening renal angiography in patients undergoing peripheral or coronary angiography will need further studies.
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PMID:Renal artery stenosis presenting as crescendo angina pectoris. 755 35

Review article informs about the physiological and pathophysiological effects of the most potent vasoconstrictor agent endothelin (ET). This vasoactive polypeptide (21-aminoacid) has three izoforms (ET-1, ET-2, ET-3) and participates on regulation of the vascular tone and on remodelling of the vascular and myocardial wall. Article is focused on the effects of endothelins on the cardiovascular system, kidney and the central nervous system with respect to their expected role in the initiation and sustaining of disorders and diseases accompanied by the local and general vasconstriction. Findings concerning the role of endothelins in the pathogenesis of arterial hypertension, myocardial infarction, congestive heart failure, atherosclerosis, shock conditions, renal failure, and vasospasm following the subarachnoidhem orrage are discussed.
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PMID:[Endothelin--a cardiovascular regulatory peptide. II. Outline of its pathophysiologic activity]. 758 20


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