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

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

Coronary artery aneurysms were found in 16 men between 37 and 62 years of age, mean 51 years. Aneurysms were of two types: saccular and fusiform. They involved the right coronary artery in 13 (87 per cent), the circumflex artery in eight (50 per cent) and the left anterior descending artery in five (31 per cent). In some patients, more than one vessel was involved. Twelve patients presented with angina pectoris, three with congestive heart failure and one with both. Five were in functional class II, eight were in class III and three were in class IV at the beginning of the study. The electrocardiogram showed evidence of previous myocardial infarction in four patients; four patients had left ventricular hypertrophy, one had left axis deviation, one had left bundle branch block, one had right bundle branch block, two had first degree atrioventricular block and seven had abnormalities in the S-T segment and T wave. Obstructive coronary disease was present in all; the obstruction score was from 1 to 4 in three patients, from 5 to 9 in four patients and from 10 to 14 in the remaining nine. Similar aneurysms were found in the pulmonary artery of one patient and in the abdominal aorta of three patients; in seven of 14 patients with adequate venous angiograms, varicosities of the coronary venous tree were observed. Left ventricular dysfunction and angina pectoris were noted in patients with significant obstructive coronary disease (greater than 70 per cent) and also in patients without obstruction but with coronary aneurysms. Ten patients were treated surgically; nine underwent aortocoronary bypass and one mitral valve replacement. Criteria for bypass was the presence of obstructive disease and medically unresponsive angina pectoris. All but one surgically treated patient showed improvement. The functional class in medically treated patients was unchanged. Fourteen patients were still alive at the completion of the study. The findings of this study suggest that angina pectoris and left ventricular dysfunction can occur with coronary artery aneurysm without coronary artery obstructions. Coronary aneurysms may be a subset of atherosclerosis, and this process may involve other vascular territories. The prognosis in those patients appears to be no worse than in patients with obstructive coronary disease and no aneurysms.
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PMID:Coronary artery aneurysms: study of the etiology, clinical course and effect on left ventricular function and prognosis. 30 May 67

Little is known of the clinical significance of myocardial bridges, which may be recognized angiographically as systolic coronary artery narrowing (SCAN). A retrospective review of a 1 year's experience (313 consecutive coronary arteriograms) revealed 5 patients with SCAN, an incidence of 1.6%. SCAN involved the proximal and/or middle segments of the left anterior descending coronary artery in all patients. It is of particular note that the administration of nitroglycerin noticeably accentuated the SCAN phenomenon in each of 3 patients to whom it was administered. Four of the 5 patients had left ventricular hypertrophy due to hypertrophic cardiomyopathy (2), aortic stenosis (1), and hypertension (1). All 5 patients with the SCAN phenomenon had anginal chest pains, and critical obstructive coronary atherosclerosis was observed in only 2 cases. The other 3 patients showed, otherwise normal coronary arteriograms. Thus, myocardial bridges appear to be angiographically manifest predominantly in patients with cardiac hypertrophy. Nitroglycerin, which accentuates SCAN, might be useful as a provocative test to enhance the angiographic recognition of this phenomenon. The possible role of myocardial bridges in the production of myocardial ischemia warrants further investigation.
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PMID:Myocardial bridges in man: clinical correlations and angiographic accentuation with nitroglycerin. 40 19

There are two mechanical determinants of coronary blood flow and its distribution: resistance and pressure gradient. Resistance is determined by blood viscosity and the anatomy and geometry of the coronary vascular bed. The coronary vascular pressure gradient is the difference between aortic root pressure and intramyocardial pressure. A number of factors such as coronary atherosclerosis, ventricular hypertrophy, and myocardial edema may adversely affect the determinants of coronary flow before, during, or after cardiopulmonary bypass, thereby lowering or eliminating regional or local coronary reserve and promoting the likelihood of a myocardial ischemic injury. The subendocardial layers of the left ventricle appear to be more vulnerable, perhaps in part because they depend entirely on diastolic coronary flow.
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PMID:Mechanical determinants of myocardial blood flow and its distribution. 80 72

A unique case is described of a 64-year-old white woman who had silent thromboembolic occlusion of the right pulmonary artery. Over the ensuing months, severe pulmonary hypertension developed, as manifested by marked dilatation and atherosclerosis of the right and left pulmonary arteries and severe right ventricular hypertrophy. Nevertheless, she remained fully ambulatory and felt generally well throughout this time. Eventually, however, the pulmonary arteries became so dilated that they compressed the recurrent laryngeal nerve as it looped under the aortic arch, and it was the resulting hoarseness that first caused the patient to seek medical attention. A work-up disclosed normal peripheral lung fields on x-ray study and a large dense right hilar mass. Accordingly, the patient was subjected to an exploratory thoracotomy on the reasonable but mistaken diagnosis of bronchogenic carcinoma. After the following operation, her condition deteriorated. She developed bronchopneumonia which, when superimposed on her already precariously reduced cardiopulmonary function, precipitated respiratory insufficiency. An independent stroke was the immediate cause of death.
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PMID:Silent, chronic, massive pulmonary thromboembolism masquerading as bronchogenic carcinoma. 96 90

Cardiovascular diseases account for approximately 50% of deaths in patients on chronic haemodialysis. Therefore we prospectively studied 54 consecutive patients on dialysis for the presence or absence of ventricular late potentials (LP). LP, i.e. low-amplitude potentials in the terminal part of the QRS complex, have been shown to be highly indicative of life-threatening arrhythmias and sudden death. The results were correlated with echocardiographic studies and the clinical outcome during a follow-up period of 18 months. Fifty patients were suitable for evaluation (29 males, 21 females; mean age 55 years; mean time on dialysis 32 months; coronary artery disease present in 5) Our analysis revealed LP in seven of 50 patients only. Left ventricular hypertrophy, i.e. mean wall diameter > 12 mm, was present in 78%, a compromised left ventricular function, i.e. shortening fraction < 28%, was found in 28% of the patients. With respect to echocardiographic parameters, patients with and without LP were similar. During follow-up, sudden cardiac death was observed in three of 11 patients deceased. LP were detectable in one of the three only. From the remaining six patients with LP, four are still alive, and two patients died due to atherosclerosis and pulmonary embolism. Our data underline the crucial role of sudden cardiac death in dialysis patients. Ventricular late potentials, however, are of no prognostic relevance with respect to identification of dialysis patients at risk of sudden death.
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PMID:Ventricular late potentials in haemodialysis patients and the risk of sudden death. 133 75

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

This hypothesis is that permanent cardiac injury could develop in some endurance athletes despite the absence of coronary atherosclerosis and ventricular hypertrophy. The proposed mechanism by which this injury could arise involves two physiological "vicious cycles". The first vicious cycle would occur between severe ischaemia and high catecholamines, the second would be between coronary vasospasm (induced by high catecholamines) and endothelial injury. The likelihood of the injury becoming permanent might increase if there is insufficient time between bouts of endurance exercise for regression of ischaemia and endothelial repair. Furthermore, magnesium ion deficiency, which can be induced by exercise, could exacerbate these vicious cycles and also contribute to catecholamine-induced thrombogenesis. In addition to ischaemia, there are several mechanisms, including the effect of free fatty acids liberated by the lipolytic effect of high catecholamines, that could cause direct myocardial injury.
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PMID:Extraordinary unremitting endurance exercise and permanent injury to normal heart. 135 47

Although clinical trials of the efficacy of antihypertensive treatment have demonstrated impressive reductions in the incidence of stroke, the reduction in coronary artery disease mortality has been less impressive. It may be that the antihypertensive drugs used in these trials induced metabolic disturbances, or produced inadequate regression of left ventricular hypertrophy, thus blunting the reduction in risk of coronary artery disease expected with blood pressure-lowering. Isradipine, a dihydropyridine calcium antagonist known to be an effective antihypertensive agent, has also displayed pronounced antiatherogenic effects in animals. Thus, a reasonable hypothesis could be that isradipine not only reduces the level of blood pressure, but also may have a positive effect on the evolution of atherosclerotic plaque in coronary and carotid arteries, thereby leading to prevention of clinical sequelae of atherosclerosis. On this basis, a 3-year clinical trial is being carried out in the United States--the Multicenter Isradipine/Diuretic Atherosclerosis Study (MIDAS)--to establish the efficacy of isradipine in inhibiting atherogenesis and retarding the progression of atherosclerosis in carotid arteries of hypertensive patients. The primary end point of the study is intima-media thickness and the extent of atherosclerotic plaque in the carotid arteries, as measured by B-mode ultrasonography.
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PMID:MIDAS: hypertension and atherosclerosis. A trial of the effects of antihypertensive drug treatment on atherosclerosis. MIDAS Research Group. 137 28

Arterial compliance in humans is generally measured by modeling analysis of pulse tracing or of pulse wave propagation in the arterial tree. It is decreased in hypertension in part because elevation of blood pressure stiffens the arteries by stretching the rigid collagen fibres of their walls. Using a modeling evaluation of the compliance-pressure relationship in large arteries, it is possible to correct compliance from the mechanical effect (passive effect) due to pressure elevation. This makes it possible to show that, at the same pressure as in normal controls, hypertensive patients maintain decreased arterial compliance. This finding suggests that functional and/or structural changes other than pressure-mediated stretching of arteries (active effect) contribute toward reducing arterial compliance. Thus, the response of compliance to antihypertensive drugs must be studied by differentiating between passive and active effects. The diameter and compliance-pressure relationship in arteries allow differentiation of a passive arterial effect due to the pressure-lowering action of the drug, and an active pharmacological effect calculated at the same pressure before and after drug administration. Four drugs--ketanserin, urapidil, nitrendipine, and nicardipine (acute administration)--are given as examples. No active or passive compliance changes are observed with urapidil and ketanserin. In contrast, an active increase in compliance is observed in isobaric conditions with calcium antagonists, together with large-artery dilation due to a potent smooth muscle-relaxing effect. This active increase in compliance is potentiated by a passive increase due to the pressure-lowering effect that reduces the mechanical stretch exerted by blood pressure on arterial bioelastomers. Finally, an optimum increase in arterial compliance is achieved by drugs that vasodilate large arteries by smooth muscle relaxation and concomitantly decrease blood pressure. This may be of importance because low compliance has adverse effects on the cardiovascular system by contributing to the pathogenesis of systolic hypertension and left ventricular hypertrophy. Loss of arterial compliance may also be an early marker of atherosclerosis.
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PMID:Role of arterial compliance in the physiopharmacological approach to human hypertension. 138 85


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