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

Eight groups of New Zealand white rabbits were used to study the effects of moderate chronic one-kidney, one clip hypertension (HT) and long-term nifedipine therapy on atherogenesis. Four groups were fed a normal diet (ND) over an 8-month study period; two groups, one of which was given nifedipine, remained normotensive (NT) throughout the study. Of the two HT groups, one remained hypertensive for 7 months; the blood pressure of the other group was normalized after 2 months with nifedipine. The other four groups of animals were similarly constructed except that they were fed a 0.1% cholesterol diet (CD). The results showed that: although scattered fibromuscular vascular lesions were present in the aortas of normal-diet, HT animals no atheroma was observed; neither moderate chronic HT nor abrupt, short-term HT exacerbated atherogenesis in the CD-animals; nifedipine therapy had no suppressive effect on either fibromuscular lesions or atherogenesis; nifedipine therapy reduced the aorta weight of the normotensive ND and CD groups; the aortic triglyceride content of both dietary groups was reduced by nifedipine; cholesterol content was unaffected; left ventricular hypertrophy was evident only in HT-untreated groups; and only the weight of the left ventricle of the ND-NT-treated group was significantly reduced, but the mitochondria volume per unit volume of left ventricle myocardial cells was reduced only in the NT-CD group treated with nifedipine. It is concluded that an antihypertensive dosage of nifedipine administered to animals with atherosclerosis does not suppress subsequent atherogenesis.
Atherosclerosis 1987 Jul
PMID:Hypertension and atherosclerosis in cholesterol-fed rabbits. II. One-kidney, one clip Goldblatt hypertension treated with nifedipine. 330 94

Risk factors for coronary disease were assessed and noninvasive methods were used to quantitate the extent of extracranial carotid atherosclerosis in 382 patients free of cerebrovascular symptoms. The ages of the participants ranged from 27 to 80 years. There were 183 men and 199 women, 30 black and 352 white persons. All patients had heart disease symptoms and were hospitalized for coronary angiography. Correlation of risk factors with extent of extracranial carotid atherosclerosis in this series of patients undergoing coronary angiography uncovered individual variability in relationships between risk factors and carotid atherosclerosis that depended on coronary status. Risk factors for carotid atherosclerosis in patients with and without coronary disease differed. Age and hypertension were independently related to carotid atherosclerosis in patients with, as well as those without, coronary disease. However, other risk factors were related to carotid atherosclerosis in only one group or the other. Risk factors correlated strongly with carotid atherosclerosis in patients with coronary disease (r2 = 0.41) but poorly in those with no coronary disease (r2 = 0.21). Certain risk factors (age, pack years of smoking, left ventricular hypertrophy) related differently to the extent of carotid atherosclerosis in patients with, than in those without, coronary disease. Clarification of the role of coronary status in the carotid atherosclerosis response to risk factors may partly explain the results of certain population-based studies that have related race, gender, and other risk factors to carotid atherosclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Individual variation in susceptibility to extracranial carotid atherosclerosis. 339 75

Acromegaly involves cardiovascular complications mostly due to the presence of hypertension, diabetes and atherosclerosis. However the appearance of cardiac decompensation and arrhythmias in the absence of predisposing factors tends to support the hypothesis of a specific myocardiopathy caused by excess GH. In order to assess the existence and course of subclinical cardiac alterations, 8 acromegaly patients were examined: 4 males and 4 females aged 31-56 with GH levels of 24-70 ng/ml (M + CD X 47 +/- 16) and no cardiovascular symptoms. One of the patients had moderate hypertension and 2 reduced glucose tolerance. The basal ECG showed sporadic ventricular extrasystoles in 2 cases and alterations compatible with left ventricular hypertrophy in another, while the effort ECG produced an asymptomatic depression of the ST segment in the hypertensive patient. The chest X-ray was normal in all cases. The echocardiography study investigated: the thickness of the interventricular septum (IVS = 13.9 +/- 2.8 mm), the thickness of the posterior wall of the left ventricle (LPW = 10.6 +/- 2.9 mm), the septum/posterior wall ratio (IVS/LPW = 1.3 +/- 0.2 the diastolic diameter (DD = 15.4 +/- 11.4 mm), the fraction of shortening (FS = 39.1 +/- 14.5%), the ejection fraction (EF = 64.1 +/- 18.4%) and revealed asymmetrical septal hypertrophy in 3 cases, concentric hypertrophy in another two. In two cases the DD and EF were distinctly altered. The patients were re-examined 2-4 years after surgical or radiation treatment. GH levels (M +/- SD = 10.3 +/- 10.1 ng/ml) were normal in 4 cases and still high, though lower in another two. The remaining two patients had borderline GH levels with high Sm-C. The ECG and chest X-ray were unchanged while echocardiography revealed a significant deterioration in heart function as far as DD (56.4 +/- 10.8 mm, p less than 0.05) were concerned with frankly pathological results in 4 and 3 cases respectively. These data confirm the view that most acromegalic patients present subclinical abnormalities in cardiac function and that the evolution of these is slightly influenced by the reduction in GH and Sm-C. levels. In fact, while the persistence of high GH and Sm-C. levels may explain the progression of cardiac alterations in some cases, it does not in others. It is also emphasised that echocardiography appears to be the most sensitive non-invasive technique for the diagnosis and follow-up of cardiac involvement in acromegaly.
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PMID:[Cardiological findings in acromegaly]. 343 27

Cardiovascular diseases responsible for sudden unexpected death in highly conditioned athletes are largely related to the age of the patient. In most young competitive athletes (less than 35 years of age) sudden death is due to congenital cardiovascular disease. Hypertrophic cardiomyopathy appears to be the most common cause of such deaths, accounting for about half of the sudden deaths in young athletes. Other cardiovascular abnormalities that appear to be less frequent but important causes of sudden death in young athletes include congenital coronary artery anomalies, ruptured aorta (due to cystic medial necrosis), idiopathic left ventricular hypertrophy and coronary artery atherosclerosis. Diseases that appear to be very uncommon causes of sudden death include myocarditis, mitral valve prolapse, aortic valve stenosis and sarcoidosis. Cardiovascular disease in young athletes is usually unsuspected during life, and most athletes who die suddenly have experienced no cardiac symptoms. In only about 25% of those competitive athletes who die suddenly is underlying cardiovascular disease detected or suspected before participation and rarely is the correct clinical diagnosis made. In contrast, in older athletes (greater than or equal to 35 years of age) sudden death is usually due to coronary artery disease, and rarely results from congenital heart disease.
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PMID:Causes of sudden death in competitive athletes. 351 Feb 33

Progression of coronary artery stenosis was measured using a quantitative, computer-assisted cinevideodensitometric method in 144 arterial segments in 44 subjects undergoing coronary arteriography on two separate occasions at least 6 months apart. Projected coronary arteriograms were digitized into 512 X 512 pixel mode and percent stenosis was calculated by comparing background-corrected videodensitometric values over stenotic and normal segments. Subjects underwent repeat coronary arteriography because of worsening symptoms of angina or heart failure; subjects with renal failure, coronary artery bypass grafts or cardiac transplant were excluded. Clinical variables determined at the time of the first arteriogram included age, sex, serum cholesterol, systolic blood pressure and presence or absence of cigarette smoking, diabetes mellitus and left ventricular hypertrophy. The mean interval between arteriograms was 29.3 months. Overall progression of coronary stenosis was observed in 40 of the 44 subjects; the mean progression at 24 months was 39% (90% confidence interval, 33 to 45%) and at 36 months was 48% (40 to 56%). The degree of overall progression was related to the length of time between arteriograms (F = 5.81, p less than 0.05) and to serum cholesterol level (F = 4.37, p less than 0.05). These data indicate that using an accurate, quantitative method, it is possible to measure progression of coronary artery atherosclerosis within 2 to 3 years of the initial arteriogram. Serum cholesterol appears to be an important determinant of disease progression.
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PMID:Progression of coronary atherosclerotic disease assessed by cinevideodensitometry: relation to clinical risk factors. 378 37

This study compares two groups of patients: Group I with 44 patients who suffered recent acute myocardial infarction and Group II: 40 control subjects. In both groups, 2D Doppler echocardiography was performed to detect carotid atheroma, to determine the respective roles of vascular risk factors for two sites of atherosclerosis. Carotid atheroma affected 73 p. 100 of subjects in Group I and 22.5 p. 100 in Group II. Carotid stenosis of more than 40 p. 100 was found mainly in hypertensive patients who presented with acute myocardial infarction, and in patients with left ventricular hypertrophy. Smoking was more frequent in Group I than in Group II (p less than 0.001) irrespective of the frequency of carotid atheroma (p less than 0.05). Hypercholesterolaemia only favoured carotid atherosclerosis after acute myocardial infarction (p = 0.01). We did not find any difference in the incidence of diabetes mellitus in the two groups of patients. Age analysis indicated that carotid atheroma occurred earlier in Group I than in Group II. An association between a dominant risk factor for coronary disease (smoking or hypercholesterolemia) was found in 9 patients, all of whom had severe bipolar atherosclerosis with multivessel coronary lesions and carotid stenosis.
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PMID:[Risk factors in the combination of myocardial infarction and carotid atheroma]. 381 69

Atherosclerosis of the pulmonary arteries is a common autopsy finding and is associated with a variety of clinical conditions. To delineate the morphologic changes associated with pulmonary artery atherosclerosis, autopsies of 337 consecutive adults (greater than 15 years of age) were studied. For each, 35 features were studied, including age, coronary vascular disease, cardiac chamber hypertrophy and dilation, pulmonary artery and aortic atherosclerosis, and pulmonary thromboemboli and emphysema. These were compared using correlation coefficients and forward and backward stepwise regression procedures for selected variables. Pulmonary artery atherosclerosis correlated significantly with age, right ventricular dilation and hypertrophy, pulmonary emphysema, and aortic atherosclerosis. Regional evaluations of systemic and pulmonary atherosclerosis showed highly significant internal correlations. In the ligamentum arteriosum, the intensity of atherosclerosis over the aortic insertion correlated with the severity of a similar atheroma at the pulmonary artery insertion. With the multiple-regression procedure, pulmonary artery atherosclerosis was a significant predictor of aortic atherosclerosis, right ventricular hypertrophy, and pulmonary embolization. Our study shows that pulmonary embolization. Our study shows that pulmonary embolization. Our study shows that pulmonary artery atherosclerosis is accelerated in patients with atherosclerosis of the systemic arteries and the pathologic lesions associated with hypertensive pulmonary vascular disease.
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PMID:Pulmonary artery atherosclerosis: correlation with systemic atherosclerosis and hypertensive pulmonary vascular disease. 621 13

This study examined the hearts of 55 patients dying of chronic obstructive pulmonary disease, with and without cor pulmonale, quantitated histologically the degree of myocardial fibrosis in the left and right ventricle, and determined the relationship to associated disease states. Comparison has been made to a control group of 17 patients free of cardiopulmonary disease. Patients with associated and advanced ischemic heart disease, as proved by marked atherosclerosis and myocardial infarction, have significantly increased myocardial fibrosis throughout all layers of the left ventricular wall in comparison to control patients or patients with chronic obstructive pulmonary disease free of associated cardiac disease. Right ventricular fibrosis was not significantly increased; however, one case showed a marked degree of fibrosis related to myocardial infarction. Subdivision of patients with chronic obstructive pulmonary disease into groups with definite anatomic right ventricular hypertrophy, a clinical diagnosis of cor pulmonale, or with chronic hypoxemia failed to show any difference in the percentage of myocardial fibrosis of the ventricles among these groups. Increased fibrosis of the right or left ventricle in patients with chronic obstructive pulmonary disease, therefore, is not related to the degree of myocardial hypertrophy pathologically, the hypoxemic state, or clinical heart failure, but to ischemic heart disease with myocardial infarction.
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PMID:Quantitation of fibrosis of the heart in chronic obstructive pulmonary disease with and without cor pulmonale. 622 97

A review of the electrocardiograms (ECG) of 108 patients with sickle cell anemia found only 3 with patterns consistent with myocardial infarction. Two of the 3 patients with ECG infarct patterns had postmortem examination confirmation of the infarction. These two patients had no significant coronary atherosclerosis nor did the other six autopsied patients in the present series. Literature reports of postmortem examinations on patients with sickle cell anemia confirm the scarcity of coronary atherosclerosis and myocardial infarction in these patients. Forty of the 108 ECGs showed signs of left ventricular hypertrophy and 20 others had nondiagnostic ST and T wave abnormalities. Nine showed first degree AV block and four right bundle branch block.
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PMID:Myocardial infarction in sickle cell anemia. 623 6

Chronic hypertension increases the risk of myocardial infarction and the morbidity and mortality associated with it. Although accelerated atherosclerosis is partially responsible, other abnormalities in the coronary circulation associated with hypertension, such as decreased coronary vascular capacity and capillary density, could also contribute. To evaluate the effects of these nonatherosclerotic abnormalities, we produced sudden coronary occlusion in nine chronically hypertensive dogs. The mean aortic pressure and left ventricular mass were about 50% greater in hypertensive dogs than in the nine controls. Before occlusion and 5 min and 49 h after occlusion, myocardial blood flow was measured with tracer microspheres. Also, the extent of infarction in selected myocardial segments was quantified histologically. We found that coronary occlusion reduced flows to a similar extent, and that, over a 48-h period, collateral flow increased to a similar extent in the two groups. In addition, the amount of necrosis associated with a given degree of ischemia was similar in the two groups. Although the extent of the left ventricle that became ischemic was greater in the hypertensive dogs (28 +/- 2 vs. 18 +/- 4%; P < 0.05), chronic hypertension and left ventricular hypertrophy did not limit the recruitment of collateral supply or increase the amount of necrosis associated with a given degree of ischemia.
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PMID:Myocardial infarction in dogs with chronic hypertension and left ventricular hypertrophy. 644 77


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