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

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.
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PMID:Role of hypertension in atherosclerosis and cardiovascular disease. 13 91

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

There is no dearth of experimental techniques for producing the hyperlipoproteinemia resulting in atherosclerotic complications and for myocardial infarction in the non human primates. Most of the recent experiments which have given information of great value have been studied with relatively expensive animals for a long period of time up to 6-7 years. It is evident that no animal model perfectly duplicates the human disease or satisfies all desirable requirements. The chimpanzees, representatives of the New World monkeys, have circulating plasma lipoproteins identical to man in composition as well as in function. The results reported above indicate that the compositional changes of chimpanzee plasma lipoproteins in response to dietary changes reflect the appearance of type II and type IV hyperlipoproteinemia similar to the human disease. Moreover, there are more indications about the existence of genotype II a in the chimpanzee, and also on the influence of stress on the plasma lipids, so that the developed intimal lesions similar to the human pathology are in this sense multifactorially influenced. From a phylogenetic point of view the chimpanzee is closer to man than any other non human primate. Furthermore, the chimpanzee lipoproteins are useful models for understanding the relationship between function and structure of the plasma lipoproteins in health and disease. Baboon and rhesus monkeys show similar results, but more differences to the human lipoproteins in health and disease were observed. At present it appears that the most useful models of human atherosclerosis are those induced in the non human primates, especially in the chimpanzee.
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PMID:The nonhuman primates as models for studying human atherosclerosis: studies on the chimpanzee, the baboon and the rhesus macacus. 17 99

Blood plasma cholesterol and triglycides concentration lipids composition of lipoproteins as contrasted to the amount of 17-KS and their hormonally active fractions excreted were investigated in 87 patients with myocardial infarction in their history and in 49 practically healthy individuals with no clinical manifestations of ischemic heart disease. In patients with coronary atherosclerosis exhibiting normal blood plasma lipids level, the excretion of 17-KS and of their fractions did not differ from that in healthy individuals. Patients with hyperlipoproteinemia of the IIa, IIb and IV types demonstrated a significantly reduced excretion of 17-KS, etiocholanolone, androsterone and dehydroepiandrosterone. No differences in the excretion of androgens depending upon the type of hyperlipoproteinemia were recorded. A significant negative correlation between the blood plasma cholesterol concentration and the amount of ethocholanolone excreted, the level of hypertriglyceridemin and the passage of dehydroepiandrosterone with urine was noted. In patients with hyperlipoproteinemia and a reduced androgens excretion a deranged lipids composition of lipoproteins was disclosed. A decrease in the amount of androgens leads to disruption of the synthesis and metabolism of lipoproteins and exerts a marked influence on the emergence and further development of hyperlipoproteinemia.
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PMID:[Lipid composition of lipoproteins and excretion of 17-ketosteroids in coronary arteriosclerosis]. 18 38

To study the incidence of hyperlipoproteinaemia in patients with myocardial infarction (MI) in the Chandigarh area, estimations of various lipids have been carried out in 83 patients. A serial study has been carried out in 31 patients. Serum lipoproteins and uric acid were also estimated. Results show an incidence of only 18% hypercholesterolaemia in patients with MI and 15% in normal subjects. Age-wise distribution of hypercholesterolaemia was slightly higher in 41-60 years old patients when compared with other age groups. No other abnormality in lipid profile was observed. Hyperuricaemia was not observed. These results, therefore, differ markedly from those of similar studies published from the western world.
Atherosclerosis 1976 Sep
PMID:Serum lipid profiles in patients of myocardial infarction in the Chandigarh area (Northern India). 18 98

Longevity and morbidity and death from myocardial infarction were examined in eight kindreds with familial hypobeta lipoproteinemia and in 18 kindreds with familial hyperalpha lipoproteinemia. Expectation of life for males and females from kindreds with hypobeta lipoproteinemia was 9 and 12 years longer (p less than or equal to 0.002) than that indicated by population statistics for U.S. white populations, whereas expectation of life for males and females from kindreds with hyperalpha lipoproteinemia was 5 and 7 years longer (p less than 0.02). Morbidity from myocardial infarction in 115 living first-degree adult relatives of probands with hypobeta and hyperalpha lipoproteinemia and in 364 living first-degree adult relatives of normolipemic spouse controls were compared. Nonfatal myocardial infarction (MI) was reported for 18 of 364 (5 per cent) relatives of normal spouse controls and in 0 of 115 relatives of hypobeta and hyperalpha subjects (p less than 0.05). The ratios (mean+/-S.E.) of C-LDL to C-HDL in familial hypobeta and hyperalpha lipoproteinemia were 0.79+/-0.06 and 1.21+/-0.06, as compared to 2.41+/-0.12 in a control population (p less than 0.001). If high-density lipoproteins confer protection against development of atherosclerosis, whereas low-density lipoproteins have opposite effects, then we speculate that the low ratio of C-LDL:C-HDL may be related to prolonged longevity and decreased morbidity from myocardial infarction in familial hypobeta and hyperalpha lipoproteinemia.
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PMID:Longevity syndromes: familial hypobeta and familial hyperalpha lipoproteinemia. 18 45

The chemical composition of ultracentrifugal fractions of VLDL (d less than 1006), LDL (d 1006-1063) and HDL (d less than 1063) has been studied in males affected by atherosclerosis of different vascular beds. Thirty-seven subjects affected by post-infarction cardiopathy (M.I.) showed significantly higher values of total-C, VLDL-C and LDL-C when compared to 52 controls. Twenty-three patients affected by non-occlusive ischaemic heart disease (I.H.D.) showed higher values than controls of total-C, VLCL-C, LDL-C, total TG, VLDL-TG, and GDL-TG. Twenty-three patients with atherosclerosis of the inferior limbs (P.A.) were characterized by increased levels of total-TG, VLDL-TG, VLDL-C, HDL-C. A group of patients who had suffered a stroke from cerebro-vascular disease (C.V.D.) did not show any significant difference from controls. In the M.I. group, 56% of the patients had a high level of C-VLDL. Patients with I.H.D. were characterized mostly by an increase in C-LDL, Patients with P.A. showed the highest values of total -TG, VLDL-TG and LDL-TG. Some of the observed differences are probably due to different metabolic backgrounds. Some other differences may be due to variations in dietary habits after heart infarction. Patients with levels of plasma cholesterol and triglyceride beyond the 90th percentile of the normal group showed many abnormalities in the chemical composition of their lipoproteins. It is noteworthy that increased amounts of cholesterol may collect in lipoprotein classes different from LDL while increased amounts of triglyceride may collect in classes different from VLDL.
Atherosclerosis 1977 Feb
PMID:Chemical composition of ultracentrifugal fractions in different patterns of human atheroslcerosis. 18 83

Acute changes in low density lipoprotein cholesterol levels may be due to both a change in the number of LDL particles/ml of plasma and an alteration in the amount of cholesterol per LDL particle. Since LDL cholesterol levels are known to alter abruptly after myocardial infarction, the composition of LDL was determined in nine patients who suffered an uncomplicated transmural myocardial infarction. In six of these, LDL cholesterol levels fell whereas in three LDL cholesterol rose during the first nine days in hospital. The contents of B protein, free cholesterol, phospholipid, cholesterol ester and triglyceride in LDL were determined in the initial sample and the subsequent sample showing the greatest changes in LDL cholesterol level. The proportion of the LDL molecule contributed by B protein, free cholesterol and phospholipid did not differ significantly between the two samples. In contrast, when LDL cholesterol fell, the decrease in the proportion of cholesterol ester was disproportionately greater than in triglyceride. The opposite was observed when LDL cholesterol rose. This inverse relation between changes in LDL cholesterol ester and triglyceride could be expressed by Y = -1.02 X -0.17 (r = -0.94). These data are consistent with a pseudomicellar model of LDL in which the surface components are present in fixed amounts but the interior shell of cholesterol ester and triglyceride varies in an inverse relation depending on the absolute LDL concentration.
Atherosclerosis 1977 Jul
PMID:Predictable changes in low density lipoprotein composition after acute myocardial infarction. 19 78

Hypercholesterolemia caused a decrease in the activity of adenylcyclase in rabbit liver tissue and in thrombocytes; hypertriglyceridemia, which developed after administration of hydrocortisone, led to an increase in the activity of adenylcyclase and in the content of 3,5-AMP in adipose tissue. Activities of adenylcyclase, phosphodiesterase and content of prostaglandines E1 and F2alpha were measured in thrombocytes of 39 healthy men without any symptoms of of ischemic heart impairment, in 52 patients with coronary atherosclerosis of the III degree (by Myasnikov's classification) as well as in 12 patients during the period of rehabilitation after myocardial infarction. The activity of adenylate cyclase system was impaired in atherosclerosis. This phenomenon might be caused by alteration in concentration of glucocorticoids in the organism.
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PMID:[Cyclic adenosine monophosphate and atherogenic factors]. 20 91

Epidemiologic studies have found associations between low levels of high density lipoprotein (HDL) cholesterol and increased risk of coronary artery disease, using myocardial infarction or angina pectoris as endpoints. However, since most studies have not correlated HDL cholesterol with the presence, severity, or location of anatomically proven coronary disease, the present study measured HDL cholesterol levels in 483 men and women undergoing coronary arteriography. Consistent and statistically significant trends of decreasing mean HDL cholesterol levels with increasing numbers of diseased coronary arteries were observed in both men and women and in younger and older age groups. Although women without coronary disease had much higher levels of HDL cholesterol than men without coronary disease, the differences between men and women with similar degrees of coronary disease were small. Low levels of HDL cholesterol were associated with left main coronary disease; patients with both triple vessel disease and left main disease had lower levels of HDL cholesterol than did patients with triple vessel disease without left main disease. These results were not explained by the possible associations of low density lipoprotein cholesterol or triglycerides with HDL cholesterol. These findings suggest that low levels of HDL cholesterol are important risk factors for the development of atherosclerosis and that they may be useful for identifying patients at high risk of certain anatomic patterns of coronary artery disease.
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PMID:The association of low levels of HDL cholesterol and arteriographically defined coronary artery disease. 22 34


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