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

Factors which are known to be associated with cerebral atherosclerosis were evaluated in Nigerian Africans. Of 465 autopsied adult Nigerians, 62 (13%) had cerebral atherosclerosis. The frequency and severity of atherosclerosis among Nigerians with hypertension, particularly male subjects, were higher than in normotensives. Although there was a similar frequency of hypertension among autopsied Nigerian and Minnesota Caucasian populations, the severity and extent of atherosclerosis were greater in the Minnesota Caucasian populations, the severity and extent of atherosclerosis were greater in the Minnesota population. The relatively short duration of hypertension in the Nigerian before death might be an important factor which did not permit progressive development of cerebral atherosclerosis. Other factors which predisposed the Nigerian to increased frequency and severity of atherosclerosis included increased heart weight and diabetes mellitus. The relatively low frequency of cerebrovascular disease in the Nigerian may be explained on the basis of a low degree of cerebral atherosclerosis and relatively short duration of hypertension.
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PMID:Cerebral atherosclerosis and its relationship to selected diseases in Nigerians: a pathological study. 12 75

This report summarizes the clinical frequencies of systemic hypertension and necropsy evidence of cardiomegaly in various cardiovascular conditions (Table I), termed "the hypertensive diseases" because of their frequent association with systemic hypertension. Although long recognized as a major risk factor, systemic hypertension appears to be an even greater risk factor to the development of various cardiovascular conditions than previously appreciated. Hypertension by itself appears to be the sole underlying factor in most cases of nontraumatic cerebral arterial or aortic (dissection = partial rupture) rupture. In association with hyperlipidemia, hypertension clearly accelerates atherosclerosis and its devastating consequences.
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PMID:The hypertensive diseases. Evidence that systemic hypertension is a greater risk factor to the development of other cardiovascular diseases than previously suspected. 12 44

Hypertension studies using laboratory animals have been conducted since 1930. These were not completely satisfactory because either surgery or pharmacologic induction were required to produce hypertensive animals. Many attempts have been made to breed spontaneously hypertensive rats, mainly from the Okamoto strain. The cause of hypertension in the rat, with specific reference to genetic aspects and pathogenicity, were reviewed. The hypertensive rat is an acceptable model for hypertension studies because of the stability of the hypertensive state and the reproducibility of experimental effects. It is a particularly useful model for screening antihypertensive agents. Development of mutant Okamato stran rats which have brain softening, cerebral hemorrhages, and myocardial infarctions would permit the screening of specific therapeutic agents with fewer side-effects. Mutants which develop obesity, hyperlipidism, and early atherosclerosis have been reported in Okamoto strain X Sprague-Dawley rat crosses.
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PMID:The use of spontaneously hypertensive rats for the study of anti-hypertensive agents. 13 78

In 80 industrial workers producing herbicides (2,4,5-trichlorphenoxyaceticacidsodium and sodiumpentachlorphenolate) in Czechoslovakia the following signs of intoxication caused by 2,3,6,7-tetrachlordibenzodioxin were found: Dermatological: Chloracne and Porphyria cutanea tarda. Internal: Disorders of the metabolism of porphyrins, fats, carbohydrates, plasmaproteins. Neurological: Mainly lesions of the peripheral neurone. Psychiatric: Neurasthenic syndrome and organic lesions. Differences from the usual course of chloracne were observed. Porphyria cutanea tarda acquisita was most obvious, one patient suffered and died from severe atherosclerosis, hypertension and diabetes. Many patients developed polyneuropathy, as verified both by EMG and autopsy. Two patients died from bronchogenic carcinoma.
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PMID:[Chloracne, porphyria cutanea tarda, and other poisonings due to the herbicides]. 13 6

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

Results of histological and histochemical studies of the choroid of the eyes of deceased old people who when alive suffered from glaucoma, hypertensive disease and atherosclerosis, are presented. It was established that hypertensive disease, general atherosclerosis, symptomatic hypertension brought about peculiar changes in the choroid vessels and stroma. There were revealed changes in the venous system of the choroid of the glaucomatous eyes, which testified to the presence of venous congestion in them, this apparently being one of pathogenetic factors in origination of primary glaucoma.
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PMID:[Comparative pathology of the choroid vessels in glaucoma, hypertension and arteriosclerosis]. 13 10

Uncontrolled hypertension increases the workload of the left ventricle causing the development of hypertrophy and an increase in myocardial oxygen consumption that may precipitate ischemia because of inadequate oxygen delivery related to accelerated coronary atherosclerosis. Control of the hypertension should prevent the further development of hypertrophy, delay the development of fibrosis and possibly also slow the rate of development of atherosclerosis. Furthermore, when myocardial function is impaired because of hypertrophy or other myocardial diseases, the level of blood pressure becomes an important determinant of left ventricular performance. Regardless of the level of arterial pressure, vasodilator drugs that lower arterial pressure may result in marked improvement in left ventricular performance and relief of symptoms of left ventricular failure. Therefore, control of blood pressure in the presence of heart disease may involve treatment of normotensive patients to bring them into a lower normotensive range as well as the more traditional treatment of hypertensives to bring them into the normotensive range. Although this scenario is consistent with conventional wisdom and clinical experience, intricacies of the relationship between hypertension, hypertrophy, myocardial oxygen delivery, atherosclerosis and intramyocardial blood flow distribution remain poorly understood. Until these aspects of the natural history of heart disease are better worked out therapy will remain largely empirical.
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PMID:Heart disease in the hypertensive patient. 14 Feb 80

In surgery for renovascular hypertension one should try to avoid prothetic material. In general, it seems preferable to use methods without transplanted tissue at all, for instance the direct desobliteration in atherosclerosis or resection and end-to-end anastomosis in fibromuscular disease. General complications should be avoided in a carefully postoperative observation of the patients with exact equilibration of blood vulume and electrolytes.
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PMID:Early and late complications following surgical correction of renovascular hypertension. 14 Jul 81

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

The abdominal aortas and right coronary arteries removed during autopsies were gathered from over 18,000 subjects in 19 location-race groups. Sudanstained intimal surfaces were graded for the percent as raised lesions (R) and fatty streaks (F). The proportions of all types of lesions (ATL = F + R) that were raised (RaL = R divided by ATL) were examined. The difference between the observed RaL (in subjects having atherosclerosis-related conditions) and the expected RaL (in age-, sex-, and ATL-matched subjects without such conditions) measured the excess of RaL, which by inference indicated the tendency for an excess of raised lesions to be produced in place of fatty streaks. In cases of coronary heart disease (CHD), a large excess of RaL was found consistently on the average. The coronary arteries and aortas of hypertensive subjects, compared with those of nonhypertensives, had only a small and inconsistent excess of RaL. Both CHD and hypertension were characterized by a marked tendency for severe involvement by ATL, including extensive fatty streaks, leaving only small remnants of normal intima. Some factors (Class A) act to form fatty streaks and also to continue advancing them into raised lesions. Once the fatty streaks are formed, some new factors (Class B2) convert them into raised lesions. We concluded that hypertension is almost, if not entirely, a Class A type of atherogenic agent, and that CHD is promoted by exceptionally strong effects of both A and B2 types of causation. This conclusion exposes a biological priniciple that, if the assumptions of the model are true, is of considerable importance: Some of the more important causes of atherosclerosis (Class B causes) begin to act only after the fatty streaks have formed.
Atherosclerosis 1979 May
PMID:Relationship of raised atherosclerotic lesions to fatty streaks in coronary heart disease and hypertension. 15 38


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