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

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.
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PMID:The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review. 9 95

High density lipoprotein (HDL) and low density lipoprotein (LdL) cholesterol levels were measured in fasting blood samples from 950 healthy subjects and 188 aged patients by a new simple method. The HDL-cholesterol levels and HDL/LDL-cholesterol ratios are significantly higher in females than in males. In the healthy subjects, there are slight decreases in the levels of HDL-cholesterol and HDL/LDL-cholesterol ratio with aging in both sexes. The patients with myocardial infarction had significantly lower HDL-cholesterol levels and HDL/LDL-cholesterol ratios as compared to those of the group without infarction. On the contrary, no differences in total lipoprotein cholesterol levels were observed in the patients with cerebral infarction. The results, obtained in respect of electrocardiographic findings after the isoproterenol stress test, suggest that the HDL-cholesterol levels and HDL/LDL-cholesterol ratios may be related not only to the established myocardial infarction, but also to the presence of coronary atherosclerosis and stenosis.
Atherosclerosis 1979 Mar
PMID:High and low density lipoprotein cholesterol in myocardial and cerebral infarction. 22 92

Evidence of cerebrovascular disease at autopsy was compared in 2 groups of men: 186 long-time residents of Hiroshima, Japan, and 253 men of Japanese ancestry long resident in Honolulu, Hawaii. They were 45 to 71 years-of-age at death. Atherosclerosis of the circle of Willis and its major branches, sclerosis of the intraparenchymal arteries and the frequency of cerebral hemorrhage and cerebral infarct were compared in the 2 populations. The Honolulu subjects had significantly more atherosclerosis of the circle of Willis, but less intraparenchymal artery sclerosis and less cerebral infarction. Cerebral hemorrhage was equally frequent in the 2 cities. It was concluded that cerebral infarction is more frequent in Japanese men in Hiroshima than Honolulu, and that men of Japanese ancestry in Honolulu are spared an appreciable risk of cerebral infarction through decreased frequency of intraparenchymal arterial sclerosis despite higher levels of atherosclerosis of large intracranial arteries.
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PMID:Autopsy study of cerebrovascular disease in Japanese men who lived in Hiroshima, Japan, and Honolulu, Hawaii. 50 76

One hundred seventeen patients, 31 with TIA and 86 with cerebral infarction, had angiographically verified atherosclerosis within the relevant carotid artery territory and normal CSF. They were treated with anticoagulants for a mean of 11.1 months. No TIA but 1 cerebral infarction, appearing during inadequate anticoagulant therapy, was registered. Seventy-six of the patients, 20 with TIA and 56 with infarction, were followed for a mean of 4.4 months after cessation of anticoagulants or during inadequate antinecessitating re-institution of anticoagulant therapy. Long-term, anticoagulant treatment can be recommended in carefully selected patients with TIA, and also with infarction in the carotid territory.
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PMID:Prognosis in patients with infarction and TIA in carotid territory during and after anticoagulant therapy. 50 92

Between the years 1964 and 1973, 225 patients with transient ischemic attacks (TIAs) due primarily to atherosclerosis were evaluated and treated. They have now been followed for from 3 to 14 years (average 5.5 years). As of 1976, 82 of the 225 patients were dead, 21 from cerebral infarction, 52 from heart disease and nine from other causes. Of the 56 untreated patients, 11 (19 percent) had cerebral infarctions, four (7 percent) of which were fatal; six (11 percent) were still having TIAs. Of the 45 patients medically treated, 10 (24 percent) had cerebral infarctions, three (7 percent) of which were fatal; 11(25 percent) still experienced TIAs. In the surgical group of 124, 27 (21 percent) had postoperative cerebral infarctions, seven (6 percent) of which were fatal; 23 (18 percent) had cerebral infarctions during follow-up, of which seven (6 percent) were fatal; and 15 (12 percent) were still having TIAs. No statistically significant differences (p less than 0.05) related to cerebral infarction or TIAs developed among the three groups. The majority (23 percent) eventually succumbed to myocardial infarction, leading us to conclude that great emphasis must be placed upon TIAs as a warning for cardiac as well as cerebrovascular disease.
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PMID:Transient ischemic attacks: a prospective study of 225 patients. 56 90

The incidence of both atherosclerosis and demential increases with age and therefore the terms "cerebral atherosclerosis" or "cerebro-vascular dementia" are commonly used for any mental deterioration in elderly persons. These names depend on the proposition of a gradual narrowing of cerebral arteries as an inevitable accompaniement of ageing which ends in dementia through a progressive reduction of cerebral blood flow. This apparently reasonnable hypothesis has now been shown to be wrong. ;t has been established that first, senile dementia is not due to cerebral atherosclerosis in spite of the frequent coexistence of degenerative and vascular lesions; and secondly, true cerebro vascular dementia results from the destruction of brain tissue following cerebral infarction; hence the proper term is "multi-infarct dementia". This neuronal destruction leads to decrease in cerebral metabolism and blood flow and to intellectual deterioration. The diagnostic criteria are therefore those of cerebral infarcts i.e: arterial hypertension and/or signs of atherosclerosis, sudden onset and/or stepwise progression, and focal neurological signs. If one follow those criteria, multi-infarct dementia accounts for only about 10% of all dementias; if one does not, the diagnosis will continue to be made to the exclusion of other potentially curable causes of dementias. Five clinico-pathological forms can be distinguished according to the size, number and site of the infarcts: lacunar state, large multiple infarcts, watershed infarction, single infarct and Binswanger's encephalopathy. This distinction is always arbitrary because the association of lacunes and large infarcts is very common in multi-infarct dementia. The almost invariable failure of all therapeutic measures once multi-infarct dementia has been established stresses the importance of prevention. This depends on prevention of cerebral infarcts, i.e. on the correction of risk factors amongst which arterial hypertension is by far, the most important. Some cases benefit also from carotid surgery, anticoagulants, and antiplatelet drugs but antihypertensive drugs are the most essential part. It is very likely that if all cases of arterial hypertension are properly treated, the incidence of multi-infarct dementia will decrease greatly.
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PMID:[Modern concepts of "cerebrovascular dementia"]. 61 Oct 16

Cerebral atherosclerosis without luminal narrowing has been found macroscopically and by angiographic examinations in some patients with cerebral hemorrhage. In order to clarify the histology of non-stenotic atherosclerosis of the cerebral vessels, we examined cleared specimens and serial sections of the main trunks of the cerebral arteries. The middle cerebral artery was selected in 20 cases of cerebral hemorrhage and 7 cases of cerebral infarction. Non-stenotic atherosclerosis was found frequently in cases of cerebral hemorrhage, while most patients with cerebral infarction showed stenotic cerebral atherosclerosis. We counted the numbers of medial smooth muscle cells in 10 autopsied cases of cerebral hemorrhage and 6 of cerebral infraction. The mean numbers of smooth muscle cells per unit area in the patient with cerebral hemorrhage were less than those in cerebral infraction. In cerebral hemorrhage, the main trunks of the cerebral arteries were dilated, probably as a result of the damage to medial muscle cells and higher blood pressure during the course of intimal thickening. It is considered that arterial hypertension spreads to the peripheral, small arteries through the main trunks without luminal narrowing of the cerebral vessels.
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PMID:Comparative angiographic and histological evaluations of intracranial atherosclerosis in hypertensive and normotensive subjects. 67 48

The relationship between the indicence of cerebral infarction and the hematocrit was studied using 432 consecutive autopsied patients with the average age of 77.1 years. The incidence of cerebral infraction was higher in patients with hematocrit values of more than 46%, (the average in younger adult subjects). The increase in the frequency of cerebral infarction with high hematocrit values was more conspicuous in patients with severe cerebral atherosclerosis than in those with slight cerebral atherosclerosis. High blood pressure per se did not influence the relationship between the hematocrit value and the incidence of cerebral infarction. With hematocrit values of more than 41%, cerebral infarction occurred more frequently in patients over 78 years of age than in the younger patients, but the difference was not significant statistically. High hematocrit values are associated with a higher risk of cerebral infarction in deep subcortical structures of the brain than for cartical infarctions. The pathogenetic and preventive implications of these results are discussed in the light of blood rheology.
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PMID:Importance of the hematocrit as a risk factor in cerebral infarction. 67 49

Observations of a series of fifteen surgically treated coiled and kinked internal carotid arteries are reported. The kinked internal carotid artery may be clinically significant and can cause cerebral infarction, even in the absence of atherosclerosis. Each patient must be thoroughly investigated and evaluated individually. One must distinguish simple tortuosity without blood flow obstruction from critical kinking of the internal carotid artery. If a patient with angiographic confirmation is symptomatic and other causes are eliminated, surgical correction should be carefully considered, especially if rotational cerebral ischemia is present. The surgical treatment of choice is resection of the redundant internal carotid artery with reimplantation and thromboendarterectomy of any associated plaque. Kinking of the internal carotid artery may lead to aneurysm formation requiring a difficult surgical resection. Although the evidence for a precise causal relationship between kinking of the internal carotid artery and cerebrovascular symptoms is sometimes difficult to establish, it is our belief that a more aggressive surgical approach may be warranted in this potentially disabling and even fatal condition.
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PMID:Kinking of the internal carotid artery. Clinical significance and surgical management. 87 13

To define the etiologic factors of Japanese cerebrovascular diseases, a pathological research was conducted on autopsy cases of stroke in Akita Prefecture. In most cases of cerebral hemorrhages, especially in the middle age group (30-59 of age), arteriosclerotic deviations in basal berebral arteries of the circle of Willis and intracerebral small arteries are not found. The authors conclude that cerebral hemorrhage may occur without relationship to disturbances of lipid metabolism, biochemically, and to atherosclerosis, pathologically. Concerning cerebral infarction, especially in the old generation (over 60 years of age), severe arteriosclerotic deviations were recognized both in basal cerebral and intracerebral arteries. These changes were highly influenced by the grade and duration of hypertension, and rarely influenced by hypercholesterolemia. According to the above-mentioned facts, the results obtained from out epidemiological survey were confirmed by the pathological studies.
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PMID:Epidemiological studies of cerebro-and cardiovascular diseases in the northeast of Japan Part I. Pathological approach to the study in Akita Prefecture. 96 61


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