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

The fibrous plaque is regarded as the vascular lesion most characteristic of atherosclerosis. The notion that these lesions develop from mural thrombi has received considerable support, and there is also much support for the idea that plaques form as a reaction to mechanical or chemical damage to the endothelium. As an alternative to these two hypotheses, Benditt and Benditt have suggested that plaques represent monoclonal proliferation of altered smooth muscle cells similar to leiomyomas. Evidence in favor of this suggestion has been obtained using tissues from human black females who are heterozygous for the X-linked enzyme glucose-6-phosphate dehydrogenase (G6PD). In such individuals, as a result of random inactivation of the X-chromosome during embryogenesis, all normal tissues contain both the A and B isoenzymes of G6PD, when assayed electrophoretically, whereas plaques and other lesions suspected of being of monoclonal origin contain predominantly one isoenzyme. A certain proportion of fatty streaks also show a single G6PD isoenzyme pattern, suggesting that some fatty streaks act as the foreunners of the fibrous plaque.
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PMID:The human atherosclerotic plaque. 84 15

Atherosclerotic segments of pigeon aorta synthesized collagen at four times the rate found in normal aorta (Athero = 2071 +/- 1339 ng/g/h; Control = 497 +/- 192 ng/g/h; P less than 0.025). Similar results were obtained when synthesis was expressed per mg DNA. Elevation in collagen synthesis was relatively specific, collagen accounting for 4% of total protein synthesis in lesion-free aorta and 11.5% in atherosclerotic aorta. Substantial increases in total collagen were observed in atherosclerotic aortas (Athero = 9.9 +/- 3.1 mg/aorta; Control = 6.0 +/- 1.3 mg/aorta; P less than 0.05). Ultrastructural studies revealed the accumulation of large amounts of dense fibrillar collagen in the sub-endothelial region of the plaque. Plaque cells contained multiple vacuoles, an extensive rought endoplasmic reticulum and many mitochondria, suggesting active protein synthesis. It is concluded that increased collagen biosynthesis and deposition is an important metabolic derangement in lipid-rich atherosclerotic lesions whihc promotes their gradual conversion to fibrous plaques.
Atherosclerosis 1977 Mar
PMID:Enhanced synthesis and accumulation of collagen in cholesterol-aggravated pigeon atherosclerosis. 84 79

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

Measurements of aortic length and circumference in 336 post-mortem specimens confirm earlier, neglected observations on the progressive increase in aortic size which occurs with advancing years. The increase is not related to atherosclerosis , or to hypertension and seems to be part of a true ageing process. The value of measurement of aortic size in body age determination merits exploration by forensic pathologists. Aortic calcification is found in raised and complicated atherosclerotic plaques and its prevalence and severity closely follows the accepted pattern of plaque severity, occurring earlier and more severely in men, in the abdominal aorta and in patients with overt vascular disease in other territories such as patients with cardiac infarcts. No association was found between the amount of calcification and the presence of hypertension, diabetes or neoplasia.
Atherosclerosis 1977 Aug
PMID:Aortic size and aortic calcification. A necropsy Study. 88

Five patients studied by the authors and 28 mentioned in the literature indicate that recurrent stenosis occurs in no less than 0.6% of patients after carotid endarterectomy. The pathology of the recurrent stenosis was stated in only 10 cases indicating atherosclerotic disease in various stages of development in 7 and a fibrous intimal hyperplasia in 3. Correlation between risk factors for the development of atherosclerosis and the pathology of the recurrent disease was poor. Six patients developed recurrent disease despite postoperative prophylactic oral anticoagulation. Surgical technique appeared to have contributed to re-stenosis in 8 patients (1) by failure to remove the distal tongue of plaque or (2) narrowing of the lumen by the arteriotomy suture or (3) damage by a vascular clamp. In 18 symptomatic patients, 44% had symptoms by 3 years, 67% by 5 years, and 83% by 7 years after operation. The 8 patients with possible errors in surgical technique did not develop symptoms earlier than the other patients. Seventeen symptomatic patients had surgical correction of the re-stenosis (endarterectomy 9, vein patch 6, arterial homograft 1, not detailed 1). The incidence of recurrent stenosis after carotid endarterectomy is low and usually the operation provides a patent artery for life.
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PMID:Recurrent stenosis at site of carotid endarterectomy. 90 60

Rabbits were fed diets including cholesterol and 10% butterfat to determine whether polyunsaturated butter (9% 18:2) would be less atherogenic than normal saturated butter (3% 18:2) when fed for 12 weeks. The cholesterol diets alone, 0.5% or 2%, produced aortic plaque development, and plasma cholesterol increased 20 times, lipids increased 10 times, and vitamin E increased 5 times. The inclusion of both fat and cholesterol in the diet produced a synergistic effect, doubling these values to 40 times for cholesterol, 20 times for lipids, and 10 times for vitamin E. The higher circulating levels of cholesterol caused increased tissue levels of cholesterol. With 2% cholesterol and fat, liver and aorta cholesterol increased 10 times, heart 4 times, and muscle cholesterol 2 times. The lower 0.5% dietary cholesterol load was successful in limiting the amount of tissue cholesterol increase. Liver, aorta, heart, and muscle levels of cholesterol were only about half the concentration attained when 2% cholesterol was fed. It was concluded that there were no differences in plasma or tissue cholesterol, vitamin E, or atherosclerosis attributable to the polyunsaturated nature of the diet. The 10% butterfat diets alone, whether saturated or unsaturated, did not induce aortic plaques and did not increase blood or tissue cholesterol, lipids, or vitamin E. Our results suggest that the lipid mobilizing effect is mediated by cholesterol, probably by conversion to bile acids and a stimulation in intestinal absorption.
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PMID:Vitamin e, cholesterol, and lipids during atherogenesis in rabbits. 93 22

Clinical experience with 5 patients who had complications of atherosclerosis within the aorta at the site of the obliterated ductus arteriosus suggested the occurrence of clinically significant preferential atherosclerosis at this location. To examine this hypothesis, the clinical findings in these patients (4 with saccular aneurysm and 1 with systemic emboli from an ulcerated plaque at this location) were correlated with postmortem examination of the aortic isthmus in 40 consecutive cadavers. The point of ductal closure was the area of most severe atheromatous involvement in 32 of the 40 cadavers, and 25 of the 40 specimens demonstrated ulcerated plaques at this location. Microscopical examination consistently demonstrated intimal irregularity or disruption and thinning of the aortic media in this area. These studies indicate that preferential atherosclerosis occurs at the aortic end of the obliterated ducts arteriosus and that these atherosclerotic changes can be a clinically significant development.
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PMID:Preferential atherosclerosis at the aortic junction of the ligamentum arteriosum: clinical significance and pathological correlation. 93 39

An operative case of 12-year-old boy with a saccular aneurysm at the anterior communicating artery was reported. He had episodes of occasional headache during one year before admission. He was attacked by a severe headache associated with nausea and vomiting, and was admitted to Ooita Pref. Hospital under the diagnosis of subarachnoid hemorrhage four days later. On admission physical examinations revealed almost normal findings except for moderate dehydration and a blood pressure of 130/70 mmHg. Routine examinations (blood, serum including total cholesterol, urine, ECG and plain chest X-film) were normal. Neurologically there were lethalgic state, moderate nuchal rigidity and bilateral abducens paresis. Slightly hemorrhagic and xanthochromic CSF was demonstrated by a spinal puncture. An aneurysm was found at the anterior communicating artery on the right carotid arteriogram. The left carotid and the left vertebral arteriograms showed no pathologic findings. Operation via right fronto-temporal approach disclosed a berry aneurysm about 4 mm in diameter arising from the bifurcation of the right anterior cerebral and the anterior communicating artery. There was a plaque presumably an atherosclerotic change at the neck of the aneurysm. Clipping of the aneurysmal neck was done. The aneurysm was not visualized on the postoperative arteriogram, and the patient was discharged in good condition two weeks after the operation. It is true that this patient had a lesion which seemed to be an atherosclerotic plaque at the neck of the aneurysm macroscopically, but he did not have any evidence of generalized atherosclerosis or other metabolic disturbance. This plaque may be of special significance in etiological respect. In general, however, degenerative lesions like atherosclerosis occur predominantly in larger arteries than smaller arteries of the brain. Also the location of this aneurysm was at the anterior communicating artery which is reported to be implicated in anomalous vascularity on occasion. From these facts the authors considered combined congenital and acquired factors in the development of this aneurysm.
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PMID:[Intracranial aneurysm in a child--a case report and some considerations on etiology (author's transl)]. 94 72

This review has highlighted some of the factors which influence the formation and fate of thrombi. Rheology and flow, the coagulation mechanism, the fibrinolytic enzyme system, and the properties of platelets to adhere and aggregate all play a significant role. Of paramount importance to neurosurgeons is the role of the vascular wall in thrombogenesis. The ulcerated atherosclerotic plaque demonstrates this point. Factors contributing to thromboembolism in this setting include stenosis and reduced flow, turbulence, and the elements in the lesion with which blood interacts. These are principally collagen, ADP, fatty acids, and the thromboplastic activity of vascular subendothelial tissue. Current concepts of the etiologies of atherosclerosis were discussed. Along with other predisposing factors, platelets may play a significant role in the initiation of the process. The current status of clinical trials with inhibitors of platelet function in the treatment of cerebrovascular disorders was reviewed. In vascular reconstructive surgery, the principles which underlie good technique are those which best insure against thrombosis. The briefest possible period of stasis during surgery should be maintained. The reconstruction should result in a smooth blood flow pattern with rapid runoff and minimal stenosis or gaps between apposed endothelial surfaces.
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PMID:Hematological and vascular concepts in relation to stroke. 97 74

The evidence for the monoclonal nature of human atherosclerotic plaques is briefly reviewed. The interpretation of the cellular monotypy found in a large percentage (75 to 80%) of discrete raised atherosclerotic plaques as being monoclonal in origin appear firm since the size of patches of cells of the same type appears to be very small (ca. 10(-4) cu mm and 10 +/- cells). Evidence for explanations other than single cell origins of each plaque do not appear, at the moment, to be compelling. If we assume then that there is reason to accept the monoclonal character of atherosclerotic plaques in human beings then we are led to a search for the presence of factors that could "initiate" the monoclonal proliferation as well as factors that may promote the growth of the plaques. Evidence is presented that increased risk of atherosclerosis found with cigarette smoking is due to absorption from the lung and circulation in the blood of aryl hydrocarbons. Experiments show that these are preferentially carried in the same parts of the serum that transport cholesterol. The possibility of intrinsic initiators derived from cholesterol is discussed. A possible mechanism for the role of hypertension in promoting atherosclerosis is considered. Finally the evidence for a possible role of viruses in the pathogenesis of atherosclerosis is discussed.
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PMID:Implications of the monoclonal character of human atherosclerotic plaques. 98 99


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