Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over the past four years, 21 patients have been operated for aneurysms of the thoracic aorta requiring aortic arch reconstruction. The causes of the aneurysms were dissecting aneurysms of the aorta (type A) in 16 patients and atherosclerosis in 5 patients. To prevent cerebral ischemia during operation, selective cerebral perfusion (SCP) (600 ml/min at 25 degrees C) was employed in 11 patients and hypothermic circulatory arrest (HCA) at 15 degrees C in 10 patients. There were three early deaths (14.3%) in the series. There were no serious neurologic complications in either group. The present data suggests that both selective cerebral perfusion SCP and HCA are useful methods for cerebral protection during resection of aortic arch aneurysms, although the latter method has the limitation of restricted cerebral arrest time.
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PMID:Surgical treatment of aneurysms of the transverse aortic arch. 274 27

The positive correlation between cerebral ischemia and carotid atherosclerosis of extracranial tract has been well established. The reliability of echotomography as diagnostic and prognostic tool in the evaluation of the carotid atherosclerotic lesions is now intensively investigated. Most of the attention has been payed to the accuracy in the determination of the carotid stenosis. A percentage of cerebrovascular accidents do not correlate to the vascular stenosis but to the other modifications induced by the atherosclerotic plaque, such as the release of emboli, acute stenosis for intraplaque haemorrhage or thrombosis. Thus the evaluation of the composition of the plaque may represent a good prognostic tool. In the present study, fifty-two carotid obtained at surgery from patients, who preoperatively underwent ultrasonographic scanning of both carotid arteries, were examined by histological methods. In calcified tissues a significant correlation between findings obtained with both techniques was observed. In the complicated plaques atheromasic gruel, intraplaque haemorrhages and thrombosis could not be discriminated by echotomography.
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PMID:Histopathological characterization of carotid plaques echotomography. 329 Mar 60

The classification, epidemiology, pathophysiology, diagnosis, and treatment of ischemic cerebrovascular disease (ischemic stroke) are reviewed, and the major drugs used in the prevention of this disease are discussed. Ischemic stroke is a major problem in terms of morbidity and mortality because of the high prevalence of atherosclerosis in the United States population. The pathogenesis of cerebral ischemia is multifactorial, beginning with an atherosclerotic plaque on the arterial wall that may result in stenosis or ulceration with subsequent thrombosis or embolization. Platelets may adhere to the exposed arterial wall endothelium, stimulating further platelet aggregation and accumulation of leukocytes and fibrin. Consequences of cerebral ischemia include transient ischemic attacks and brain infarcts. Diagnosis is based mainly on patient history and ancillary radiologic studies. Treatment of ischemic cerebrovascular disease is primarily preventive, since the brain has limited capacity to recover neurologic function after an infarction. Transient ischemic attacks are treated with either antiplatelet agents, anticoagulants, or surgery. Treatment of stroke is also preventive, although anticoagulation is sometimes used to prevent stroke progression. Agents that may reverse neurologic impairment following an acute stroke, such as prostacyclin, calcium-channel blockers, and opiate antagonists, are being investigated. Antiplatelet therapy is indicated in subsets of patients with cerebral vascular insufficiency. Anticoagulation therapy, if needed, should be given for only three to four months.
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PMID:Current concepts in clinical therapeutics: ischemic cerebrovascular disease. 331 77

Twenty five carotid endarterectomies were performed in 24 patients with cerebral ischemia due to atherosclerosis. Four of these patients were asymptomatic, 7 suffered from hemispheric TIA (hemispheric attack group), 7 suffered from nonhemispheric TIA (nonhemispheric attack group) and other 6 had previous completed stroke (completed stroke group). The average length of follow-up study was two and half years with a range of 2 months to 6 years. Completed strokes occurred in 1 patient following the operation and in 3 patients during the follow-up period (16.7%). Two patients were reoperated upon because of recurrent carotid stenosis (8.3%). Four patients continued to have neurologic symptoms postoperatively. Ultimately 10 of 24 patients had some neurologic complications even following carotid endarterectomies (41.7%). The first postoperative year was the worst period because almost all late neurologic complications occurred in that time. Kaplan-Meier's analysis demonstrated a relatively favorable result in the hemispheric attack group among these 3 groups. The completed stroke group was followed by that and the nonhemispheric attack group was proved to be the worst, although there was no statistical significance.
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PMID:[Carotid endarterectomies for cerebral ischemia: a follow up study of surgical results and late neurologic complications]. 339 33

In a group of 1621 patients with vascular brain lesions (849 males, 772 females) the authors found seizures in 108 cases (56 males, 52 females): in 26 cases of subarachnoid haemorrhage (aneurysms), 6 cerebral haemorrhages, 24 cerebral arterial thromboses, 18 atherosclerosis of brain vessels, 13 cases of embolia, 4 cases of transient cerebral ischaemia, 4 cases of vertebrobasilar insufficiency, 4 cases of cerebrocardiac syndromes, 2 cases of cerebral form of the Winiwarter-Buerger disease and 1 cases each of cerebellar haemorrhage and aortic arch syndrome. In 8 cases family history of epilepsy was elicited. The authors suggest administration of anticonvulsants in justified cases.
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PMID:[Epileptic seizures in patients with vascular brain lesions]. 358 13

To investigate the association between carotid plaque hematoma and symptoms of cerebral ischemia a retrospective review of 200 consecutive carotid endarterectomies at the Neurological Institute of New York was carried out. Data analyzed included cerebral ischemic symptoms, angiographic findings, preoperative use of antithrombotic agents, and microscopic pathology of endarterectomy specimens. No association was found between ischemic symptoms ipsilateral to the endarterectomy and presence, size, or age of plaque hematomas. Plaque hematomas were less common among patients who took antithrombotic agents preoperatively than among those who did not. The presence of plaque hematoma was associated with angiographic carotid cross-sectional area stenosis of greater than 75%. Patients with stenosis of less than 75% were more likely than those with stenosis of greater than 75% to have ischemic symptoms ipsilateral to the endarterectomy, suggesting that criteria for surgical treatment of carotid atherosclerosis differ for those who are symptomatic vs. those who are asymptomatic. These results demonstrate the limitation of using a surgical series to extend causal inferences about the relation between plaque hematoma and cerebral ischemic symptoms to the general population of people with carotid atherosclerosis.
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PMID:Lack of association between carotid plaque hematoma and ischemic cerebral symptoms. 362 46

Serotonin, which is released when platelets aggregate at carotid lesions, may contribute to cerebral ischemia. Our goal was to test the hypothesis that dietary treatment of atherosclerosis reverses the augmented cerebral vasoconstrictor response to serotonin. We studied normal cynomolgus monkeys, atherosclerotic monkeys, and atherosclerotic monkeys that were fed a normal (regression) diet for 18 months. Morphometric studies indicated that the regression diet reduced intimal area in the carotid arteries by about 50-75%. Cerebral blood flow was measured with microspheres, and microvascular pressure was measured with a micropipette in pial arteries that were approximately 300 micron in diameter. Values for cerebral blood flow and arteriolar pressure were used to calculate resistance of large cerebral arteries (greater than 300 micron diameter). Infusion of serotonin produced a modest increase in the resistance of large cerebral arteries in normal monkeys. Vasoconstrictor responses to serotonin were increased more than fivefold in atherosclerotic monkeys. The major finding of the study is that dietary treatment of atherosclerosis abolishes augmented cerebral responses to serotonin.
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PMID:Cerebral vasoconstrictor responses to serotonin after dietary treatment of atherosclerosis: implications for transient ischemic attacks. 368 79

Isolated supraclinoid occlusive disease of the internal carotid artery is a rare cause of cerebral ischemia. The authors of the only review of this subject concluded that it is caused predominantly by factors other than atherosclerosis. We examined 6 patients with isolated supraclinoid occlusive lesions. Five of them had one or more risk factors for atherosclerosis. Thus, the isolated stenosis of that part of the internal carotid artery does not seem to represent a particular pathologic entity.
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PMID:Isolated supraclinoid occlusive disease of the internal carotid artery. 381 84

As a result of the examination of 76 patients with atherosclerosis (57 with ischemic stroke and 19 with chronic cerebrovascular insufficiency) the authors have established a definite correlation between the blood levels of carotinoids and the degree of hypoxia and cerebral ischemia, as well as between pigment concentrations and the oxygen consumption by tissues which indicates an active participation of carotinoids in the processes of body adaptation to hypoxia. The necessity of the drug correction of carotinoid concentrations in patients with ischemic vascular lesions of the brain is justified.
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PMID:[The role of carotenoids in the development of compensatory reactions of the body to hypoxia]. 382 87

Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.
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PMID:Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. 1110 78


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