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)

Utilizing the initial BP assessment in the 462 patients who entered the Italian Multicenter Study of reversible cerebral ischemia, an analysis of the effect of each BP component in respect of presence, extent and severity of atherosclerotic lesions, as displayed by angiography, was carried out separately for lesions located at either intra- or extracranial level. In a multivariate statistical model, among the following variables: sex, age, systolic BP, diastolic BP, cholesterol and smoking, systolic BP was found the best predictor of extent and severity of atherosclerotic lesions at extracranial level. None of the same variables was predictive of the severity of intracranial atherosclerosis. The results of this clinical study may confirm the indication, coming from physiopathologic observations, of a predominant role of systolic hypertension in the process of maintenance and acceleration of atherosclerosis in the large pre-cerebral arteries.
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PMID:The Italian Multicenter Study of reversible cerebral ischemic attacks: IV--Blood pressure components and atherosclerotic lesions. 396 27

Juvenile distal cerebral ischemia has been attributed to small artery atherosclerosis (Arnold, Benoit, Merlen, Dobbelaere, Delandsheer, 1979), based on clinicopathologic findings in one male patient and results of big toe pulp biopsy in three other cases. Pathological findings were obstruction of small artery lumens by hypertrophic endothelium and loose fibrocellular bands, their origin being the result possibly of partial intimalization of media by elastic neogenesis. Appearances were similar to those described by Dahl in human cerebral atherosclerosis in 1976, and approached those of the initial stages of experimental atheroma (Ross, Glomset, 1976). Arterial exiguity was also present in the 4 cases. Results of biologic, metabolic, inflammatory and immunologic examinations were negative. The present study concerns 4 additional cases of juvenile distal encephalic ischemia. One case in a female patient not on oral contraceptives confirmed the hypothesis of intimalization of media of arterioles of big toe pulp. Elastic neogenesis was present in the tunica media in areas where there was a change of direction of myocytes, and was apparent at a distance from the internal elastic layer. The latter was fragmented, sometimes doubles and of variable color. In another case, a woman taking oral contraceptives, there was almost total obstruction of the pulp arteriolar lumens with a very thin tunica media. Elastic neogenesis encircled two very narrow lumens in the center of the vessel and there were also elastic changes common to both.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Juvenile distal cerebral ischemia: value of pulp biopsy]. 398 17

Platelet scintigraphy was performed on 62 patients with cerebral ischaemia. Pathological scintigraphic images were obtained in 29 of the 62 patients. In 79.3% of these 29 patients the scan was abnormal in the vessel clinically affected. Platelet scintigraphy was abnormal in 21 of 34 patients with normal angiogram or only slight atherosclerosis. In patients undergoing antiplatelet therapy, platelet scintigraphy was less often positive than in untreated patients. It is suggested that platelet scintigraphy could be an appropriate technique for detecting small mural thrombi of the carotid artery, which are the source of arterio-arterial emboli, and for controlling the efficiency of antiplatelet therapy.
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PMID:The clinical use of platelet scintigraphy with 111-In-oxine. 619 27

Prospective longitudinal cerebral blood flow values were serially plotted over a four-year interval against the course of cerebral ischemia before, during, and after onset of clinical symptoms. Of 161 normal subjects (mean age, 62 years), 86 were risk free and 75 had hypertension, heart disease, diabetes mellitus, and/or hyperlipidemia. Twenty-one subjects developed cerebrovascular symptoms during the prospective trial. Mean hemispheric cerebral blood flow values were significantly lower for at risk than for risk-free subjects. Symptomatic subjects showed lower values than those in either of the two asymptomatic groups at every session. Statistical analysis of cerebral blood flow values for symptomatic patients compared one and two years prior to onset of symptoms, at the onset of symptoms, and 1 year later showed reductions compared to asymptomatic risk-factored subjects tested in a similar prospective manner. Measurable declines in cerebral perfusion accompany development and progression of aortocerebral atherosclerosis prior to clinical appearance of signs and symptoms of cerebrovascular disease. If confirmed, these observations should permit the institution of preventive medical and/or surgical interventive measures and an evaluation of their outcome.
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PMID:Progressive cerebral ischemia antedates cerebrovascular symptoms by two years. 648 37

Systematic blood coagulation analyses were conducted in 32 severely hypertensive patients treated with the angiotensin converting enzyme inhibitor captopril. Two hours after the first captopril dose, fibrin monomer complexes had already increased. This rise was even more distinct after 26 h and 1 week. Tests after 6 and 12 months of therapy showed a regression of fibrin monomer complexes to pretreatment values. In several patients with a marked increase in fibrin monomer complexes, the partial thromboplastin time (PTT) became shorter and antiplasmin activity increased. The most pronounced increase in fibrin monomer complexes was seen in patients with a rapid and excessive blood pressure reduction. The concentration of fibrin monomer complexes also rose in 15 healthy normotensive subjects, after a single oral dose of captopril (25 mg). Additionally, the PTT was shortened and antiplasmin significantly rose. An inhibition of fibrinolysis by captopril could be demonstrated by the effect on fibrin plates and thrombus weight after streptokinase. Out of 58 patients with severe hypertension and atherosclerosis treated with captopril, 7 patients suffered vascular complications during antihypertensive therapy: myocardial infarction (n = 2), coronary insufficiency (1), cerebral ischemia (1), renal insufficiency (3). These ischemic lesions may be partly explained by the alterations of coagulation and fibrinolysis under captopril therapy.
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PMID:Effects of the converting enzyme inhibitor captopril on blood coagulation and fibrinolysis in man. 675 Feb 21

THe records of 78 young adults, who had suffered cerebral infarction, were reviewed with regard to possible pathogenetic mechanisms. Atherosclerosis risk factors appeared to play a major role between the age of 40 and 50, especially in males. Non atherosclerotic factors of cerebral ischemia were found predominant among females under 40, owing to contribution of migraine, oral contraceptive use and pregnancy/puerperium. In 18% of the patients no etiology could be identified.
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PMID:[Juvenile cerebral infarct. Retrospective analysis of risk factors in 78 cases]. 730 Nov 82

56 cerebral ischemia patients up to the age of 40 were investigated using a strict clinical and instrumental protocol in order to elicit the relative importance of the various iatrogenic factors involved. In addition to atherosclerosis risk factors (smoking, hypertension, ischemic heart disease, diabetes, dyslipidemia) other possible causes of cerebral ischemia were sought (arteritis, migraine, head injury, oral contraceptives, coagulation disorders, cardiogenic embolism, etc.). 50% of the patients examined had at least two atherosclerosis risk factors and 55% had other causes singly or in association with atherosclerosis.
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PMID:Cerebral ischemia in young adults. 733 59

Nicardipine is a second generation dihydropyridine-type Ca2+ antagonist with high vascular selectivity and strong cerebral and coronary vasodilatory activity. The compound is used in the treatment of hypertension, primarily in the elderly. In this review the main evidence of the cerebrovascular activity of nicardipine in preclinical studies using in vitro and in vivo models is detailed. A particular physico-chemical property of nicardipine is the almost complete protonation in acid environment. This allows its accumulation in ischemic brain regions and makes it a candidate for the treatment of cerebrovascular disorders characterised by impaired brain perfusion. The main clinical data on the use of nicardipine in cerebral ischemia and related disorders, subarachnoid haemorrhage and stroke, are also reviewed. These studies included 5940 patients affected by chronic cerebrovascular insufficiency (cerebral ischemia, cerebral atherosclerosis mainly associated with hypertension, transient ischemic attacks, sequelae of cerebral infarction, thrombosis or embolia, hypertensive encephalopathy), 1540 patients affected by sequelae of subarachnoid haemorrhage and 206 patients affected by stroke. Both preclinical studies and clinical trials have shown that nicardipine is a safe Ca2+ antagonist with powerful cerebrovascular activity. This suggests its possible use in cerebrovascular disorders in which blockade of Ca2+ channels of the L-type and/or selective cerebral vasodilatation is desirable. Further studies are necessary to establish if modulation of neuronal Ca2+ channels of the L-type by nicardipine may have a neuroprotective effect independent by the cerebrovascular activity of the compound.
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PMID:Nicardipine and treatment of cerebrovascular diseases with particular reference to hypertension-related disorders. 765 45

Syncope is a brief sudden loss of consciousness and muscle tone secondary to cerebral ischaemia, inadequate oxygen or glucose delivery to the brain. The causes of syncope may be benign and require very little in the way of evaluation or treatment. However, syncope may be the harbinger of sudden death, and extensive evaluation, monitoring and detailed recommendations regarding advisability of participating in sports should be reviewed with the patient. The history is the most important clue when attempting to identify which patient with syncope is at risk for sudden death. A careful cardiac and neurological examination should be performed in any patient presenting with syncope. Selective use of laboratory testing and cardiac monitoring may assist the practitioner in making the diagnosis. Most often patients with syncope will have a benign cause such as vaso-vagal events, hyperventilation or orthostatic hypotension. Patients with a cardiac condition causing their syncope are at increased risk for sudden death. The ominous, cardiac-related causes of syncope in the younger population include hypertrophic cardiomyopathy, aberrant coronary arteries and aortic dissection secondary to Marfan's syndrome. In the older athletic population, coronary atherosclerosis may present with syncope. Dysrhythmias may be the cause of syncope in both populations.
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PMID:Syncope in athletes. 778 60

Aneurysms of the extracranial internal carotid artery are rare but can be responsible for severe complications such as rupture, thrombosis, or embolism. Between 1961 and 1985 we operated on 38 aneurysms of the extracranial internal carotid artery in 35 patients, 22 males and 13 females, whose ages ranged from 6 to 73 years. The underlying causes of aneurysm included atherosclerosis (12 cases), fibromuscular dysplasia (eight cases), a congenital defect (five cases), infection (one case), and trauma (six cases); in six cases aneurysm was secondary to spontaneous dissection. Signs of cerebral ischemia were present in 26 (74%) patients and a cervical mass was found in six. The aneurysm was proximal (i.e., below the angle of the mandible) in 16 patients and distal (i.e., above the angle of the mandible) in 22. After resection of the aneurysm, arterial continuity was restored in 37 patients by resection and grafting (12 cases), resection and anastomosis (11 cases), or arteriorrhaphy (14 cases). One death occurred 13 days after operation due to myocardial infarction. Two patients experienced a reversible neurologic event. Transient paresis of cranial nerves was observed in eight patients. During a follow-up period that ranged from 6 to 30 years, four patients were lost to follow-up and 25 patients remained asymptomatic. Three patients had asymptomatic thrombosis of the carotid artery detected at follow-up investigations. The potential risks of cerebral ischemia and rupture and the satisfactory long-term results achieved with surgery are strong arguments in favor of surgical treatment for aneurysms of the extracranial internal carotid artery.
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PMID:Surgical treatment of extracranial internal carotid artery aneurysm. 781 77


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