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)

Prognosis of transient ischemic attack (TIA) in 45 patients, diagnosed as TIA out of 75 suspected TIAs, was investigated for an average follow-up of 12.9 months. Twelve (27%) of the 45 patients progressed to complete stroke during the follow-up period. Patients with severe atherosclerotic lesions and with intracranial arterial lesions or with lesions of both intracranial and extracranial sites were predominant among the 29 cases examined angiographically, and the majority progressed to stroke. The prognosis was poorer than in the cases with mild atherosclerotic lesions or cases with only extracranial arterial lesions. From such characteristics of cerebral atherosclerosis of TIA in the Japanese with predominant intracranial severe arterial lesions, a different genesis for the development of cerebral atherosclerosis between Japanese and Americans or other Caucasians may be expected in cases with TIAs. With respect to the relation of recurrence of TIA to prognosis, a single episode of TIA in the past placed the patient at a greater risk of early infarction, where a high incidence (57%) of progression to stroke was found during the follow-up period. Treatment by superficial temporal artery to middle cerebral artery anastomosis or anticoagulant drug medication seemed to improve the prognosis of TIA as compared with antiplatelet aggregation therapy. These results suggest that embolus formation from an embolic source of arterial lesions may play some part in the pathogenesis of TIA and occurrence of subsequent stroke.
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PMID:Transient ischemic attacks: racial differences, treatment, and prognosis. 614 Jun 53

That an elevated haemoglobin or haematocrit is a risk factor in stroke is suggested by the prospective epidemiological evidence from Framingham. Our own study of a series of patients with transient ischaemic attacks revealed that even when due allowance was made for interaction between haematocrit, hypertension and smoking, there was still evidence that both male and female patients had a higher haematocrit than age and sex matched controls. Toghi's autopsy study further shows that cerebral infarction is more frequently found in the elderly population in subjects with a high haematocrit, the effect being most obvious in the presence of severe cerebral atherosclerosis. Cerebral blood flow is inversely related to haematocrit, reflecting the physiological maintenance of oxygen supply according to the metabolic demands of cerebral tissue. When oxygen carriage is enhanced at high haematocrit, flow falls. This could however, predispose in the face of atheroma to thrombosis, a suggestion given some support by the finding that amongst TIA patients the greatest proportion with a haematocrit over 50 were found among those with thrombotic carotid occlusion. The effect of haematocrit on flow might become limiting when considering collateral flow, and flow in a maximally dilated vascular bed in the territory of recent infarction. This hypothesis is supported by the finding that the size of the cerebral infarct accompanying carotid occlusion is greater in patients with an elevated haematocrit.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hematocrit and cerebrovascular accidents]. 622 21

63 patients with mitral annulus calcification (MAC) were followed for an average of 3.4 years. Two patients experienced TIA, both ipsilateral to a previous endarterectomy site, and IV-DSA demonstrated normal extracranial vessels. There were 3 strokes (5%), all fatal, but none could be attributed to embolism. Embolic stroke due to MAC is rare and difficult to prove due to coexistent atherosclerosis. Associated cardiac conditions such as atrial fibrillation, which might increase the risk of embolism, usually occur with MAC greater than or equal to 5 mm. In many patients, MAC may be better viewed as a marker of generalized calcific atherosclerosis rather than as an immediate embolic source.
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PMID:Risk of stroke in patients with mitral annulus calcification. 647 29

A prospective study was made of the morbidity and mortality from ischemic heart disease in 390 patients with focal TIA caused by atherosclerotic vascular disease. The 5-year cumulative rate of myocardial infarction or sudden death in these patients was 21.0%, a rate only slightly less than that of fatal or nonfatal cerebral infarction (22.7%). Risk factors including diabetes, angina, and ECG abnormalities were associated with an increase in morbidity and mortality from ischemic heart disease. A major factor associated with these cardiac events was the presence of atherosclerotic obstructive or ulcerative lesions in the carotid arteries. These observations indicate that focal TIA caused by carotid atherosclerosis is a predictor not only of cerebral infarction, but also of serious cardiac disease and death.
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PMID:Risk of ischemic heart disease in patients with TIA. 653 54

A 42-year-old man with generalized atherosclerosis underwent surgery of the left carotid artery with eventual placement of a Dacron graft bypassing the left carotid sinus. Subsequently, symptoms suggestive of pheochromocytoma developed, and 24-hour urine catecholamine levels were elevated. Clonidine testing resulted in suppression of plasma norepinephrine levels but was complicated by severe hypotension and a transient ischemic attack. Baroreceptor dysfunction may have been involved. Caution is advised and recommendations are offered for future usage of the clonidine suppression test.
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PMID:Symptomatic hypotension following the clonidine suppression test for pheochromocytoma. 663 44

Serum high density lipoprotein (HDL) cholesterol and other lipoproteins were measured in 27 TIA-patients with a mean age of 49 +/- 10 years before and during phenytoin therapy. The pretreatment concentrations of HDL-cholesterol (mmol/l, mean +/- SD) were lower (p less than 0.001) in male (1.03 +/- 0.25) and in female patients (1.15 +/- 0.44) than in healthy male (1.28 +/- 0.34) and female controls (1.52 +/- 0.31) respectively. After one month's phenytoin therapy HDL cholesterol concentrations reached normal levels (men 1.33 +/- 0.38, women 1.61 +/- 0.27) and after 9 months of therapy even surpassed them (men 1.47 +/- 0.27, p less than 0.05; women 1.91 +/- 0.33, p less than 0.01). Percent increase of HDL cholesterol after 9 months of therapy was 42 +/- 25 in men and 68 +/- 46 in women. There was a positive correlation (r = 0.43, p less than 0.05) between serum phenytoin level and increase of HDL cholesterol. HDL/LDL cholesterol ratio increased (p less than 0.01) also during 9 months of therapy (men from 0.26 +/- 0.05 to 0.36 +/- 0.10, women from 0.26 +/- 0.07 to 0.43 +/- 0.13) and showed a positive correlation (r = 0.91, p less than 0.001) with increase of serum HDL cholesterol. The HDL cholesterol levels achieved have been maintained with a mean serum phenytoin level of 5.6 +/- 3.6 mg/l. Phenytoin induced increase in serum HDL levels should not yet be equated with protection against atherosclerosis.
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PMID:Increase of low serum concentrations of high-density lipoprotein (HDL) cholesterol in TIA-patients treated with phenytoin. 665 26

A sample of in all 119 young adults below the age of 55, with ischemic cerebrovascular disease (TIA and minor stroke), was investigated later than three months after acute disease. Factor VIII biological activity and antithrombin antigen were significantly (p less than 0.001) increased as compared to 80 healthy controls. In combination, these two variables correctly classified 85 percent of patients and controls at a stepwise discriminant analysis. Factor VIII related antigen was increased (p less than 0.02) in patients with atherosclerotic signs at cerebral angiography and in postmenopausal female patients (p less than 0.001). It is suggested that high levels of factor VIII might predispose for thrombosis/atherosclerosis. Antithrombin biological activity was normal in spite of high antithrombin antigen levels, possibly indicating a relative insufficiency in the antithrombin defense line. It is concluded that young stroke patients provide good opportunities to look for early operating factors and predictors in human atherosclerosis and arterial thromboembolism.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. I. Abnormalities in factor VIII and antithrombin. 681 Apr 96

The study includes 119 patients with minor ischemic cerebrovascular lesions before the age of 55 during 1976-78. Atherosclerotic signs were found in 65% at aortocranial angiography and/or exercise test (ST depression). Abnormalities in hemostasis (defective fibrinolytic response in 50%, high Factor VIII activity in 45% of those investigated, and high Factor VIII related antigen (VIII R:Ag) in 20%) could not be explained by accumulation of atherosclerotic risk factors as most often no significant independent correlations were found at stepwise multiple regression. Significant correlations with aortocranial atherosclerosis was found for age, VIII R:Ag and blood pressure reaction at exercise test. Only E-SR showed significant correlation to ST depression at exercise test. These results indicate different determinants and risk indicators for atherosclerosis with different locations. An early evaluation of the longitudinal study (mean 42 months' follow up) showed that 16 patients had suffered new occlusive vascular incidents. The malign prognostic subgroup (cerebral or myocardial infarction or death; n = 10) showed significantly higher levels of VIII R:Ag (p less than 0.005) and triglycerides (p less than 0.05) than the benign group (new TIA, n = 6). This indicates that VIII R:Ag may be a useful marker for development of atherosclerosis and predictor for the outcome of ICD.
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PMID:A study of hemostasis in ischemic cerebrovascular disease. V. A multivariate evaluation of risk indicators and predictors. Early results of a longitudinal study. 681 52

When a physician is faced by a patient suffering from transient ischemic attacks, the diagnosis is almost invariably determined by the clinical history. It becomes necessary to eliminate certain other medical conditions including migraine, focal epilepsy and cardiac disorders. Once he is satisfied with the diagnosis of TIA, then he must consider whether to employ medical or surgical therapy or a combination of both. It must be recognized that TIAs are not benign events since more than 50 p. 100 of individuals who develop completed strokes will have antecedent TIAs. Identification of the pathogenetic mechanism becomes important in choosing the specific therapy. Where the origin of the attacks is clearly thromboembolic, secondary to atherosclerosis, surgical intervention may be appropriate if the lesion is readily accessible. However, consideration of surgery is also determined by the risk of post-operative stroke or death at the hands of less experienced surgeons. The risk of stroke in a patient who is having frequent TIAs may be reduced initially by utilizing anticoagulants for a limited period. Long-term medical therapy requires the use of anti-platelet agents which have been shown to have a more beneficial effect in preventing strokes in men. The evidence for protection in females is less satisfactory. Surgical treatment should be followed by long-term medical therapy since it is very unlikely that only one lesion is present in a high-risk patient. It is still clear that the best way to manage cerebro-vascular accidents is to prevent them. This requires education of the public, as will as physicians, with respect to risk factors and the value of various modes of therapy.
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PMID:[Medical or chirurgical treatment in transient cerebral ischemia? (author's transl)]. 702 7

From 1978 to 1980, thirty-one patients aged forty years or less, had cerebral ischemic events as TIA, RIND or complete stroke. These patients have been studied, both clinically and with laboratory tests to assess the most common causes of their disorder. It was found that hypertension, excess smoking, diabetes and disorders of the lipid metabolism are the most common causes of the atherosclerosis, which plays a role in enhancing ischemic cerebro-vascular accidents during youth. The detection as well as the localization of the site of the ischemic lesions was difficult; only in six out of the seventeen patients examined it was possible to show angiographically a stenosis of one cerebral vessel. Comparison between the 31 patients and 31 subjects of the same age without clinical symptoms or neurological signs, showed a significant incidence of causes of atherosclerosis in the control subjects. In view of the limited number of controls it was not possible to predict a clearcut prognosis.
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PMID:[Risk of cerebral infarct in young adults (author's transl)]. 711 91


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