Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adouble-blind trial of aspirin for the treatment of cerebral ischemia was begun in 1972 and continued for 37 months. This was accomplished despite difficulties in controlling a long-term study of a drug which has widespread availability and consumption. The study design, criteria for selection of patients, follow-up surveillance, and methods of data analysis are presented. We report only subjects without carotid surgery before randomization. Patients (178) who had carotid transient ischemic attacks (TIAs) were randomly allocated to aspirin or placebo and followed to determine the incidence of subsequent TIAs,death, cerebral infarction or retinal infarction. Analysis of the first six months of follow-up revealed a statistically significant differential in favar of aspirin when death or cerebral or retinal infarction and the occurrence of TIAs were grouped and considered together as end points. Significance in favor of aspirin treatment was mainly revealed in patients with a history of multiple TIAs and was most evident in those individuals having carotid lesions appropriate to the TIA symptoms. It cannot be inferred from this study that aspirin prevents stroke because when end points were restriced to death or cerebral or retinal infarction, there was no statistically significant differential between the aspirin and placebo treatments.
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PMID:Controlled trial of aspirin in cerebral ischemia. 32 36

Acetyl salicylic acid, sulfinpyrazone, dipyridamole, hydroxychloroquine, ticlopidine, clofibrate, nicergoline are the most used antiplatelet drugs. A. S. A. and sulfinpyrazone have been tested in several large scale clinical trials. A. S. A. seems beneficial in the prevention of cerebral ischemia for patients, specially men who have previously had a transient cerebral ischemic attack. Sulfinpyrazone appears to be effective in reducing cardiac deaths during the first year after myocardial infarction.
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PMID:[Antiplatelet drugs (author's transl)]. 52 34

Fifty-seven cases admitted to the Karolinska Hospital 1973-1976 with the diagnosis transient cerebral ischemia were reviewed. Seventeen cases were excluded as not fulfilling the strict TIA definition. An analysis of the records and the supplementary questionnaire of the remaining cases showed considerable sex differences in the stroke-prone profile. In the male group arteriosclerosis in the extracranial cerebral arteries was demonstrated in 90% of these examined by angiography. In the female group factors recognized as interfering with the coagulation system were obvious in more than 70% and two women had fibromuscular dysplasia. These differences may have therapeutic and prognostic implications. In the total material only 35% had hypertension. Diabetes was not present in any of the patients. Of the men 46.6% had abnormal blood lipids against 15.4% of the women. Seventy-five percent of the patients with verified arteriosclerosis were regular smokers. At a mean follow-up time of 18.7 months only one patient, in the untreated group, developed completed stroke.
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PMID:Pathogenetic profile of TIA before 55. A three-year investigation. 68 66

The clinical features of 102 cases with transient attacks due to cerebral ischemia were evaluated, and 94 out of 102 cases were followed for an average of 6 years. 1) The clinical study makes comparisons between two groups of patients grouped under the somewhat new definition of Reversible Ischemic Attacks (RIA): classical Transient Ischemic Attacks (TIA) and Stroke with Full Recovery (SFR), in which a complete recovery took place over a longer period, on the average 3 weeks. 2) SFR constitutes the 34.31% of the total cases with transient ischemic episodes. In the carotid district the onset was more frequently gradual in SFR than in TIA and aphasia more frequent in TIA than in SFR. Multiple attacks prevailed in TIA over the SFR group. The definition of transient attack due to ischemia is discussed. 3) Completed strokes occurred in 11 cases (11.7%) with RIA. Hypertension and cardiac disease were significantly frequent in cases with subsequent stroke. The conclusion was reached that TIA is a symptom, not a pathological state, and TIA should be considered an important symptom but not a specific harbinger of completed stroke.
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PMID:Clinical features and long-term follow-up of patients with reversible ischemic attacks (RIA). 69 35

Blood pressure and clinical status of 1,736 patients with cerebrovascular disease were observed during 12 months of treatment with nicardipine. The most common diagnoses were chronic cerebral ischemia (53.2%), transient ischemic attacks (TIA; 25.1%), and cerebral infarct (8.7%); 50.1% of patients were classed as hypertensive [systolic blood pressure (SBP) > or = 160 mm Hg or diastolic blood pressure (DBP) > or = 90 mm Hg]. Most patients (91.2%) received a daily dose of 60 mg nicardipine. Additional treatments included diuretics (37%), beta-blockers (11.5%), other antihypertensive drugs (15.8%), platelet antiaggregants (25.1%), and cardiotonic drugs (15.1%). A total of 282 patients (16.2%) were lost to follow-up, 21 (1.2%) patients withdrew due to side effects, 32 (1.8%) died, and 9 (0.5%) patients had treatment interrupted due to concomitant illness. In the hypertensive subgroup, blood pressure (SBP/DBP) was reduced from a mean baseline value of 175 +/- 22/97 +/- 14 mm Hg to 152 +/- 17/85 +/- 11 mm Hg at 3 months and 149 +/- 23/81 +/- 11 mm Hg after 12 months of treatment. The incidence of TIA or stroke among these patients was reduced from 29 cases (3.5%) during the first 3 months to 11 cases (1.54%) during months 4-12 (p < 0.01). In normotensive patients there were 18 (2.15%) cases during months 1-3 and 13 (1.55%) cases during months 4-12 (difference not significant). In the 280 patients treated with nicardipine alone, the most frequent side effects during the first month were facial flushing (6.8%), gastrointestinal problems (5%), dizziness (3.2%), headache (3.2%), drowsiness (3.2%), and hypotension (1.1%). Most of these side effects were transient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of nicardipine in patients with high risk of stroke. 136 3

In a retrospective study we analysed two groups each consisting of 100 consecutive patients of similar age and sex distribution who underwent surgery for carotid disease with an intervening period of 5 years (group A 1980/82, group B 1986/87) between the collectives. Against a background of changing indications, tactics and techniques the aim of the study was to detect any differences between the two groups. Group A had a higher proportion of coronary and peripheral vascular disease. The states of cerebral ischemia I, II and III were distributed equally, but state IV was seen more frequently in group B (p less than 0.05). The number of shunt/without shunt operations in group A was 97/2, in group B 10/84 (p less than 0.005). The external carotid artery was deobliterated in 58/81 cases group A versus group B (p less than 0.005). We closed the artery by direct suture in 8/31 (p less than 0.005), by autologous venous patch in 53/26 (p less than 0.005) and by Dacron patches in 39/41 patients. In group A the operative mortality was zero and in group B 1 patient died; one patient in group B developed sudden occlusion (with TIA) postoperatively. Transient intra-/postoperative neurological deficits occurred in 1/2, permanent in 4/2 patients (n.s.). 54/25 patients have died up to 31/08/91. Coronary heart disease was the main cause of late complications and deaths in group A (p less than 0.025). Statistically, there was no dependence of neurological deficits on group, sex, age or intraoperative management. Only patients with preoperative PRINDS hat a higher postoperative neurological deficit rate than the others.
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PMID:[Immediate and late results following endarterectomy of the carotid bifurcation]. 138 98

Arterio-arterial embolism of carotid origin is one major cause of cerebral ischemia. To evaluate the role of blood platelets in this process, In-111 labeled platelet scintigraphy was performed in a series of 250 patients. Of this number, one patient with an 80% carotid stenosis and a normal intracerebral angiogram suffered a transient ischemic attack (TIA) several hours after the injection of radiolabeled platelets. The scintigram showed a pathologic platelet accumulation in the symptomatic carotid area as well as in the ipsilateral brain hemisphere. The authors conclude that this scintigraphic finding of hemispheric platelet aggregates recorded directly after a clinically observed TIA, together with previous observations of retinal emboli after amaurosis fugax attacks, provides strong evidence for the arterio-arterial embolic mechanism of TIA.
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PMID:Intracerebral platelet accumulation as evidence for embolization of carotid origin. 139 46

To evaluate the prevalence and prognostic role of silent coronary artery disease (CAD) in patients with symptomatic high-grade carotid stenosis (70 to 99%) undergoing carotid endarterectomy, and with neither history nor symptoms of CAD, 106 patients (76 men, 30 women, mean age 58.7 years [range 42 to 71]) with recent cerebral ischemia were prospectively studied. Patients were stratified as to the presence (n = 27, 25%) or absence (n = 79, 75%) of silent CAD defined by concordant abnormal exercise electrocardiographic testing and thallium-201 myocardial scintigraphy. The male sex, the severity of the symptomatic carotid lesion (greater than 90%), and the coexistence of contralateral carotid disease identified patients with higher probability of coexisting CAD. The 106 patients underwent 121 operations (bilateral in 15). In the perioperative period, no deaths or cardiac events occurred, 1 patient suffered a recurrent stroke and 3 had a transient ischemic attack. During a mean follow-up period of 5.4 years, 9 patients died (1.7%/year): fatal myocardial infarction occurred in 5 (all in the silent CAD group), cancer in 3 and vertebrobasilar stroke in 1. Nonfatal events occurred in 9 patients: myocardial infarction in 1 (without silent CAD), unstable angina in 3 (with silent CAD), and cerebral ischemic attacks in 5. After 7 years, the Kaplan-Meier estimated survival free from coronary events was 51% in patients with silent CAD, and 98% in patients without CAD (p less than 0.01). In conclusion, among patients with symptomatic high-grade carotid stenosis undergoing carotid endarterectomy, even in absence of history or symptoms of CAD, a silent CAD is detectable in one fourth of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency and prognostic significance of silent coronary artery disease in patients with cerebral ischemia undergoing carotid endarterectomy. 843 Jun 60

1. We investigated the alterations in binding sites of three major second messengers, phorbol 12,13-dibutyrate, inositol 1,4,5-trisphosphate and forskolin following transient cerebral ischemia in gerbils, and examined the effects of a novel vinca alkaloid derivative, vinconate against the alterations in the binding of the second messengers following ischemia. 2. Transient cerebral ischemia produced by bilateral occlusion of the common carotid arteries was induced for 10 min, and intraperitoneal administration of vinconate (100 mg/kg and 300 mg/kg) was given 10 min before ischemia. 3. Morphological study indicated that transient ischemia can produce severe neuronal damage in striatum, hippocampal CA1 sector and hippocampal CA3 sector. 4. Transient cerebral ischemia caused the postischemic alterations in the binding of three second messengers. 5. The postischemic alterations in the binding of second messengers were ameliorated by pretreatment with vinconate. This effect was especially observed in the striatum which was most vulnerable to ischemia. 6. These findings are discussed in relation to the mechanism of ischemic neuronal damage.
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PMID:Protective effect of a novel vinca alkaloid derivative, vinconate, against alterations in binding sites of second messengers after transient cerebral ischemia in gerbils. 159 19

For vascular reconstruction in cases of atherosclerotic stenosis at the origin of the vertebral artery, we use vertebral to subclavian artery transposition. We discuss the advantages and effectiveness of such treatment based on a study of 32 cases. We have experienced neither surgical mortality nor morbidity and the outcome at the time of discharge has been favourable. Follow-up revealed no deaths, however, three cases exhibited symptoms of cerebral ischaemia. One had a supratentorial completed stroke, and the other two hat TIA or RIND, but without any notable lesion in the angiograms. There were no cases of cerebral infarction of the posterior fossa. We believe that this method should be the first choice for treatment of cases without lesions of the subclavian artery for the following reasons: serious operative complications have not been encountered, surgical invasion is minimal, temporary occlusion of the common carotid artery is unnecessary, the operation can be done by occluding only the vertebral artery, and unlike various bypass operations, anastomosis is required at only one location and is consequently technically uncomplicated. Following anastomosis the cerebral blood pathway is physiological.
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PMID:Treatment of proximal vertebral artery stenosis. Vertebral to subclavian transposition. 176 78


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