Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The importance of atrial fibrillation (AF) as a risk factor (RF) for cerebral infarction (CI) is well-known. It is probably caused by cardiac embolism but other explanations can also justify this association. Our aim was to analyse the features of the patients with CI and AF and sinus rhythm (SR), as well as to form hypotheses as regards the pathogenesis. 250 patients with CI, 204 in RS and 46 in AF (31 non-valvular and 15 associated to a valvular disease) were studied, analysing the prevalence of RF and initial blood tests. The group of patients with valvular AF of probably embolic mechanism had a minor prevalence of RF (hypertension, diabetes, smoking, alcoholism) but higher mortality. The group with non-valvular AF, had a lower RF prevalence compared to the SR group (non-embolic mechanism), without statistical significance and with a similar mortality rate. We concluded that the atherothrombotic mechanism can be the cause of a considerable proportion of CI in patients with non-valvular AF.
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PMID:[Atrial fibrillation and cerebral infarct]. 191 88

We investigated the anticardiolipin antibody (ACA) in a series of patients with cerebral infarction without systemic lupus erythematosus (SLA). Clinical and laboratory data were assessed from a series of 250 non-SLE patients with cerebral infarction who visited our clinic from 1988 to 1990. The concentration of anticardiolipin IgG antibody was measured by an enzyme-linked immunosorbent assay technique. An elevated ACA level was defined as one which was greater than 3 standard deviations above the mean level for normal controls. We examined the CT findings and risk factors for stroke such as hypertension, diabetes mellitus, hyperlipidemia and cardiac disease. Laboratory data such as the platelet count, the presence of lupus anticoagulant and a biologic false-positive test for syphilis were also investigated. Among the 250 patients with infarction, IgG ACA was detected in 22 (8.8%). There was no significant difference in incidence of ACA between the patients with cerebral thrombosis and those with cerebral embolism. On CT scan, multiple cerebral infarcts were noted in 18 of the 22 patients. As regards the location of the infarct, the cerebral cortex together with the basal ganglia was more common than isolated lesions of the cortex or basal ganglia. Concerning the risk factors for stroke, hypertension was noted in 12, diabetes mellitus in 2, hyperlipidemia in 2 and cardiac disease in 2. Lupus anticoagulant and thrombocytopenia were not detected in any of the cases. A biologic false-positive test for syphilis was observed in one case. Dementia was present in 12 of the 22 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anticardiolipin antibody in cerebral infarction]. 191 23

A 44-year-old woman with a history of cerebral infarction and hypertension developed sudden onset of speech and visual disturbance. On admission, her general physical examinations showed high blood pressure of 210/120 mmHg and Raynaud's phenomena. The neurological examinations revealed right upper quadratic hemianopsia, left oculomotor nerve paresis and left hyperreflexia. Laboratory findings showed that antinuclear and anti-DNA antibodies were positive. The activity of Fletcher factor was reduced to 50%, and the activated partial thromboplastin time (APTT) was prolonged to 82.6 seconds. And a 1:1 dilution with normal plasma failed to correct the prolonged APTT, indicative of circulating anticoagulant to Fletcher factor. Plasma fibrinogen increased to 500 mg/dl but FDP was normal. The CT scan demonstrated the recurrently developed cerebral infarction in the left occipital lobe. Cerebral angiogram revealed mild atherosclerosis of basilar and bilateral posterior cerebral arteries, but any occlusive lesions were not found. Although she had a history of hypertension, this case suggests the possibility that the disturbance in fibrinolytic system may have been caused by the circulating anticoagulant to Fletcher factor, and contributed to her cerebral infarctions.
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PMID:[A case of cerebral infarction with circulating anticoagulant to Fletcher factor]. 191 33

We studied the pattern and outcome of strokes in 200 Saudi patients. Cerebral infarction constituted 87% of strokes, subarachnoid hemorrhage 4.5%, cerebral hemorrhage 6.5%, and venous infarction 2%. The vessel most commonly involved was part or all of the middle cerebral artery, constituting 52% (90) of the 174 arterial infarcts. Lacunar infarcts were seen in 21% (37) of the patients with arterial infarcts. Among all 200 patients, 8% died and 8% had secondary generalized seizures. Hypertension occurred in 41% of the 174 patients with arterial infarcts and 62% of the 13 with cerebral hemorrhages. The highest incidence of hypertension as a risk factor was among those with lacunar infarcts (81%), ganglionic cerebral hemorrhages (80%), and infarcts of deep branches of the middle cerebral artery (57%). Embolic infarcts due to rheumatic heart disease constituted 11% of all arterial infarcts. We conclude that our pattern of strokes is similar to that of the west rather than that of the Japanese, but with less frequent arteriovenous malformations and aneurysms.
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PMID:Cerebrovascular disease in Saudi Arabia. 192 60

We prospectively studied clinical and computed tomographic (CT) scan findings in 79 patients with a transient ischemic attack (TIA) and a relevant cerebral infarction on CT, also known as cerebral infarction with transient signs (CITS). We compared the results with those of 527 concurrent patients with TIA and without cerebral infarction and also with 646 patients with persistent neurological symptoms and a relevant infarct on CT. All patients were participating in a multicenter trial. In both groups, most infarcts were of the lacunar type. Compared with TIAs without cerebral infarction, patients with CITS slightly more often had a history of hypertension (52% vs 33%), the attacks lasted longer (greater than 1 hour, 52% vs 34%) and disappeared more slowly (over the course of hours, 39% vs 24%), and the symptoms more frequently involved speech (61% vs 41%). Despite these small differences, the reverse--the prediction of evidence on CT of infarction on the basis of the nature or time course of symptoms--proved impossible, since in each category the majority of patients had a normal CT scan. In comparison with patients with stroke and visible infarction, patients with CITS slightly more often had abnormal speech (61% vs 45%) and had a larger number of attacks (multiple attacks, 46% vs 18%). In conclusion, we found only minor clinical differences between patients with TIA with or without a relevant infarct on CT and equally small differences between patients with CITS and patients with stroke and cerebral infarction. These clinical similarities do not exclude a difference in prognosis.
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PMID:Transient ischemic attacks with and without a relevant infarct on computed tomographic scans cannot be distinguished clinically. Dutch Transient Ischemic Attack Study Group. 195 15

A prospective series of 265 patients with aneurysmal subarachnoid hemorrhage (SAH) of Grades I to III (Hunt and Hess classification) upon admission were evaluated as to neurological outcome and computerized tomography (CT) findings 1 to 3 years (mean 1.4 years) after the SAH and surgery. A total of 73 patients underwent acute surgery (within 72 hours after the bleed: Days 0 to 3), 86 were operated on subacutely (between Days 4 and 7), and 91 had late surgery (on Day 8 or later). Fifteen patients died before surgery was undertaken and another 20 patients died during the follow-up period. A total of 104 patients received nimodipine and the rest of the patients received either placebo (109 patients) or no medication (52 patients). A logistical regression analysis revealed the following prognostic factors for cerebral infarction, in order of importance: the amount of blood on the primary CT scan; postoperative angiographic vasospasm; the timing of the operation; and a history of hypertension. The use of nimodipine was associated with a significant reduction of cerebral infarcts visualized by CT scanning in patients who received intermediate or late surgery. In patients who underwent acute surgery no significant difference between the incidence of cerebral infarcts was observed.
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PMID:Risks factors for cerebral infarction in good-grade patients after aneurysmal subarachnoid hemorrhage and surgery: a prospective study. 186 62

To determine the prevalence, demographics and morbidity of vein patch rupture, the authors polled members of the Western Vascular Society. Forty-eight surgeons (53% of the members) reported an experience with 23,873 carotid operations. A vein patch was used in 1,760 operations (7.4%), and rupture of the patch occurred in 13 patients (0.7%), 10 women and three men. Indications for the patch were a small artery in 10 patients and restenosis in three. Saphenous vein was used for all patches and was harvested from the ankle in 12 patients and from the groin in one patient. All ruptures occurred from a split in the vein patch. Hypertension was present in seven of the 13 patients. None of the ruptures were associated with infection. Two ruptures occurred on the first postoperative day, six on the second day, three on the third day, one on the eighth day, and one on the twenty-first day. Four patients died: airway obstruction (1), hemorrhagic cerebral infarction (1), and myocardial infarction (2) were the causes. Three had a stroke and survived, one had a retinal embolus, and five underwent reoperation without complication. Vein patch of the carotid artery is used infrequently by members of the Western Vascular Society. The incidence of rupture of the patch is low (0.7%), but when it occurs, there is significant mortality (30.7%), and morbidity (30.7%). Patients with a vein patch should be observed in the hospital for three days after endarterectomy because rupture demands immediate reoperation.
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PMID:Vein patch rupture after carotid endarterectomy: a survey of the Western Vascular Society members. 199 80

Lacunar stroke was diagnosed in 337 (26%) of the 1,273 patients with cerebral infarction among the 1,805 total in the Stroke Data Bank. We analyzed the 316 patients with classic lacunar syndromes. Among these, 181 (57%) had pure motor hemiparesis, 63 (20%) sensorimotor syndrome, 33 (10%) ataxic hemiparesis, 21 (7%) pure sensory syndrome, and 18 (6%) dysarthria-clumsy hand syndrome. No striking differences were found among the risk factors for the lacunar subtypes, but differences were found between lacunar stroke as a group and other types of infarcts. Compared to 113 patients with large-vessel atherosclerotic infarction, those with lacunar stroke had fewer previous transient ischemic attacks and strokes. Compared to 246 with cardioembolic infarction, patients with lacunar stroke more frequently had hypertension and diabetes and less frequently had cardiac disease. We found a lesion in 35% of the lacunar stroke patients' computed tomograms, with most lesions located in the internal capsule and corona radiata. The mean infarct volume was greater in patients with pure motor hemiparesis or sensorimotor syndrome than in those with the other lacunar stroke subtypes. In patients with pure motor hemiparesis and infarcts in the posterior limb of the internal capsule, there was a correlation between lesion volume and hemiparesis severity except for the few whose infarct involved the lowest portion of the internal capsule; in these patients severe deficits occurred regardless of lesion volume. Taken together, the computed tomographic correlations with the syndromes of hemiparesis showed only slight support for the classical view of a homunculus in the internal capsule.
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PMID:Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank. 200 81

The records of 36 patients (37 eyes) with central retinal artery occlusion (CRAO, 19 patients, 19 eyes), branch retinal artery occlusion (BRAO, 15 patients, 16 eyes), and cilioretinal artery occlusion (CIAO, 2 patients, 2 eyes) were reviewed with respect to underlying systemic disorders. Hypertension was the most common disorder (58%). Half of the patients had cardiovascular disorders including ischemic heart disease, valvular disease, atrial fibrillation, internal carotid artery obstruction, and atrial myxoma. Seventeen percent of the patients had diabetes mellitus, and 8% had hyperlipemia. Cerebral infarction was detected in a quarter of the patients. The incidence of the disease was one CRAO patient per 1,000 outpatients. Age distribution showed a peak in the seventh decade. Men were twice more frequently affected than women. Right eyes were more commonly involved.
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PMID:[Retinal arterial obstruction and systemic disorders]. 204 31

A consecutive series of 145 patients with acute aneurysmal subarachnoid hemorrhage (SAH) were operated on within 7 days of SAH and were prospectively evaluated over a 4-year period to determine if the timing of aneurysm surgery influenced the development of delayed cerebral ischemia. All patients were managed with a standardized policy of urgent surgical clipping and treatment with aggressive prophylactic postoperative volume expansion. Patients with delayed ischemic symptoms were additionally treated with induced hypertension. Forty-nine patients underwent surgery on Day 0 or 1 (Group 1) post-SAH, 60 patients on Day 2 or 3 (Group 2), and 36 patients on Days 4 through 7 (Group 3). Postoperative delayed cerebral ischemia developed in 16% of (Group 1) patients, in 22% of Group 2 patients, and in 28% of Group 3 patients. Cerebral infarction resulting from delayed cerebral ischemia developed in only 4% of Group 1 patients, 10% of Group 2 patients, and 11% of Group 3 patients. A bad clinical outcome as a result of delayed cerebral ischemia occurred in one Group 1 patient (2%), two Group 2 patients (3%), and one Group 3 patient (3%). Preoperative grade was not significantly correlated with the incidence or severity of delayed cerebral ischemia at any time interval except that patients in modified Hunt and Hess Grade I or II who underwent surgery on Day 0 or 1 after SAH had no strokes or bad outcomes from delayed cerebral ischemia. This study demonstrates that there is no rationale for delaying aneurysm surgery based on the time interval between SAH and patient evaluation.
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PMID:Relationship between the timing of aneurysm surgery and the development of delayed cerebral ischemia. 204 19


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