Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Semicarbazide-sensitive amine oxidase (SSAO) has been suggested to be involved in the development of vascular endothelial damage. The source of the soluble form of SSAO found in the blood serum is unknown. However, it has been speculated that it is secreted from cells within the vascular wall where high activity of the enzyme is found. Altered SSAO activity has been reported in atherosclerotic plaques of the human aorta. Stroke is a manifestation of long-term atherosclerotic disease, and in this study, plasma SSAO activities were estimated in 42 patients with cerebral thrombosis and 26 patients with cerebral embolism, and compared to two control groups of 45 individuals in total. No statistically significant differences were found between the patient groups and controls regarding plasma SSAO activity, suggesting that changes in the soluble form of SSAO found in the circulation do not play a major role in this type of acute cerebrovascular event. Furthermore, it does not seem likely that the involvement of vascular tissue occurring in stroke results in release of the enzyme into the circulation. Nevertheless, further studies on tissue-bound SSAO in cerebral vessels would be of great interest.
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PMID:Plasma semicarbazide-sensitive amine oxidase in stroke. 988 24

To clarify the relationship between long-term prognosis of patients with stroke and their MRI findings, 103 patients with initial cerebral thrombosis, who survived more than three months after the ictus, were studied for five years. The mean age of 98 patients (T group), who were followed up completely, was 73.1 years-old and 65 were men. The age-matched controls consisted of two groups: 65 subjects, who had hypertension and/or diabetes without a history of stroke (R group), and 85 subjects, who had any hypertension, diabetes and stroke (N group). MRI findings were divided into six categories: 1) types of causative lesion, 2) grades of periventricular hyperintensity (none, rims/caps, patchy, diffuse PVH), 3) number of spotty lesions, 4) presence of silent infarction. 5) ventricular dilatation, and 6) extents of brain atrophy. Types of causative lesion were subdivided into 3 subtypes; infarction of the perforating artery territory (P type), infarction of the cortical artery territory (C type), and brainstem infarction (B type). The presence of vascular risks and dementia, and the extent of activity of daily living (ADL) were assessed. The P, C, and B types were identified by MRI in 46, 36, and 16 of the T group, respectively. Motor impairment, dementia, and an ADL status of complete dependence at discharge were also seen in 84, 44, and 22, respectively. In the T group, 33 patients died during five years, which resulted in a cumulative mortality rate of 33.7% and an annual mortality rate of 8.2%. Based on log-rank analysis, the survival rate of the T group revealed was significantly lower than those of the R and N groups. The recurrent rate in the T group (annual stroke recurrence rate was 4.0%) was higher than in the R and N groups, but stroke recurrence was not the cause of death and two thirds of deaths were due to aspiration pneumonia and/or asphyxia. Cox hazard regression analysis for death due to respiratory diseases showed that the hazard ratios of infarction, patchy PVH, and more than 4 spotty lesions were 8.87 (p < .001), 0.31 (p = .058), and 0.44 (p = .098), respectively. Compared to the survival group, rates of complete dependence in ADL, dementia, and brain atrophy were significantly higher in the death group with low incidences of the P type and patchy PVH, which indicated small vessel disease. These findings suggested that in patients with cerebral thrombosis, even in the chronic phase, care should be taken to prevent pneumonia and/or asphyxia due to bulbar palsy. Furthermore, no MRI findings were distinct predictors of long-term prognosis, although infarction based on the small vessel disease had rather good outcome in terms of respiratory disease.
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PMID:[Long-term prognosis of patients with initial cerebral thrombosis and the MRI findings]. 1036 31

Ischaemic stroke accounts for 70-85% of stroke incidence worldwide, causing substantial morbidity and mortality. Antiplatelet agents and carotid endarterectomy are effective in stroke prevention but active therapy for acute stroke is limited at present. Treatments investigated to date include thrombolysis and antiplatelet agents, both of which have been shown to modify the effects of stroke and provide a small long-term benefit in selected patients, and anticoagulation with heparin derivatives and oral agents. The value of unfractionated heparin (UFH) in modifying the acute effects of stroke has never been clearly established, and the risk of intracranial bleeding has limited its clinical application. However, disability and death following stroke stem from both the acute cerebral event and the secondary development of venous thromboembolism (VTE). Antithrombotic therapy may therefore, in principle, provide the dual benefit of retarding ongoing cerebral thrombosis and preventing secondary VTE. Low-molecular-weight heparins (LMWHs) and one heparinoid may have an improved ratio of antithrombotic action to haemorrhagic effect compared with UFH. Recent trials with these agents demonstrated a significant reduction in deep vein thrombosis and pulmonary embolism. Evidence has also emerged of improved long-term outcomes in terms of combined rates of death and residual disability, but data from different studies are conflicting. The potential role of LMWHs and heparinoids in acute stroke remains to be clarified.
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PMID:Anticoagulation in acute ischaemic stroke: deep vein thrombosis prevention and long-term stroke outcomes. 1049 41

Adherence of erythrocytes to human umbilical vein endothelial cells (HUVEC) in patients with cerebral thrombosis and transient ischemic attack (TIA) were quantitatively studied in the flow chamber system, compared with that in healthy subjects. We found: (a) The adherence of erythrocytes to HUVEC in patients with cerebral thrombosis and TIA increased, compared with that in healthy subjects; (b) The adhesion of erythrocytes to HUVEC in patients with TIA was not significantly different from that of patients with cerebral thrombosis. These suggested that the increased adhesion of erythrocytes to endothelial cells might play an important role in the pathologic process of ischemic stroke.
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PMID:[Properties of adherence of erythrocytes to endothelial cells in patients with ischemic stroke]. 1068 33

This study sought to understand the mechanism for the increased adhesion of leucocytes and endothelial cells in ischemic stroke. 20 patients with acute cerebral thrombosis and 20 healthy subjects as controls for expression of CD11a and CD11b (adhesion molecules on surface of leucocytes) were tested in vitro by flow cytometry (FCM) method. The results showed that compared with the control group, the patient group had significantly higher rates for expression of CD11a on monocytes, granulocytes and lymphocytes (P < 0.05). The CD11b expression in the patient group was positively elevated on monocytes and granulocytes (P < 0.05), but it was of lower positive rate on lymphocytes and no statistical difference was noted between the patient and control groups. These indicate that the expression of CD11a and CD11b on leucocytes increases in cerebral ischemic damage; thus adhesion of leucocytes and endothelial cells obviously increases. This change may aggravate post-ischemic delayed neuronal death.
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PMID:[The expression of CD11a and CD11b on leucocytes in cerebral thrombosis]. 1074 41

This study was conducted to clarify the relationship between long-term prognosis of functional status after stroke and the magnetic resonance imaging (MRI) findings as well as complications in the course. A total of 98 patients with initial cerebral thrombosis were enrolled, and 65 patients surviving 5 years after the event, were studied in terms of cognitive function and activity of daily living (ADL). Mean age at registration (3 months after the event) was 72.0 years-old and 44 were male. MRI findings were divided into eight categories including the size and laterality of infarction, in addition to six categories as previously described. The presence of dementia was identified according to the HDS-R and the DSM-III-R scales, and the extent of dementia, assessed with the CDR scale, was divided into 3 grades: none, mild, and severe. The extent of ADL status was also graded into 3 classes: independent, partially dependent, and completely dependent. Recurrence of stroke, pneumonia, and motor disorders (hip joint fracture) were counted as complications during the course. At baseline, dementia was identified in 44, consisting of 30 mild and 14 severe dementias. During 5 years, 11 cases with mild dementia showed deterioration, and 1 case without dementia developed mild dementia. At registration, there were 46 cases with partially dependent ADL status and 22 cases completely dependent, while deterioration of ADL was seen in 17 during 5 years. Multiple regression analyses showed that diffuse PVH and pneumonia were contributory factors to the development of dementia, while dementia, pneumonia and motor disorders were risk factors for deterioration of ADL. These findings suggested that in patients with cerebral thrombosis, especially in patients with diffuse PVH, pneumonia and motor disorders should be taken care of in order to prevent functional decline.
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PMID:[Dementia and disability after initial cerebral thrombosis evaluated by MRI and their clinical course]. 1079 60

Inhibitors of angiotensin converting enzyme (ACE) have been developed recently for therapeutic purposes in hypertension and ischemic cardiovascular diseases. Ogiku et al. reported that one such inhibitor, imidapril, significantly prolonged survival in stroke-prone spontaneously hypertensive rats (SHRSP). The present study was designed to investigate the effect of imidapril on cerebral blood vessels in SHRSP to clarify role of the ACE inhibitor in mechanisms of cerebral thrombosis and stroke. Imidapril was administered orally at 1.0 and 5.0 mg/kg/day for 3 weeks from the age of 7 weeks, and was shown to prevent the usual increase in blood pressure seen in these animals. It also delayed He-Ne laser-induced cerebral thrombosis and increased significantly the plasma concentration of nitric oxide metabolites (NO2/NO3). To confirm the association between nitric oxide (NO) and these effects of imidapril, an inhibitor of nitric oxide synthase, N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) was dissolved in drinking water and administered to the animals for 3 weeks. Four of six rats died from stroke when L-NAME was given alone. When imidapril (5.0 mg/kg/day) was administered with L-NAME, however, the animals showed no signs or symptoms of stroke. In these instances, therefore, the concurrent administration of L-NAME with imidapril reversed significantly the effects of imidapril. Intravenous injection of imidaprilat (100 microg/kg), an active metabolite of imidapril, also decreased blood pressure significantly and increased the plasma levels of NO2/NO3 after 5 min. Moreover, imidaprilat enlarged arteriolar diameters and caused an increase in red cell velocity and mean blood flow in pial arterioles after 15 min. The results strongly suggested that imidapril protects cerebral vessels in SHRSP by elevating the release of NO, thereby improving the cerebral circulation and reducing the tendency to thrombosis and stroke.
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PMID:Protective effects of imidapril on He-Ne laser-induced thrombosis in cerebral blood vessels of stroke-prone spontaneously hypertensive rats. 1082 69

The association between apolipoprotein E (apoE) genetic polymorphism and stroke has not been concordant in different racial populations. We investigated the association between apoE genotypes and stroke subtypes by a case-control study in Bangladesh for the first time among south Asian countries. First-ever-stroke patients (n=227; cerebral infarction, n=147, cerebral hemorrhage, n=80) and 190 controls were recruited from a hospital in Dhaka, Bangladesh. The diagnosis of stroke was based on CT and clinical findings. Cerebral infarction was classified anatomically into cortical and penetrating region. Infarction in the cortical region was further categorized etiologically into thrombosis and embolism. Cerebral hemorrhage was considered as a whole in all analyses. ApoE genotypes were determined by restriction fragment length polymorphism. In the multivariate conditional logistic regression analysis adjusted for potential confounders both the epsilon3/epsilon4 genotype and epsilon4 carrier conferred an approximately 3-fold increased risk for cerebral thrombosis in the cortical artery region (OR 3.5, 95% CI 1.2 to 10.4 and OR 3.1, 95% Cl 1.1 to 9.0, respectively) compared with epsilon3/epsilon3 genotype. However, when the analysis was restricted to the elderly (>60 years), epsilon 2 carrier was associated with a risk of hemorrhagic stroke (OR 19.2, 95% CI 1.3 to 295.2). Our study suggested that both apoE epsilon3/epsilon4 genotype and epsilon4 carriers were risk factors for cerebral thrombosis in cortical artery region, whereas epsilon 2 carrier was a risk factor for hemorrhagic stroke in the elderly.
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PMID:Apolipoprotein E genetic polymorphism and stroke subtypes in a Bangladeshi hospital-based study. 1143 25

Antithrombotic therapy for the acute stage of cerebral infarction consists of thrombolysis, anticoagulant therapy and antiplatelet therapy, and their indications depend on the clinicopathological type of lesion, time after onset, and severity of illness. Tissue plasminogen activator has been approved in the United States for use in cerebral infarction within 3 hours after onset. The usefulness of heparin as anticoagulant therapy at the acute stage of cerebral infarction was not proved by the International Stroke Trial due to hemorrhagic complication. A selective thrombin inhibitor (argatroban) is used in Japan for atherothrombotic cerebral infarction within 48 hours after onset. A selective thromboxane A2 synthetase inhibitor (sodium ozagrel) had been approved for cerebral thrombosis within 5 days after onset. Aspirin (160-300 mg/day) is effective, but slightly, in the acute stage of cerebral infarction by the International Stroke Trial and Chinese Acute Stroke Trial. To prevent recurrence of stroke in the chronic stage of cerebral infarction, antiplatelet therapy (with aspirin or ticlopidine) is used for atherothrombotic cerebral infarction, and anticoagulant therapy with warfarin for cardioembolic cerebral infarction.
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PMID:[Antithrombotic therapy in cerebral infarction]. 1146 70

Argatroban, a direct thrombin inhibitor derived from arginine, is an effective anticoagulant indicated for prophylaxis or treatment of thrombosis in patients with heparin-induced thrombocytopenia (HIT). Argatroban has been used as an alternative anticoagulant in patients with HIT in various clinical conditions including interventional cardiovascular procedures that require anticoagulation. Satisfactory clinical outcomes with acceptable complications have been reported in these patients. Whether argatroban offers additional clinical advantage over conventional heparin therapy in patients without HIT remains unclear. Argatroban has been evaluated as an alternative anticoagulant to replace heparin in various clinical studies, especially in patients with coronary artery disease or cerebral vascular disease. To date, it remains unclear if argatroban is more effective than heparin, although the agent seems to cause less bleeding complications. This article reviews the pharmacology of argatroban and its clinical application beyond the management of HIT, with particular emphasis on interventional cardiology procedure, acute myocardial infarction, unstable angina pectoris, cerebral thrombosis or ischemic stroke, peripheral obstructive arterial disease, and extracorporeal circulation.
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PMID:Argatroban: a direct thrombin inhibitor for heparin-induced thrombocytopenia and other clinical applications. 1197 90


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