Stroke; a journal of cerebral circulation
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Few studies have assessed the overall importance of genetic factors on stroke risk, and the results have been contradictory. We used a large, population-based twin register and nationwide registries of death and hospitalization with long-term follow-up to estimate the effect of genetic factors on the risk of stroke. ⋯ The observed increased risk of stroke death and stroke hospitalization in monozygotic compared with dizygotic co-twins suggests that genetic factors increase the risk of stroke and that the size of this effect is moderate.
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Multicenter Study Comparative Study
Characteristics of brain arteriovenous malformations with coexisting aneurysms: a comparison of two referral centers.
Patients harboring a brain arteriovenous malformation (BAVM) often have coexisting arterial aneurysms. Experts have argued about the clinical significance of these aneurysms, which may be important for risk stratification in patient management and clinical trials. We studied the association between coexisting aneurysms and initial presentation with intracranial hemorrhage (ICH) in patients with BAVM evaluated at two tertiary-care centers. ⋯ Although many BAVM characteristics were similar at the referral centers studied, the association between initial presentation with ICH and coexisting aneurysms was not. This heterogeneity between populations undermines the validity of inferences on the role of aneurysms from any single referral series, and emphasizes the complexity in creating BAVM risk-stratification models that incorporate aneurysms.
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Potassium channels or nitric oxide or both are major mediators of acidosis-induced dilation in the cerebral circulation. However, these contributions depend on a variety of factors such as species and vessel location. The present study was designed to clarify whether potassium channels and endothelial nitric oxide are involved in acidosis-induced dilation of isolated rat cerebral arterioles. ⋯ Endothelial nitric oxide and smooth muscle ATP-sensitive potassium channels contribute to acidosis-induced dilation of rat cerebral arterioles. Endothelial damage caused by pathological conditions such as subarachnoid hemorrhage or traumatic brain injury may contribute to reduced blood flow despite injury-induced cerebral acidosis.
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Thrombolytic therapy with tissue plasminogen activator (tPA) for acute ischemic stroke remains complicated by risks of hemorrhagic transformation. In this study we used a previously established quantitative rat model of tPA-associated hemorrhage to test the hypothesis that matrix metalloproteinases (MMPs) are involved. ⋯ These results indicate that (1) tPA treatment increases levels of MMP-9 after embolic focal cerebral ischemia, (2) MMPs are involved in the mechanism of tPA-associated hemorrhage, and (3) combination therapies with MMP inhibitors may be useful for decreasing the risk and severity of this dreaded complication of thrombolytic therapy.