Stroke; a journal of cerebral circulation
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The goal of this study was to analyze the association of hemorrhagic presentation with infratentorial brain arteriovenous malformations (AVMs). ⋯ Our findings suggest that infratentorial AVM location is independently associated with hemorrhagic AVM presentation.
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Clinical Trial
Electrocardiographic abnormalities and serum magnesium in patients with subarachnoid hemorrhage.
ECG abnormalities and hypomagnesemia frequently occur after aneurysmal subarachnoid hemorrhage (SAH). Because hypomagnesemia is associated with several ECG abnormalities, we studied whether hypomagnesemia mediates ECG abnormalities after SAH. ⋯ In patients with SAH, lower serum magnesium levels are related to less pronounced increase in the QTc interval. Although the direction of the relation was unexpected, decreased serum magnesium might be the missing link between SAH and ECG abnormalities.
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Successful acute stroke intervention depends on early hospital presentation. Our study aimed to examine the extent of and factors associated with prehospital delays after acute stroke in Taiwan, where people are new to thrombolytic therapy for stroke. ⋯ The time interval between symptom onset and the decision to call for medical care is far from optimal and is the underlying cause of prolonged prehospital delay. Educational efforts to reduce extent of delay are urgently needed.
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Microvascular basal lamina damage occurs after cerebral ischemia and is important for the development of hemorrhage. The aim of this study was to determine whether hypothermia could maintain microvascular integrity in ischemic stroke. ⋯ Hypothermia maintains microvascular integrity and reduces hemorrhage and the activities of MMP-2, MMP-9, uPA, and tPA.
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Subarachnoid hemorrhage (SAH) frequently results in myocardial necrosis with release of cardiac enzymes. Historically, this necrosis has been attributed to coronary artery disease, coronary vasospasm, or oxygen supply-demand mismatch. Experimental evidence, however, indicates that excessive release of norepinephrine from the myocardial sympathetic nerves is the most likely cause. We hypothesized that myocardial necrosis after SAH is a neurally mediated process that is dependent on the severity of neurological injury. ⋯ The degree of neurological injury as measured by the Hunt-Hess grade is a strong, independent predictor of myocardial necrosis after SAH. This finding supports the hypothesis that cardiac injury after SAH is a neurally mediated process.