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myocardial stunning/edema

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Pulmonary Edema and Stunned Myocardium in Subarachnoid Hemorrhage

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Aneurysmal subarachnoid hemorrhage is a life-threatening event that can cause permanent disability. This life-threatening event can be further complicated by subsequent cardiac and pulmonary disability. The presence of a neurogenic cardiomyopathy and pulmonary edema increases the morbidity and

Isolated Pulmonary Edema without Myocardial Stunning in Brainstem Strokes.

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BACKGROUND Ischemic stroke has been associated with stunned myocardium and neurogenic pulmonary edema (NPE). We studied a population of patients with large vessel brainstem ischemic stroke to see if there was an increased risk of pulmonary edema associated with strokes in this region independent of
This study tested the hypothesis that preventing neutrophil adhesion during reperfusion, by blocking either the neutrophil membrane CD18 integrin complex or its endothelial and myocyte ligand, intercellular adhesion molecule-1 (ICAM-1), would reduce myocardial inflammation and edema and improve
Transfusion-related acute lung injury (TRALI) is a frequently under-diagnosed, although potentially fatal, condition that represents a leading cause of transfusion-related morbidity and mortality even in pediatric patients. Its main clinical features are characterized by rapidly evolving respiratory
Neurogenic pulmonary edema (NPE) and neurogenic stunned myocardium are known complications of acute neuropathology, but these conditions have only rarely been reported with ventriculoperitoneal shunt malfunction. Furthermore, shunt malfunction presenting with NPE has not been described in a
Neurogenic stunned myocardium (NSM) is syndrome of myocardial dysfunction following an acute neurological insult. We report a case of NSM that occurred intraoperatively in a pediatric patient undergoing endoscopic fenestration and shunt revision. Accidental outflow occlusion of irrigation fluid and
Neurogenic stunned myocardium is a significant complication of subarachnoid hemorrhage. Diagnosis of neurogenic stunned myocardium is complicated by variable presentation. We present a case of a 23-year-old woman admitted with a subarachnoid hemorrhage from an arteriovenous malformation and
A case of transiently increased wall thickness in the left ventricular apex after stunned myocardium due to severe attack of vasospastic angina is described. "Ace of spades" configuration, documented by left ventriculogram and increased apical wall thickness of the left ventricle, as revealed by

Neurogenic stunned myocardium and cardiac transplantation: a case report.

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We present the case of a 46-year-old woman referred to our center for urgent heart transplantation assessment, initially diagnosed as having cardiogenic shock of uncertain etiology. Some hours before she had suffered syncope without regaining consciousness. When she arrived at our hospital, the

[Neurogenic stunned myocardium].

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The existence of stunned myocardium and reversible myocardial dysfunction is widely described and accepted in patients suffering ischemic heart disease. However, it cannot be exclusive to coronary disease. Classically, the appearance of electrocardiographic changes in the critical neurological
Prominent T-wave inversions are well recognized electrocardiographic signs that can occur in acute myocardial infarction (AMI). However, the giant negative T waves may be associated with myocardial stunning without AMI.This case report describes 2 patients without AMI who developed rare giant T-wave

Pulmonary edema in near hanging.

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OBJECTIVE To study the incidence and outcome of pulmonary edema in patients admitted with near hanging. METHODS A retrospective analysis of 19 cases of near hanging admitted in our Emergency Department between January 2007 and December 2010 was performed. Occurrence of pulmonary edema;
Myocardial stunning represent a consequence of brief ischemia with reversible regional contractile dysfunction dependent persist from minute to days after reperfusion, despite the absence of irreversible damage and restoration of coronary blood flow. The evolution of these new ischemic entity were
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