myocardial stunning/stroke

The so-called stunned myocardium, defined as transitory myocardial contractile dysfunction, has been clearly demonstrated in diverse clinical situations. However, stunned myocardium related to ischemic stroke has been poorly identified. We describe two patients with diagnosis of acute ischemic

A 44-year-old woman with a history of complicated type 2 diabetes mellitus presented with a diagnosis of right-hemispheric ischaemic stroke. She developed acute respiratory distress with radiological evidence of pulmonary oedema. The ECG showed poorly significant ST-segment changes, with a minimal

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

Neuromediated stunned myocardium is a well-known complication of subarachnoid hemorrhage but has rarely been reported in association with other central nervous system disorders. The pathophysiology of this entity remains unclear, but a catecholamine-induced neurocardiogenic injury has been proposed

Neurogenic stunned myocardium (NSM) after subarachnoid hemorrhage (SAH) is well known, but there is a paucity of data regarding its occurrence following acute stroke. The aim of this study is to investigate the clinical characteristics of NSM in acute non-hemorrhagic stroke. We performed an

UNASSIGNED The diagnosis of stress cardiomyopathy is often made during coronary angiography. At this point hemodynamic parameters should be assessed; a right heart catheterization with measurement of cardiac output by Fick and thermodilution methods is helpful. Patients with acute neurologic

In vitro studies suggest that interventions targeted at myocardial gene regulation of endogenous cytoprotective elements, such as heat-shock protein, may attenuate myocardial ischemic injury. We tested the hypothesis that heat shock-induced expression of myocardial heat-shock protein before ischemia

Takotsubo cardiomyopathy has been described as a consequence of stroke or a cardioembolic source of stroke. We present the case of a 43 year-old woman who suffered from Takotsubo cardiomyopathy and subsequently developed a large left cerebellar infarct without significant neurological deficits nor

BACKGROUND Preconditioning has been shown to reduce myocardial stunning after reversible global ischemia. To determine whether preconditioning improves functional recovery after cardiac transplantation, 16 sheep were randomly assigned to a preconditioning protocol or to a control

BACKGROUND Inhibition of the sodium-hydrogen exchanger isoform 1 with HOE-642 (cariporide) has been shown to protect against ischemia-reperfusion injury and to decrease myocardial cell death in numerous animal preparations; however the effects of cariporide in stunned myocardium are not as well

Myocardial stunning has been poorly described in patients with cerebrovascular accidents. We present a patient in whom severe anteroapical wall motion abnormalities and extensive anterior ST-segment elevation developed after subarachnoid hemorrhage. Total recovery ensued within 2 days. Coronary

When activated neutrophils are recruited and bind to endothelial tissues, they release leukotrienes, proteolytic enzymes, and free radicals. The latter has been implicated in myocardial stunning following periods of ischemia and reperfusion, as may occur following cardiopulmonary bypass (CPB). The

Takotsubo cardiomyopathy is a phenomenon of transient acute left ventricular dysfunction without obstructive coronary disease seen predominantly in postmenopausal women in the setting of acute emotional or physical stress. Neurocardiogenic injury from acute neurologic events such as intracranial

BACKGROUND Neurogenic stunned myocardium (NSM) is a frequent complication of aneurysmal subarachnoid hemorrhage (aSAH), with a significant impact on disease course. The presumed cause is catecholamine surge at the time of aneurysm rupture. Beta-blockers, which reduce the impact of the catecholamine