Neurocardiogenic injury in subarachnoid hemorrhage: A wide spectrum of catecholamin-mediated brain-heart interactions

Abstract

The purpose of this review was to summarize the up-to-date knowledge on clinical presentation and management of neurocardiogenic injury and to deliver the evidence of common pathophysiology of this broad spectrum of disorders. Medline and EmBase databases were searched to obtain original research articles and review papers using the following key words: neurocardiogenic injury, stress cardiomyopathy,tako-tsubo, subarachnoid hemorrhage, ECG abnormalities, catecholamine toxicity, neuropulmonary edema. Various forms of cerebral pathology, most importantly subarachnoid hemorrhage (SAH), are accompanied by transient cardiac dysfunction with ST-segment elevation and QT interval prolongation and T wave inversion with simultaneous release of cardiac troponin. In the past 20 years a great deal of data emerged concerning stress cardiomyopathy ('tako-tsubo') presenting as a rare transient apical ballooning syndrome following stressful life events with symptoms and signs resembling acute myocardial infarction (AMI), yet without significant coronary artery stenosis. Both forms of cardiac dysfunction are mediated by catecholamine toxicity, triggered by physical and psychological distress, leading to a specific type of neurogenic myocardial stunning reflected by histopathological image of contraction band necrosis. Neurocardiogenic injury should be carefully differentiated from AMI. Cardiac dysfunction in SAH heralds increased mortality. The criteria for the diagnosis of stress cardiomyopathy should be revised to comprise the diversity of its clinical symptomatology and to include cardiac dysfunction accompanying cerebral pathology.