Neurogenic Stunned Myocardium Following Acute Subarachnoid Hemorrhage

Abstract

Neurogenic stunned myocardium (NSM) is a triad of transient left ventricular dysfunction, electrocardiogram changes, and elevation in cardiac enzymes, often mimicking a myocardial infarction. It has been described following acute brain injury. The purported mechanism is catecholamine excess resulting in cardiac dysfunction. From the clinical standpoint, the most frequently encountered electrocardiographic changes are QTc prolongation and ST-T changes, with modest elevations in troponin levels. Basal and mid-ventricular segments of the left ventricle are most commonly involved. NSM poses therapeutic challenges when it occurs secondary to aneurysmal subarachnoid hemorrhage, particularly in the setting of coexisting vasospasm. Overall, NSM carries good prognosis if recognized early, with appropriate management of hemodynamic and cardiopulmonary parameters.

The evaluation of myocardial function of patients in the early stage of acute ischemic stroke by two‐dimensional speckle tracking echocardiography

“…The most widely accepted theory is metabolic myocardial stunning due to the cardiotoxic effects of high levels of circulating plasma catecholamines in relation to the affected cerebral area. Instead of the positive inotropic effects of plasma catecholamine at physiologic levels, supraphysiologic levels exhibit myocardial depressive effects . NSM is associated with ischemic ECG changes and elevated plasma troponin levels.…”

Cardiac Troponin Elevation and Outcome after Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

“…1 In addition to the impact caused by the initial bleeding and subsequent neurologic damage, neurocardiogenic injury has been linked with increased morbidity and mortality in patients with SAH. [2][3][4] Neurocardiogenic injury is believed to be a neurally mediated process as a consequence of brain damage rather than manifestation of coronary artery disease, 5,6 which could further aggravate the changes in cerebral blood flow induced by SAH. 6 Cardiac troponins (cTn) T and I provide largely identical information and are widely used as the preferred biomarkers for the diagnosis of myocardial infarction 7 and cardiac damage after SAH.…”

“…[2][3][4] Neurocardiogenic injury is believed to be a neurally mediated process as a consequence of brain damage rather than manifestation of coronary artery disease, 5,6 which could further aggravate the changes in cerebral blood flow induced by SAH. 6 Cardiac troponins (cTn) T and I provide largely identical information and are widely used as the preferred biomarkers for the diagnosis of myocardial infarction 7 and cardiac damage after SAH. [8][9][10] Cardiac abnormalities including cTn elevation were associated with poor outcome in patients with SAH in a previous meta-analysis.…”

Management of catecholamine-induced stunned myocardium—a case report

“…The onset of cardiac dysfunction late on the 11th POD, involvement of apical segments of myocardium, and a normal ECG result go against neurogenic stunned myocardium. Neurogenic stunned myocardium is generally seen immediately after SAH because of catecholamine surge, usually involves the basal myocardium, and is associated with elevation of cardiac enzymes and ECG changes mimicking myocardial infarction [4]. Although her respiratory distress was initially thought to be due to infection, negative bacterial cultures and the findings on cardiac output monitoring pointed toward a cardiac etiology.…”