Ogłuszone serce neurogenne — czy uwzględniamy to rozpoznanie u chorych z ostrym uszkodzeniem ośrodkowego układu nerwowego i niewydolnością serca?

Abstract

Neurogenic stunned myocardium (NSM) is defined as myocardial injury and dysfunction of a sudden onset, occurring after various types of acute brain injury as a result of an imbalance in the autonomic nervous system. The typical spectrum of clinically observed abnormalities includes acute left ventricular failure, not uncommonly progressing to cardiogenic shock with hypotension that requires inotropic agents, pulmonary oedema and various arrhythmias. Commonly-seen electrocardiographic changes include: prolonged QT interval, ST segment changes, T-wave inversion, a new Q-wave or U-wave. Echocardiography shows both an impaired both systolic and diastolic function of the left ventricle. Biochemical markers of NSM comprise metabolic acidosis and increased cardiac enzymes and markers: creatine kinase (CK), and CK-MB, troponin I and B-type natriuretic peptide. The main cause of NSM is myocardial injury induced by local catecholamine release from nerve endings within the myocardium. Recently, a theory has been proposed to classify NSM as one of the stress-related cardiomyopathies, together with Takotsubo cardiomyopathy, acute left ventricular failure in the critically ill, cardiomyopathy associated with pheochromacytoma and exogenous catecholamine administration. The occurrence of NSM increases the risk of life-threatening complications, death, and worsens neurologic outcome. As far as we know, treatment should generally focus on the underlying neurologic process in order to maximize neurologic recovery. Improvement in neurologic pathology leads to rapid improvement in cardiac function and its full recovery, as NSM is a fully reversible condition if the patient survives. Awareness of the existence of NSM and a deeper knowledge of its etiopathology may reduce diagnostic errors, optimise its treatment.

Myocardial ischemic changes of electrocardiogram in intracerebral hemorrhage: A case report and review of literature

“…Until recently, neurogenic stunned myocardium (NSM) was defined as the myocardial injury and dysfunction of a sudden onset, occurring after acute brain disease as a result of autonomic disturbances, which may be responsible for the cardiac injury after stroke[6,7]. The clinical features observed include arrhythmia, myocardial necrosis, ECG changes, pulmonary edema, and acute left HF which is not uncommon to progress to cardiogenic shock[8].…”

“…Oppenheimer et al[9] induced ECG changes in rats similar to those found after ischemic stroke, supporting the notion of neurogenic cardiac injury. NSM, which can develop in any acute CNS pathology, has a poorly understood pathology[8]. Most models for the etiopathology of NSM involve a subarachnoid hemorrhage (SAH)[10].…”

“…There is currently no test available to distinguish whether elevated troponin is due to concurrent exacerbation of CAD or neurogenic cardiac involvement. In patients with cardiac injury after stroke, most cTn concentrations in CCS are modest, even though an obvious abnormal contraction is observed[8]. On the contrary, cTn levels typically reach concentrations of up to 50 times the upper reference limit when measured 18-24 h after ACS[42].…”

“…In the majority of cases, the return of normal LV function is seen within 5-14 d, sometimes several weeks[47]. Some view acute myocardial ischemic-like changes after stroke as a stress cardiomyopathy similar to Takotsubo cardiomyopathy which presents with ST-segment changes, increased troponin concentrations and hypokinesis or akinesia of the apex LV[8,47,48]. Unlike Takotsubo cardiomyopathy, the most common echogenic abnormalities include hypokinesis or akinesia of basal and intraventricular segments with sparing of the apical or global hypokinesis of the LV[10,47].…”

Early prediction of cerebral-cardiac syndrome after ischemic stroke: the PANSCAN scale

“…CCS was diagnosed according to the following criteria [ 10 ]: (1) no previous history of heart disease; (2) clear diagnosis of acute ischemic stroke; (3) any secondary cardiac damage manifestations. The manifestation includes: (1) ECG changes, including ST segment elevation or depression, T wave changes and QT prolongation [ 11 – 13 ]; (2) cardiac dysfunctions in echocardiography such as left ventricular diastolic dysfunction, [ 14 ] abnormal ventricular wall motion, [ 15 ] and decreased left ventricular ejection fraction [ 16 ]; (3) elevated peripheral cardiac markers by laboratory tests including troponin [ 17 ] and B-type natriuretic peptide [ 18 ].…”