ABSTRACT

Despite improvements in medical and surgical treatment, aneurysmatic subarachnoid hemorrhage (SAH) remains one of the main causes of early mortality. Cardiac and pulmonary complications are the main causes of mortality. One of the most severe cardiac complications is neurogenic stress cardiomyopathy. Left ventricular dysfunction which is seen in neurogenic stress cardiomyopathy, although it is usually reversible within a few days, can cause severe hypotension, pulmonary edema and cardiogenic shock. Traditional treatment of heart failure after SAH is based on the use of noradrenaline, dobutamine and high volume of fluids. However, it is difficult to treat reduced cardiac output in SAH. Because, myocardial cells are already under stress due to increased adrenergic stimulation. The use of exogenous catecholamines may cause additional neurocardiogenic damage in myocardial cells, excessive calcium burden, decreased cerebral blood flow, and delayed cerebral ischemia. By reducing the use of exogenous catecholamines with levosimendan, the vicious circle of cardiotoxicity induced by catecholamines can be broken. Levosimendan is a nonadrenergic inotropic calcium sensitizer that allows rapid recovery of cardiac output and optimizes cerebral perfusion without increasing myocardial oxygen consumption. If we consider that reduction in left ventricular systolic function plays a role in the pathogenesis of delayed cerebral ischemia, the risk of developing neurological complications may be reduced by administration of levosimendan in these patients. Moreover, new evidence from experimental studies also indicates that levosimendan may have neuroprotective effects in the SAH. In this review, the use of levosimendan in the treatment of hemodynamic disorders which develops in the course of SAH has been discussed in company with current literature.

Keywords: Subarachnoid hemorrhage, traumatic, aneurysm, intracranial vasospasm, critical care, levosimendan, neurogenic stress cardiomyopathy