Background: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in acute heart failure and cardiogenic shock following acute myocardial infarction. Limited data are available on its use in patients with impaired right ventricular function. We hypothesised that levosimendan, due to its vasodilating and positiv inotropic profile, could ameliorate right ventricular hemodynamic function in critically ill patients with cardiogenic shock following myocardial infarction.
Methods: Patients (n=25) with cardiogenic shock received initial conventional inotropic therapy after reperfusion of infarct related artery. After insufficient hemodynamic improvement patients received levosimendan (2μg/kgbw/h) over 24 hours. Hemodynamic measurements were routinely performed initially i.e., − 24 hours, at baseline (prior to levosimendan infusion) at 3 hours, 24 and 48 hours after start of levosimendan infusion using a Swan-Ganz thermodilution catheter.
Results: With conventional catecholamine therapy (i.e., norepinephrine and/or dobutamine) we observed only marginal change of right ventricular perfomance parameters. In contrast, upon levosimendan infusion there was a significant decrease in pulmonary vascular resistance, while right ventricular Cardiac Power Index, a new measure of right ventricular performance similar to left ventricular CPI, significantly increased. Central venous pressure did not change which makes a significant dependency on preload unlikely.
Conclusion: Levosimendan infusion in patients with cardiogenic shock following acute MI and PCI seems to improves substantially and persistently right ventricular hemodynamic parameters, superior to conventional catecholamine therapy. Further studies addressing the benefit of levosimendan in right ventricular failure like in cardiogenic shock due to right myocardial infarction or acute pulmonary embolism are warranted.
Hemodynamic Parameters With Catecholamine Teatment and Additional Levosimendan
676 Value of evaluation of right ventricular function, postsystolic left ventricular contraction and pulmonary venous flow for prediction of post myocardial infarction remodeling