Key result
Intracoronary levosimendan (3.75 and 12.5 microg/min) exerted mild inotropic and lusitropic effects in patients with left ventricular dysfunction, without altering force-frequency relationships.
Why the study?
Does intracoronary levosimendan improve inotropic and lusitropic responses in patients with left ventricular dysfunction caused by nonischemic dilated cardiomyopathy?
Does intracoronary levosimendan improve inotropic and lusitropic responses in patients with left ventricular dysfunction caused by nonischemic dilated cardiomyopathy?
Levosimendan exerts direct mild positive inotropic and lusitropic effects in failing human myocardium in vivo without altering force-frequency or relaxation-frequency relationships.
No takes yet. Share an insight, caveat, or question.
Shows direct mild inotropic and lusitropic effects in vivo; extends in vitro data but leaves open clinical utility in nonischemic cardiomyopathy.
Givertz et al. (2007) studied left ventricular dysfunction caused by nonischemic dilated cardiomyopathy (n=10). Levosimendan vs. 5% dextrose in water was evaluated on Inotropic (peak +dP/dt) and lusitropic (Tau) responses. Intracoronary levosimendan (3.75 and 12.5 microg/min) exerted mild inotropic and lusitropic effects in patients with left ventricular dysfunction, without altering force-frequency relationships.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: