. " "@en . . . . . "Eliminination half-life is approximately 1 hour."@en . . . . . . . "For short term treatment of acutely decompensated severe chronic heart failure (CHF). Also being investigated for use/treatment in heart disease."@en . . . . . "98% bound to plasma protein."@en . . . "approved"@en . . . . "Humans and other mammals"@en . . "Levosimedan"@en . . . . . . . "# \"Link\":http://www.medicinescomplete.com/mc/martindale/current/17095-k.htm # Mebazaa A, Nieminen MS, Packer M, Cohen-Solal A, Kleber FX, Pocock SJ, Thakkar R, Padley RJ, Poder P, Kivikko M: Levosimendan vs dobutamine for patients with acute decompensated heart failure: the SURVIVE Randomized Trial. JAMA. 2007 May 2;297(17):1883-91. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/17473298 # Kasikcioglu HA, Cam N: A review of levosimendan in the treatment of heart failure. Vasc Health Risk Manag. 2006;2(4):389-400. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/17323593"@en . . . . "Levosimendanum"@en . . . "Levosimendan appears to increase myofilament calcium sensitivity by binding to cardiac troponin C in a calcium-dependent manner. This stabilizes the calcium-induced conformational change of troponin C, thereby (1) changing actin-myosin cross-bridge kinetics apparently without increasing the cycling rate of the cross-bridges or myocardial ATP consumption, (2) increasing the effects of calcium on cardiac myofilaments during systole and (3) improving contraction at low energy cost (inotropic effect). Calcium concentration and, therefore, sensitization decline during diastole, allowing normal or improved diastolic relaxation. Levosimendan also leads to vasodilation through the opening of ATP-sensitive potassium channels. By these inotropic and vasodilatory actions, levosimendan increases cardiac output without increasing myocardial oxygen demand. Levosimendan also has a selective phosphodiesterase (PDE)-III inhibitory action that may contribute to the inotropic effect of this compound under certain experimental conditions. It has been reported that levosimendan may act preferentially as a Ca²⁺ sensitizer at lower concentrations, whereas at higher concentrations its action as a PDE-III inhibitor becomes more prominent in experimental animals and humans."@en . "Levosimendan"@en . . . "Simdax"@en . "Dharmaraj Ramachandra Rao, Rajendra Narayanrao Kankan, Manjinder Singh Phull, Ashwini Amol Sawant, \"Process for Preparing Levosimendan and Intermediates for Use in the Process.\" U.S. Patent US20120165524, issued June 28, 2012."@en . . . "141505-33-1"@en . "Levosimendan is a calcium sensitiser used in the management of acutely decompensated congestive heart failure. It increases the sensitivity of the heart to calcium, thus increasing cardiac contractility without a rise in intracellular calcium. Levosimendan exerts its effect by increasing calcium sensitivity of myocytes by binding to cardiac troponin C in a calcium-dependent manner. It also has a vasodilatory effect, by opening adenosine triphosphate (ATP)-sensitive potassium channels in vascular smooth muscle to cause smooth muscle relaxation."@en . . . "The bioavailability of oral levosimendan is 85 ± 6% in healthy volunteers and 84 ± 4% in patients."@en . "investigational"@en .