The clinical experience with levosimendan in anesthesiology and in the intensive care unit.
In the present review striking data showing that intensive care unit patients with acute heart failure and high-risk surgical patients may markedly benefit from the use of levosimendan are presented. Indeed, levosimendan is an effective new agent that acts via two complementary mechanisms. It enhances cardiac contractility by improving the response of the myofilaments to intracellular calcium, and it reduces the cardiac workload by opening the adenosine triphosphate-dependent potassium channels for the dilation of blood vessels. Because the therapeutic levels of levosimendan do not increase the intracellular calcium concentrations, levosimendan is less likely than traditional inotropes (beta-agonist inotropes or phosphodiesterase inhibitors) to elicit arrhythmias or impair diastolic relaxation. In fact, the results of recent clinical studies indicate that levosimendan offers significant hemodynamic and survival benefits when given to patients who are hospitalized for acute heart failure. Indeed, in the near future, it is likely that levosimendan may also prove effective for the treatment of patients with diastolic heart failure or for those with a low cardiac output following coronary artery bypass grafting. In addition, levosimendan has the potential of supporting the cardiac function during the initiation of beta-blocker therapy, for weaning patients from cardiopulmonary bypass, for individuals with valvular abnormalities and for those with myocarditis. Preliminary results also suggest that levosimendan may be beneficial for the treatment of patients with right ventricular heart failure. Although the use of levosimendan has been fully validated for the most common causes of acute heart failure, additional clinical trials are needed to safety broaden its therapeutic indications.
Cavana
Marco
M
Department of Anesthesiology and Critical Care Medicine, Hôpital Lariboisière, 2 Rue Ambroise Pare, 75475 Paris, France.
Pignataro
Claudia
C
Fraticelli
Amanda
A
Mebazaa
Alexandre
A
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000758:Anesthesia; D020746:Calcium Channels, L-Type / Q000627:therapeutic use*; D002303:Cardiac Output, Low / Q000503:physiopathology / Q000628:therapy; D006348:Cardiac Surgical Procedures; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D006333:Heart Failure / Q000503:physiopathology / Q000628:therapy*; D006801:Humans; D006835:Hydrazones / Q000627:therapeutic use*; D007362:Intensive Care Units; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology; D011724:Pyridazines / Q000627:therapeutic use*; D012770:Shock, Cardiogenic / Q000503:physiopathology / Q000628:therapy; D000077464:Simendan; D013599:Systole / Q000187:drug effects / Q000502:physiology; D018487:Ventricular Dysfunction, Left / Q000503:physiopathology / Q000628:therapy
D000319:Adrenergic beta-Antagonists; D020746:Calcium Channels, L-Type; D002316:Cardiotonic Agents; D006835:Hydrazones; D011724:Pyridazines; D000077464:Simendan