Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock.
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Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock. / Russ, Martin A; Prondzinsky, Roland; Christoph, Arnd; Schlitt, Axel; Buerke, Ute; Soeffker, Gerold; Lemm, Henning; Swyter, Michael; Wegener, Nikolas; Winkler, Matthias; Carter, Justin M; Reith, Sebastian; Werdan, Karl; Buerke, Michael.
In: CRIT CARE MED, Vol. 35, No. 12, 12, 2007, p. 2732-2739.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock.
AU - Russ, Martin A
AU - Prondzinsky, Roland
AU - Christoph, Arnd
AU - Schlitt, Axel
AU - Buerke, Ute
AU - Soeffker, Gerold
AU - Lemm, Henning
AU - Swyter, Michael
AU - Wegener, Nikolas
AU - Winkler, Matthias
AU - Carter, Justin M
AU - Reith, Sebastian
AU - Werdan, Karl
AU - Buerke, Michael
PY - 2007
Y1 - 2007
N2 - OBJECTIVES: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in patients with acute exacerbation of congestive heart failure. We wanted to determine the hemodynamic effects of levosimendan following ineffective conventional therapy (with catecholamines) in patients with cardiogenic shock following myocardial infarction. DESIGN: Observational hemodynamic study. SETTING: Tertiary care center university hospital. PATIENTS: Fifty-six patients with cardiogenic shock secondary to myocardial infarction were treated with percutaneous revascularization (intra-aortic balloon pump where appropriate) and commenced on conventional inotropic therapy. INTERVENTIONS: Patients with persisting cardiogenic shock 24 hrs after revascularization were additionally treated with levosimendan (rapid bolus of 12 microg/kg for 10 mins, then 0.05-0.2 mug/kg/min for 24 hrs) (n = 25). MEASUREMENTS AND MAIN RESULTS: With conventional catecholamine therapy (norepinephrine and dobutamine), we observed only marginal improvement in mean arterial pressure or cardiac index. In contrast, the addition of levosimendan produced a significant increase in cardiac index (2.1 +/- 0.56 to 3.0 +/- 1.11 L/min/m2, p <.01) and cardiac power index (0.32 +/- 0.08 to 0.44 +/- 0.18 W, p <.01), whereas systemic vascular resistance decreased significantly (1208 +/- 333 to 858 +/- 299 dyne.sec.cm(-5), p <.01). There was no significant change in blood pressure during levosimendan treatment. Hemodynamic improvement was sustained after levosimendan infusion was stopped. CONCLUSIONS: Levosimendan infusion in cardiogenic shock following acute myocardial infarction improved cardiovascular hemodynamics without leading to hypotension.
AB - OBJECTIVES: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in patients with acute exacerbation of congestive heart failure. We wanted to determine the hemodynamic effects of levosimendan following ineffective conventional therapy (with catecholamines) in patients with cardiogenic shock following myocardial infarction. DESIGN: Observational hemodynamic study. SETTING: Tertiary care center university hospital. PATIENTS: Fifty-six patients with cardiogenic shock secondary to myocardial infarction were treated with percutaneous revascularization (intra-aortic balloon pump where appropriate) and commenced on conventional inotropic therapy. INTERVENTIONS: Patients with persisting cardiogenic shock 24 hrs after revascularization were additionally treated with levosimendan (rapid bolus of 12 microg/kg for 10 mins, then 0.05-0.2 mug/kg/min for 24 hrs) (n = 25). MEASUREMENTS AND MAIN RESULTS: With conventional catecholamine therapy (norepinephrine and dobutamine), we observed only marginal improvement in mean arterial pressure or cardiac index. In contrast, the addition of levosimendan produced a significant increase in cardiac index (2.1 +/- 0.56 to 3.0 +/- 1.11 L/min/m2, p <.01) and cardiac power index (0.32 +/- 0.08 to 0.44 +/- 0.18 W, p <.01), whereas systemic vascular resistance decreased significantly (1208 +/- 333 to 858 +/- 299 dyne.sec.cm(-5), p <.01). There was no significant change in blood pressure during levosimendan treatment. Hemodynamic improvement was sustained after levosimendan infusion was stopped. CONCLUSIONS: Levosimendan infusion in cardiogenic shock following acute myocardial infarction improved cardiovascular hemodynamics without leading to hypotension.
M3 - SCORING: Zeitschriftenaufsatz
VL - 35
SP - 2732
EP - 2739
JO - CRIT CARE MED
JF - CRIT CARE MED
SN - 0090-3493
IS - 12
M1 - 12
ER -