Russ Martin A, Prondzinsky Roland, Christoph Arnd, Schlitt Axel, Buerke Ute, Söffker Gerold, Lemm Henning, Swyter Michael, Wegener Nikolas, Winkler Matthias, Carter Justin M, Reith Sebastian, Werdan Karl, Buerke Michael
Department of Internal Medicine III, Martin-Luther-University Halle-Wittenberg, Halle/Saale, Germany.
Crit Care Med. 2007 Dec;35(12):2732-9. doi: 10.1097/01.CCM.0000287524.17358.48.
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.
Observational hemodynamic study.
Tertiary care center university hospital.
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.
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).
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.
Levosimendan infusion in cardiogenic shock following acute myocardial infarction improved cardiovascular hemodynamics without leading to hypotension.
左西孟旦是一种新型的血管扩张剂，已被证明可改善充血性心力衰竭急性加重患者的血流动力学功能。我们想确定在心肌梗死后心源性休克患者中，在常规治疗（使用儿茶酚胺）无效后使用左西孟旦的血流动力学效应。
观察性血流动力学研究。
三级医疗中心大学医院。
56例心肌梗死后心源性休克患者接受了经皮血管重建术（必要时使用主动脉内球囊泵），并开始接受常规的强心治疗。
血管重建术后24小时仍存在心源性休克的患者，额外接受左西孟旦治疗（快速推注12微克/千克，持续10分钟，然后以0.05 - 0.2微克/千克/分钟的速度持续24小时）（n = 25）。
使用常规儿茶酚胺治疗（去甲肾上腺素和多巴酚丁胺）时，我们观察到平均动脉压或心脏指数仅有轻微改善。相比之下，添加左西孟旦后心脏指数显著增加（从2.1±0.56升至3.0±1.11升/分钟/平方米，p < 0.01），心脏功率指数也显著增加（从0.32±0.08升至0.44±0.18瓦，p < 0.01），而全身血管阻力显著降低（从1208±333降至858±299达因·秒·厘米⁻⁵，p < 0.01）。在左西孟旦治疗期间血压无显著变化。停止输注左西孟旦后，血流动力学改善得以持续。
急性心肌梗死后心源性休克患者输注左西孟旦可改善心血管血流动力学，且不会导致低血压。
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