Acute heart failure with low cardiac output: Can we develop a short-term inotropic agent that does not increase adverse events?

被引：14

作者：

Campia U. ^{[1
]}

Nodari S. ^{[2
]}

Gheorghiade M. ^{[1
]}

机构：

[1] Center for Cardiovascular Quality and Outcomes, Northwestern University, Feinberg School of Medicine, Chicago, IL 60611

[2] Section of Cardiovascular Diseases, Department of Experimental and Applied Medicine, University of Brescia, Brescia

来源：

Current Heart Failure Reports | 2010年 / 7卷 / 3期

关键词：

Acute heart failure; Digoxin; Inotropic drug; Istaroxime; Low cardiac output; Lusitropic drug; Myosin activator; Omecamtiv mecarbil;

D O I：

10.1007/s11897-010-0021-9

中图分类号：

学科分类号：

摘要：

Acute heart failure represents an increasingly common cause of hospitalization, and may require the use of inotropic drugs in patients with low cardiac output and evidence of organ hypoperfusion. However, currently available therapies may have deleterious effects and increase mortality. An ideal inotropic drug should restore effective tissue perfusion by enhancing myocardial contractility without causing adverse effects. Such a drug is not available yet. New agents with different biological targets are under clinical development. In particular, istaroxime seems to dissociate the inotropic effect exerted by digitalis (inhibition of the membrane sodium/potassium adenosine triphosphatase) from the arrhythmic effect and to ameliorate diastolic dysfunction (via sarcoendoplasmic reticulum calcium adenosine triphosphatase activation). Additionally, the myosin activator omecamtiv mecarbil appears to have promising characteristics, while genetic therapy has been explored in animal studies only. Further investigations are needed to confirm and expand the effectiveness and safety of these agents in patients with acute heart failure and low cardiac output. © 2010 Springer Science+Business Media, LLC.

引用

页码：100 / 109

页数：9

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