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

Umberto Campia, Savina Nodari, Mihai Gheorghiade*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

13 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)100-109
Number of pages10
JournalCurrent Heart Failure Reports
Volume7
Issue number3
DOIs
StatePublished - Sep 1 2010

Keywords

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

ASJC Scopus subject areas

  • Emergency Medicine
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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