Inotropes and inodilators for acute heart failure: Sarcomere active drugs in focus

L. Nagy, Piero Pollesello, Z. Papp

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Acute heart failure (AHF) emerges as a major and growing epidemiological concern with high morbidity and mortality rates. Current therapies in patients with acute heart failure rely on different strategies. Patients with hypotension, hypoperfusion, or shock require inotropic support, whereas diuretics and vasodilators are recommended in patients with systemic or pulmonary congestion. Traditionally inotropic agents, referred to as Ca2+ mobilizers load the cardiomyocyte with Ca2+ and thereby increase oxygen consumption and risk for arrhythmias. These limitations of traditional inotropes may be avoided by sarcomere targeted agents. Direct activation of the cardiac sarcomere may be achieved by either sensitizing the cardiac myofilaments to Ca2+ or activating directly the cardiac myosin. In this review, we focus on sarcomere targeted inotropic agents, emphasizing their mechanisms of action and overview the most relevant clinical considerations.

Original languageEnglish
Pages (from-to)199-208
Number of pages10
JournalJournal of Cardiovascular Pharmacology
Volume64
Issue number3
Publication statusPublished - Sep 1 2014

Fingerprint

Sarcomeres
Heart Failure
Pharmaceutical Preparations
Cardiac Myosins
Myofibrils
Vasodilator Agents
Diuretics
Cardiac Myocytes
Oxygen Consumption
Hypotension
Cardiac Arrhythmias
Shock
Morbidity
Lung
Mortality
Therapeutics

Keywords

  • Acute heart failure syndrome
  • Ca<sup>2+</sup> mobilizer
  • Levosimendan
  • Omecamtiv mecarbil
  • Sarcomere targeted agent

ASJC Scopus subject areas

  • Pharmacology
  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

Inotropes and inodilators for acute heart failure : Sarcomere active drugs in focus. / Nagy, L.; Pollesello, Piero; Papp, Z.

In: Journal of Cardiovascular Pharmacology, Vol. 64, No. 3, 01.09.2014, p. 199-208.

Research output: Contribution to journalArticle

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