Routine use of positive inotropes in heart failure is associated with increased myocardial oxygen demand, arrhythmias, and mortality, limiting their use to patients with hypoperfusion or shock.
Impaired cardiac contractility is a fundamental component of the heart failure syndrome, initiating the cycle of vasoconstriction, neurohormonal and inflammatory activation, and adverse ventricular remodeling that leads to heart failure progression. Based on this core paradigm, drugs that increase cardiac contractility (positive inotropes) are theoretically appealing as a heart failure therapy, and such agents have been extensively investigated in both acute and chronic heart failure. Although these agents clearly improve cardiac output, their use in heart failure has consistently been associated with increased myocardial oxygen demand, cardiac arrhythmias, and mortality in a variety of clinical settings. Based on these data, the routine use of inotropes as heart failure therapy is not indicated in either the acute or chronic setting. Inotropes may be a necessary evil in a subset of acute heart failure patients, such as those with acute heart failure decompensation in the setting of clinically evident hypoperfusion or shock, or as a bridge to more definitive treatment, such as revascularization or cardiac transplantation. Currently available inotropes, such as dobutamine and milrinone, act (directly or indirectly) by increasing cyclic adenylate monophosphate and therefore intracellular calcium flux. Whether newer inotropes with differing mechanisms of action will realize the potential clinical benefits of inotropic therapy without the risk remains a subject of ongoing investigation.
Petersen et al. (Tue,) conducted a review in Acute heart failure. Inotropes was evaluated. Routine use of positive inotropes in heart failure is associated with increased myocardial oxygen demand, arrhythmias, and mortality, limiting their use to patients with hypoperfusion or shock.