Evolving concepts in the treatment of heart failure: should new inotropic agents carry promise or paranoia?

Heart failure is a common disorder caused by many different diseases. At the root of the problem is diminished myocyte contractility, which ultimately results in failure of the pump to generate adequate peripheral flow. An interplay of hemodynamic, neurohumoral, and inflammatory perturbations initially improves cardiac flow and cellular respiration, but ultimately worsens the syndrome. Inotropic drug therapy was an attractive option in patients with heart failure even before the pump failure aspect of the disease was recognized. Increased contractility should lead to increased cardiac output, which would likely ameliorate hemodynamic and metabolic derangements. Although inotropes increase cardiac contractility at least transiently, this effect does not generally translate into improved survival in clinical trials. Indeed, in patients with advanced heart failure, these drugs frequently increase death rates. It is important to put the issue of inotropic therapeutics into perspective when considering treatment options for these patients. It may well be that certain inotropes in yet to be defined dosages will substantially improve morbidity and mortality when combined with drugs designed to interdict metabolic and neurohumoral components of the syndrome.