Combination Therapy With Beta Blocker and Inotrope in Decompensated Heart Failure: A Clinical Observation.
Inotropic support is contemplated in the presence of ongoing end-organ hypoperfusion or
refractory symptoms in decompensated heart failure (DHF). However, inotropic agents may
cause tachycardia leading to increased myocardial oxygen demand and arrhythmogenesis.1
Introduction of beta blocker (BB) therapy in DHF patients requiring inotrope support is discouraged due to the negative hemodynamic impact of acute BB therapy.2-5 On the other
hand, reduction in heart rate by BB therapy results in decreased myocardial oxygen demand
and increased ventricular diastolic filling.6,7 Additionally, early introduction of BB therapy
improves outcome in heart failure.
We describe our clinical experience in two DHF patients with end-organ hypoperfusion while receiving intravenous milrinone who tolerated and derived benefit from addition of BB therapy. We discuss the molecular mechanisms that may support improvement in hemodynamics after addition of BB therapy to intravenous milrinone in DHF. When used together, BB may improve hemodynamics by enhancing inotropic effect of milrinone and mitigates cardiotoxic effects and the risk of arrhythmias associated with milrinone. Moreover, milrinone might counter negative hemodynamic effects of acute BB therapy. We propose that DHF patients receiving intravenous inotrope support with milrinone may benefit from addition of BB therapy in the absence of systemic hypotension.
In addition, BB therapy attenuates adverse effects associated with PDEI by modulation of intramyocardial calcium handling.19,20 Improvement in calcium handling, through targeted SERCA gene expression has shown to retard development of action potential duration alternans and hence decrease arrhythmogenesis. Moreover, these changes may result in improvements in inotropy and lusitropy without increasing arrhythmogenesis and cardiotoxicity. Addition of beta blocker (BB) therapy to intravenous milrinone support in DHF may result in hemodynamic and
clinical improvement.
Heart Res Open J. 2017; 4(1): 18-22. doi: 10.17140/HROJ-4-136
