Hemodynamic effects of ivabradine use in combination with intravenous inotropic therapy in advanced heart failure
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Hemodynamic effects of ivabradine use in combination with intravenous inotropic therapy in advanced heart failure Mohammed Elzeneini 1 & Juan M. Aranda Jr 2,3 & Mohammad Al-Ani 2,3 & Mustafa M. Ahmed 2,3 & Alex M. Parker 2,3 & Juan R. Vilaro 2,3 Accepted: 15 September 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Intravenous inotropic therapy can be used in patients with advanced heart failure, as palliative therapy or as a bridge to cardiac transplantation or mechanical circulatory support, as well as in cardiogenic shock. Their use is limited to increasing cardiac output in low cardiac output states and reducing ventricular filling pressures to alleviate patient symptoms and improve functional class. Many advanced heart failure patients have sinus tachycardia as a compensatory mechanism to maintain cardiac output. However, excessive sinus tachycardia caused by intravenous inotropes can increase myocardial oxygen consumption, decrease coronary perfusion, and at extreme heart rates decrease ventricular filling and stroke volume. The limited available hemodynamic studies support the hypothesis that adding ivabradine, a rate control agent without negative inotropic effect, may blunt inotrope-induced tachycardia and its associated deleterious effects, while optimizing cardiac output by increasing stroke volume. This review analyzes the intriguing pathophysiology of combined intravenous inotropes and ivabradine to optimize the hemodynamic profile of patients in advanced heart failure.
Keywords Ivabradine, Inotrope, Cardiogenic shock, Cardiac output Abbreviations LV Left ventricle cAMP Cyclic adenosine monophosphate HCN Hyperpolarization-activated cyclic nucleotide-gated
Advanced heart failure refers to patients with heart failure symptoms at rest refractory to goal-directed medical or device therapy, with severe limitation in functional capacity or recurrent hospitalizations for episodes of fluid retention or low cardiac output [1]. This is also termed Stage D heart failure by the American College of Cardiology/American Heart Association (ACC/AHA) and requires consideration for advanced therapies including continuous intravenous inotropic * Juan R. Vilaro [email protected] 1
Department of Internal Medicine, University of Florida, Gainesville, FL, USA
2
Division of Cardiovascular Medicine, University of Florida, Gainesville, FL, USA
3
Advanced Heart Failure & Transplant Cardiology, University of Florida, 1329 SW 16th Street, Suite 5130, PO Box 100288, Gainesville, FL 32608, USA
therapy, mechanical circulatory support and/or cardiac transplantation, or end-of-life care [2]. Based on the 2013 ACC/ AHA guideline for the management of heart failure, ambulatory intravenous inotropic therapy is reasonable in these patients as a bridge to cardiac transplantation or mechanical circulatory support (Class IIA recommendation) [3–5], and may be considered as palliative therapy for symptom control (Class IIb recommendation) [3, 6], based on limited evidence (Level of Evidence: B). The hemod
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