Cardiac Contractility Modulation in Heart Failure: Mechanisms and Clinical Evidence
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Heart Failure (W Tang, Section Editor)
Cardiac Contractility Modulation in Heart Failure: Mechanisms and Clinical Evidence Alexis Barnes, MD1 Courtney Campbell, MD, PhD2 Raul Weiss, MD2 Rami Kahwash, MD2,* Address 1 Department of Internal Medicine, The Ohio State University, Columbus, OH, 43210, USA *,2 Division of Cardiology, Department of Internal Medicine, The Ohio State University, 452 W 10th Avenue, Columbus, OH, 43210, USA Email: [email protected]
Published online: 10 October 2020 * Springer Science+Business Media, LLC, part of Springer Nature 2020
This article is part of the Topical Collection on Heart Failure Keywords Heart failure I Cardiac contractility modulation I OPTIMIZER device
Abstract Purpose of review Device-based therapy utilizing cardiac contractility modulation (CCM™) was approved by the FDA in March 2019 for patients with moderately to severely symptomatic heart failure with reduced ejection fraction between 25 and 45% on optimal guideline-directed medical therapy in normal sinus rhythm and not a candidate for cardiac resynchronization therapy. This review explores the mechanism of action behind CCM, the most recent clinical trials, and the expansion of therapy to additional patient populations. Recent findings The most recent trial on CCM explored a two-lead system, which was as equally efficacious as three-lead model. Importantly, CCM was shown to be effective in patients with atrial fibrillation (AF), who made up 15% of the population studied. Furthermore, emerging data from the European Registry suggests improvement in mortality with the use of CCM. Summary New developments of a two-lead system have allowed for expansion into a broader array of patient populations, including those with AF, while maintaining the safety and efficacy of this therapy.
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Curr Treat Options Cardio Med (2020) 22: 43
Introduction Heart failure (HF) currently affects over 6 million Americans with projections that the prevalence will increase by 46% from 2012 to 2030 [1]. While heart failure with reduced ejection fraction (HFrEF) has dominated the literature, mid-range heart failure and heart failure with preserved ejection fraction (HFpEF) make up over 50% of heart failure patients [2]. Our current therapies for heart failure remain inadequate. For HFrEF patients, the mainstays of optimal guideline-directed medical therapy (GDMT) are betaadrenergic blockade, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin receptor blockade (ARB), and mineralocorticoid receptor antagonists (MCRAs). The only new additions to GDMT in two decades are the combination neprilysin inhibitor and ARB, sacubitril/valsartan, and the cardiac pacemaker c u r r en t , I ( f ) , i n hi bi t o r , i v a b r a d i n e . C a r d i a c resynchronization therapy (CRT), a device that stimulates the left and right ventricle to contract simultaneously, improves cardiac function and quality of life while decreasing hospitalization and mortality for patients with an ejection fraction (EF) of G 35% and wide QRS (9 1
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