PURPOSE OF REVIEW: Heart failure often progresses despite optimal medical and device therapies, and advanced mechanical circulatory support has limited availability and substantial associated morbidity. Cardiac contractility modulation (CCM) provides nonexcitatory stimulation to ventricular myocardium which increases cardiac contractility without increasing oxygen demand. This review describes the emerging role of CCM in heart failure treatment. RECENT FINDINGS: The FIX-HF-5C2 study demonstrated similar safety and efficacy profile of the two-lead Optimizer device in comparison with the prior three-lead system, thereby decreasing procedural complexity and minimizing endocardial hardware. The FIX-HF-5C trial underscored the benefit of CCM in patients with mild-moderate left ventricular dysfunction (ejection fraction, 25-45%) with New York Heart Association (NYHA) Class III symptoms. The summarized randomized trial data show consistent improvements in peak VO2, 6-min walk distance, and NYHA functional class with CCM. Future trials are planned to determine the role of CCM in heart failure patients with preserved ejection fraction, obligate ventricular pacing, and atrial arrhythmias. SUMMARY: Nonexcitatory extracellular electric potentials can facilitate inotropic improvements in the failing heart. The mechanism of CCM does not increase myocardial oxygen consumption and has been shown to mitigate heart failure symptoms, decrease hospitalizations, and work in synergy with guideline-directed therapy for heart failure.
PURPOSE OF REVIEW: Heart failure often progresses despite optimal medical and device therapies, and advanced mechanical circulatory support has limited availability and substantial associated morbidity. Cardiac contractility modulation (CCM) provides nonexcitatory stimulation to ventricular myocardium which increases cardiac contractility without increasing oxygen demand. This review describes the emerging role of CCM in heart failure treatment. RECENT FINDINGS: The FIX-HF-5C2 study demonstrated similar safety and efficacy profile of the two-lead Optimizer device in comparison with the prior three-lead system, thereby decreasing procedural complexity and minimizing endocardial hardware. The FIX-HF-5C trial underscored the benefit of CCM in patients with mild-moderate left ventricular dysfunction (ejection fraction, 25-45%) with New York Heart Association (NYHA) Class III symptoms. The summarized randomized trial data show consistent improvements in peak VO2, 6-min walk distance, and NYHA functional class with CCM. Future trials are planned to determine the role of CCM in heart failure patients with preserved ejection fraction, obligate ventricular pacing, and atrial arrhythmias. SUMMARY: Nonexcitatory extracellular electric potentials can facilitate inotropic improvements in the failing heart. The mechanism of CCM does not increase myocardial oxygen consumption and has been shown to mitigate heart failure symptoms, decrease hospitalizations, and work in synergy with guideline-directed therapy for heart failure.