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Review
. 2024 Feb;11(1):1-12.
doi: 10.1002/ehf2.14575. Epub 2023 Nov 10.

Enhancing myocardial function with cardiac contractility modulation: potential and challenges

Zihan Li  1   2 , Qiming Liu  1 , Shenghua Zhou  1 , Yichao Xiao  1
Affiliations
Review

Enhancing myocardial function with cardiac contractility modulation: potential and challenges

Zihan Li et al. ESC Heart Fail. 2024 Feb.

Abstract

Cardiac contractility modulation (CCM) offers a novel therapeutic avenue for heart failure patients, particularly those unresponsive to cardiac resynchronization therapy within specific QRS duration ranges. This review elucidates CCM's mechanistic underpinnings, its impact on myocardial function, and utility across patient demographics. However, CCM is limited by insufficient data on mortality and hospitalization rate reductions, as well as the need for specialized device implantation skills. While prevailing research has concentrated on left ventricular effects, a knowledge gap persists for other patient subsets. Future inquiries should address combinatory treatment strategies, extended usage and the impact of atrial fibrillation on device implantation. Such expanded studies could refine therapeutic outcomes and widen the scope of beneficiaries.

Keywords: Cardiac contractility modulation; Cardiac devices; Device implantation; Heart failure.

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Conflict of interest statement

The authors have nothing to disclose.

Figures

Figure 1
Figure 1
Primary mechanism of CCM in treating HF. CCM enhances cardiac contractility by up‐regulating MHC‐α expression, promoting intracellular calcium handling, and increasing sympathetic nerve activity in the muscles. CCM, cardiac contractility modulation; PLB, phospholamban; SERCA‐2a, sarcoplasmic reticulum calcium ATPase; SR, sarcoplasmic reticulum.
Figure 2
Figure 2
Main changes after 3 months of CCM therapy.
Figure 3
Figure 3
Main mechanism of factors affecting CCM. CCM, cardiac contractility modulation; SR, sarcoplasmic reticulum; PKA, protein kinase A. Ca2+ can be released by SR, which can be promoted by activated CaV1.2 channels; PKA can excite CaV1.2 channels after the action of adrenaline on beta receptors.
See this image and copyright information in PMC

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