Key result
Multiscale mathematical models of the failing heart demonstrate that cellular remodeling, including action potential prolongation and altered calcium handling, contributes to arrhythmogenesis and contractile dysfunction.
This review provides an overview of human models used to simulate cellular remodeling in heart failure, bridging the gap from single-cell membrane excitation to whole-heart contraction.
Models support mechanistic understanding of HF remodeling; extends computational approaches but leaves open clinical validation.
Heart failure is characterized as any heart condition resulting from impairment of the heart's ability to pump blood, with high prevalence in both aged and diseased hearts. Numerous population-based studies have shown that, in patients with impaired left ventricular systolic function, additional structural and functional cardiovascular abnormalities are often found, making it difficult to understand the underlying pathophysiological processes. Advances in experimental and modeling tools have led to the identification of many cellular mechanisms that contribute to cardiac failure. Still, the mechanism by which cardiac myofiber adaptation ultimately leads to failure remains unclear. Several human cell, tissue, and organ models are used to model heart failure. In this mini review, several available human models are summarized with a focus on the simulation of cellular remodeling: from membrane excitation at the level of the single cell to contraction of the ventricle.
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Ani Amar (2018) conducted a review in Heart failure. Multiscale mathematical models of the failing heart demonstrate that cellular remodeling, including action potential prolongation and altered calcium handling, contributes to arrhythmogenesis and contractile dysfunction.
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