Congestive heart failure (CHF) is a debilitating disease that is generally initiated by some index cardiac event and ultimately characterized by left ventricular (LV) remodeling which dramatically alters the mechanical environment about the heart. It is well established that mechanical stimuli (e.g., stress or strain) are important epigenetic factors in cardiovascular development, adaptation, and disease.1–3 Interestingly, abnormal cardiac kinematics is often considered a symptom of heart failure when in actuality it is likely a primary contributing factor to the relentless progression of the disease.4 Cellular responses to pathologic mechanical factors lead to further pathologic remodeling and a positive feedback loop emerges such that eventually a threshold is reached wherein the neurohormal compensatory mechanisms activated to maintain homeostasis following the initial cardiac event are no longer sufficient to deter further progression of the disease. Consequently, treatment strategies that fail to remedy the aberrant mechanical environment become increasingly ineffective as the disease progresses.

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