Integrative Physiology

After myocardial infarction (MI), the left ventricle (LV) undergoes molecular, cellular, and extracellular matrix (ECM) changes that dramatically alter the size, shape, and function at the organ level.1 Macrophages phagocytose ne-crotic myocytes, apoptotic neutrophils, and ECM debris, as well as produce cytokines and growth factors that stimulate the activation of fibroblasts.2,3 Activated fibroblasts (myofi-broblasts) promote abundant ECM synthesis and scar forma-tion in the infarct area.4 Matrix metalloproteinases (MMPs) are activated to degrade ECM components to facilitate the re-modeling process. The balance of ECM turnover is critical for stable scar repair. Excessive ECM deposition increases wall stiffness and diastolic dysfunction, whereas insufficient ECM accumulation and impaired collagen cross-linking contribute to cardiac rupture post-MI.5,6 The inflammatory component regulates ECM synthesis, by promoting fibroblast prolifera