Unchecked disease-related stress and hypertrophic remodeling in ventricular pressure overload become maladaptive and predispose to cardiovascular morbidity and mortality.
H ypertrophic growth of ventricular myocytes is a hallmark feature of numerous forms of cardiovascular disease. ther cellular elements within the ventricle, fibroblasts, vascular smooth muscle cells, and endothelium, also manifest intricate stress responses, resulting in fibrosis, inflammatory cell infiltration, endothelial dysfunction, and vascular stiffness. Current thinking holds that these events, the reaction of the heart to a host of pathological stresses, provide short-term benefit. However, if disease-related stress remains unchecked, these remodeling events become maladaptive and predispose to cardiovascular morbidity and mortality.
Schiattarella et al. (Tue,) conducted a review in Ventricular pressure overload and hypertrophy. Inhibition of hypertrophy was evaluated. Unchecked disease-related stress and hypertrophic remodeling in ventricular pressure overload become maladaptive and predispose to cardiovascular morbidity and mortality.