Why the septum thickens in hypertrophic cardiomyopathy
Abstract
In hypertrophic cardiomyopathy (HCM), hypertrophy often disproportionately affects the interventricular septum, especially in the obstructive form (oHCM). The reasons for this septal predilection remain debated. Here, we review emerging evidence that septal hypertrophy in HCM represents a localised, load-driven remodelling response, an adaptive "retrofitting" of the heart's wall to withstand abnormal stress. Congenital differences in septal fibre architecture and chronic sarcomeric hypercontractility create a focal mechanical burden that predisposes the septum to near-isometric contraction (low septal mobility) and drives early hypertrophic remodelling. When present, systolic anterior motion of the mitral valve and left ventricular (LV) outflow tract obstruction (LVOTO) further amplify this load, increase wall stress, and accelerate this process. Analogous to earthquake engineering, where rigid buildings are retrofitted with dampers to absorb shocks, the septum adapts by accumulating viscoelastic elements (e.g., microtubules, titin, collagen) that thicken and stiffen the wall. This structural adaptation protects against further damage by limiting myocardial shortening and reducing wall tension (according to Laplace's law), albeit at the cost of diastolic dysfunction and energetic inefficiency. We integrate haemodynamic studies and new patient-specific computational modelling data to confirm this load-centric model. When LVOTO develops, the added external load activates the…
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