Left ventricular hypertrophy is typically characterized by myocyte disarray

Pathophysiology of HCM:

Left ventricular hypertrophy is typically characterized by myocyte disarray, with cardiomyocytes varying in size and shape and forming abnormal intercellular connections. There is also small vessel disease, in which intramural coronary vessels are apparently narrowed by medial hypertrophy.

Systolic septal bulging into the LVOT and hyperdynamic LV contraction (causing the Venturi effect) contribute to the creation of a variable LVOT gradient that increases with decreased afterload.

Approximately 25% of patients have dynamic LVOT obstruction caused by contact between the anterior or, less commonly, the posterior mitral valve leaflet and the interventricular septum during systole (systolic anterior motion—SAM).

Severe LV hypertrophy results in increased chamber stiffness and diastolic dysfunction.

Intrinsic abnormalities of the mitral apparatus, including fibrous leaflet thickening, prolapse, and malposition of the anterior papillary muscle, occur in an estimated 20% of patients with HCM and contribute to the obstruction