Hypertrophic cardiomyopathy (HCM) is a poorly understood, heritable cardiac disease affecting > 1 in 500 persons. HCM is characterised by progressive enlargement of the primary pumping chamber of the heart, the left ventricle, wherein the heart muscle is abnormally thick. Patients with HCM can develop left ventricular outflow tract obstruction (LVOTO), a blockage of the path by which blood is pumped out of the heart. Drug-refractory patients with HCM LVOTO can be treated by a septal myectomy (SM), where parts of the heart are surgically removed, alcohol septal ablation (ASA), where alcohol is injected in the heart to kill unwanted tissue, or potentially through Mavacamten a novel sarcomere modulator, however which treatment is best in each patient is not known.
Physics based patient specific models of the heart have been used to optimise therapies for rhythm disorders. In this study we will create patient specific models of HCM patients. We will:
Develop workflows to rapidly create patient specific biomechanical models from routine clinical images in HCM patients.
Test if inferred myocardial properties (shape, stiffness, contraction, pre-load or after-load) correlate with known genetic causes of HCM.
Create models to simulate the effect of Mavacamten, SM and ASA on cardiac contraction.
Test if simulations of each therapy based on pre-procedural data predicts post procedural measurements in patients undergoing each procedure.