The impact of disopyramide on exercise capacity among patients with obstructive hypertrophic cardiomyopathy: beyond left ventricular outflow tract gradient

Hypertrophic cardiomyopathy (HCM) is a genetic cardiomyopathy de- fined by thickening of the left ventricle not explained by other causes. Approximately two-thirds of HCM patients suffer from left ventricu- lar outflow tract obstruction (LVOTO), i.e. obstructive HCM (oHCM), which frequently manifests with syncope, dyspnoea, and exercise intolerance.1,2 Treatment of oHCM focuses on symptoms. First-line treatments consist of cardioselective beta-blockers or non- dihydropyridine calcium channel blockers.3 Disopyramide, a class Ia antiarrhythmic with a strong negative ino- tropic and chronotropic effect, has traditionally been considered after failure of first-line agents but prior to septal reduction strategies.4–7 In recent years, the selective myosin ATPase inhibitor mavacamten has shown favourable results in terms of symptom relief, cardiac bio- markers improvement, LVOTO reduction, and improvements in car- diopulmonary exercise test (CPET) parameters such as peak oxygen consumption (pVO2).8,9 While beta-blockers and calcium channel blockers have failed to demonstrate improvements in pVO2, there is limited evidence about the impact of disopyramide on CPET parameters as well as on dynamic left ventricular gradient. Therefore, this study aims to examine the effects of disopyramide on exercise capacity and dynamic left ventricular gradient assessed by CPET combined with concomitant transthoracic stress echocardiog- raphy (TTE-CPET).