Abstract Body (Do not enter title and authors here): Background:
Obstructive hypertrophic cardiomyopathy (oHCM) features left ventricular hypertrophy, dynamic LV outflow tract (LVOT) obstruction, and diastolic dysfunction, often causing symptoms and reduced quality of life. Mavacamten, a selective cardiac myosin inhibitor, targets oHCM’s underlying pathology. However, real-world data on its full impact—including atrial and right ventricular remodeling—are limited.
Methods:
This single-center retrospective study analyzed 46 symptomatic oHCM patients treated with Mavacamten, assessed at baseline, short-term (1–3 months), and long-term (6–9 months). Serial echocardiographic measurements included left ventricular global longitudinal strain (LV GLS), interventricular septal (IVS) and posterior wall thickness (LVPW), left atrial volume index (LAVI), left atrial (LA) strain, right ventricular (RV) strain, tissue Doppler and transmitral diastolic indices, and RV function metrics: tricuspid annular plane systolic excursion (TAPSE) and fractional area change (FAC). Clinical endpoints were NYHA class, LVOT gradients, and serum B-type natriuretic peptide (BNP).
Results:
Mavacamten was associated with significant symptomatic and structural improvements. At long-term follow-up, 69.5% of patients were NYHA Class I; none required septal reduction therapy. LVOT gradients significantly decreased at rest and with Valsalva (p<0.001). LV GLS improved from 15.1±2% to 20.7±2% (p<0.001), along with reductions in IVS and LVPW thickness, LAVI, and E/E′ ratio (p<0.001).
LA strain rose significantly from 18.9±6% to 37.3±6% (p<0.001), indicating better atrial compliance and reservoir function. RV strain improved from 18.5±4% to 24.1±4% (p<0.001), despite no change in TAPSE or FAC—suggesting early RV myocardial recovery not detected by traditional indices. BNP dropped markedly (267±308 to 40±80 pg/mL, p<0.001). One patient developed asymptomatic LVEF reduction (<50%), prompting discontinuation.
Conclusion:
In this real-world symptomatic oHCM cohort, Mavacamten yielded robust multidimensional cardiac benefits. Beyond LVOT gradient reduction and symptom improvement, it induced significant reverse remodeling with enhanced diastolic function, myocardial strain, and atrial and RV mechanics. Improvements in LA and RV strain—even without TAPSE or FAC changes—highlight strain imaging’s value for early therapy response. These findings affirm Mavacamten as a disease-modifying agent with broad hemodynamic and structural effects in oHCM.