[Left ventricular remodeling in patients with hypertrophic obstructive cardiomyopathy treated with percutaneous alcohol septal ablation: an echocardiographic study].

INTRODUCTION In patients with hypertrophic obstructive cardiomyopathy, obstruction in the left ventricular outflow tract may generate more hypertrophy. Our aim was to evaluate the impact of reducing ventricular outflow tract obstruction on left ventricular hypertrophy and remodeling after alcohol septal ablation. PATIENTS AND METHOD 20 patients with hypertrophic obstructive cardiomyopathy who underwent alcohol septal ablation were included. Doppler echocardiography was performed in all patients at baseline, immediately after alcohol septal ablation, and at 3 and 12 months' follow-up. Left ventricular diameters and wall thickness and pressure gradients in the ventricular outflow tract were determined. RESULTS Immediately after alcohol septal ablation, ventricular outflow tract pressure gradient decreased from 63.0 27.7 to 28.2 24.7 mmHg (p < 0.001), without significant changes in left ventricular dimensions. However, after 12 months we observed an increase in left ventricular end-diastolic (from 47.1 4.9 to 50.8 4.5 mm) and end-systolic diameter (from 27.1 3.0 to 33.7 4.6 mm), as well as a reduction in septal (from 19.5 4.0 to 15.5 2.7 mm) and posterior wall thickness (from 14.0 2.2 to 12.9 1.3 mm) (p < 0.01 in all cases). Left ventricular end-diastolic and end-systolic volumes increased (from 106.4 26.9 to 123.1 28.7 ml and from 50.2 17.3 to 56.7 18.3 ml, respectively, p < 0.01 in both cases), without changes in left ventricular ejection fraction. The reduction in ventricular outflow tract pressure gradient at 12 months' follow-up correlated significantly with the increase in left ventricular end-systolic diameter (r = 0.63; p < 0.01). CONCLUSIONS In patients with hypertrophic obstructive cardiomyopathy who underwent alcohol septal ablation, relief of ventricular outflow tract obstruction is associated with an increase in left ventricular chamber diameters and volume. These findings suggest that middle- and long-term ventricular remodeling and regression of hypertrophy occur in these patients, which may contribute to their clinical improvement.