Long mitral valve leaflets determine left ventricular outflow tract obstruction during exercise in hypertrophic cardiomyopathy
Development of left ventricular outflow tract obstruction (LVOTO) in patients with hypertrophic cardiomyopathy (HCM) is important for explaining symptoms and designing management. LVOTO is mostly caused by a combination of septal hypertrophy and systolic anterior movement of the mitral valve (SAM). The aim of the present study was to determine predictors of exercise induced LVOTO in a group of HCM patients.
We performed supine exercise Doppler echocardiography, including measurements of LV morphology and function and anterior mitral leaflet length, in 51 mildly symptomatic HCM (septal thickness ≥ 15 mm) and compared them with 50 healthy controls. Measurements were made at 1) rest, 2) Valsalva maneuver, 3) peak exercise and 4) post exercise. LVOTO was diagnosed as a LVOT gradient of >30 mm Hg at rest, after Valsalva and after exercise or ≥50 mm Hg at peak exercise.
All patients stopped exercise because of exhaustion. 35% of the patients had resting LVOTO and 48% during Valsalva. At peak exercise, only 37% had LVOTO, who increased to 64% post exercise. Patients who developed LVOTO at peak exercise were more prone to continue having it post exercise (p < 0.001), to have attenuated systolic blood pressure rise (p = 0.011) and to have long anterior mitral valve leaflets (p < 0.001). Backward multiple regression analysis showed the anterior mitral leaflet length as the strongest single independent predictor (β = 0.36, p = 0.010) for increased LVOT velocities, followed by basal septal thickness.
In patients with HCM, LV outflow tract obstruction seems to be relatively uncommon during exercise but rather occurring minutes after stopping exercise. Exercise LVOTO seems to be determined by long anterior mitral leaflets in addition to the well established septal hypertrophy.
Keywords:Anterior mitral leaflet, Exercise echocardiography, Hypertrophic cardiomyopathy, Obstruction, Systolic anterior motion
Autor / Fonte:Michael Henein, Sandra Arvidsson, Björn Pilebro, Christer Backman, Stellan Mörner, Per Lindqvist International Journal of Cardiology 2016 March 16, 212: 47-53