Muscular subaortic stenosis: The temporal relationship between systolic anterior motion of the anterior mitral leaflet and the pressure gradient

Abstract

Recent studies indicate that in patients with muscular subaortic stenosis at rest, left ventricular outflow tract obstruction is associated with severe systolic anterior motion (SAM) of the anterior mitral leaflet and prolonged SAM-septal contact. We correlated the temporal relatioships between echocardiographic and hemodynamic events in 18 patients with muscular subaortic stenosis (gradient of 73 ± 18 mm Hg [mean ± SD]). After the ECG R wave, aortic ejection began at 72 ± 12 msec and the onset of SAM 23 msec later, at 95 ± 22 msec. The onset of the pressure gradient at 162 ± 22 msec after the R wave was almost simultaneous with the onset of SAM-septal contact at 168 ± 28 msec. SAM-septal contact was maintained for 195 msec and ceased at 363 ± 41 msec after the R wave. Peak posterior left ventricular wall movement occurred at 387 ± 48 msec, 219 msec after peak SAM (the onset of SAM-septal contact). The excursion and mean rate of development of SAM from onset to septal contact (14 ± 2 mm and 208 ± 55 mm/sec, respectively) were almost three times the excursion and mean rate of inward movement of the posterior wall in the same period of systole (5 ± 1 mm and 75 ± 16 mm/sec, respectively). In terms of the systolic ejection period, SAM began at 6.0 ± 6%, and the onset of the pressure gradient and SAM-septal contact were almost simultaneous, at 23 ± 5% and 25 ± 7%, throughout this period. The end of SAM-septal contact occurred at 76 ± 10% of the systolic ejection period and peak posterior left ventricular wall movement occurred at 82 ± 12%. We conclude that the onset of SAM is a very early systolic event. The onset of the pressure gradient occurs just before or with the onset of SAM-septal contact, suggesting a cause-and-effect relationship. Posterior wall hyperkinesis plays no part in the genesis of SAM in these patients, judging by the differing rate and extent of excursion of SAM and the posterior wall and the fact that peak left ventricular wall movement occurs 219 msec after peak SAM (onset of SAM-septal contact). Tethering of the anterior mitral leaflet by the papillary muscles is not the cause of SAM, since SAM-septal contact ceases at 76 ± 10% of the systolic ejection period, whereas a tethering effect should last until end-systole. SAM is most likely caused by a Venturi effect related to rapid early systolic ejection.