“…Increasingly, primary abnormalities of the mitral valve apparatus in HCM, including abnormal leaflet coaptation, leaflet elongation, chordal slack, and papillary muscle displacement, have been recognized as promoting SAM and generating obstruction [14, 15]. Even in the absence of HCM, SAM has still been shown to occur following treadmill exercise or dobutamine stress [16, 17]. In these settings, intrinsic abnormalities of the mitral apparatus were postulated to be sufficient to cause SAM, independent of significant LV septal wall hypertrophy being present.…”