Role of noninvasive imaging modalities to better understand the mechanism of left ventricular outflow tract obstruction and tailored lesion-specific treatment options

Abstract

Left ventricular outflow tract obstruction (LVOTO) has important prognostic implications in patients with hypertrophic cardiomyopathy (HCM). Echocardiography provides critical information to establish LVOTO as a unique feature of HCM by demonstrating heterogeneity of hypertrophy patterns and the systolic anterior motion of mitral leaflets, resulting in mitral-septal contact. Currently, 2 treatment strategies are available for reduction of muscle mass to relieve LVOTO: surgical myectomy and percutaneous alcohol septal ablation. Both focus on mechanical removal of the hypertrophied septum. However, this alone is not the best approach to abolishing LVOTO, because recurrence is common and requires additional septal reduction. Recent 3-dimensional in vivo measurements and other noninvasive cardiac imaging modalities have confirmed primary alterations of the mitral valvular apparatus, including leaflet elongation with increased surface area and abnormal displacement of papillary muscles. More importantly, these extra-myocardial changes appear to be independent factors associated with the development of LVOTO. Other important anatomical changes include anomalous papillary muscle insertion into the anterior mitral leaflet and midventricular obstruction because of apposition of the hypertrophied mid-septum and the papillary muscle. Thus, the myocardium is not the only tissue affected in patients with HCM. A tailored approach to correcting primary changes of the mitral valvular apparatus and hypertrophy pattern based on a comprehensive evaluation using noninvasive imaging modalities is necessary to improve long-term outcomes.