Enlargement of left ventricular outflow tract using an autologous pericardial patch for the anterior mitral valve leaflet and septal myectomy through trans-mitral approach for the hypertrophic obstructive cardiomyopathy Zhang et al (1) describe their experience in septal myectomy for hypertrophic obstructive cardiomyopathy. Of 247 consecutive cases with HOCM treated during 2016-2019 with a variety of techniques, this report is on 16 patients who underwent trans-mitral septal myectomy and enlargement of left ventricular outflow with an autologous pericardial patch in transverse configuration. The technique reportedly decreased the gradient from average 90+ to 10+ mm Hg and resolved systolic anterior leaflet motion in all with only mild residual mitral regurgitation. There were no deaths or any other major complications in this group. It is a small group of patients with excellent result but no definitive conclusion can be drawn regarding validity of the technique from this study. The controversy remains regarding the approach, trans-aortic vs. trans-mitral and whether leaflets should be left alone, plicated or lengthened as well as whether mitral valve should be repaired or replaced in addition to septal myectomy. One certainty remains, extended myectomy done either way, is the foundation of the surgical treatment of hypertrophic cardiomyopathy.

It is an elegant albeit limited study reporting effects of pre op LVEF on long term results in patients with RHD undergoing DVR. Study includes146 pqtients out of 201 who underwent DVR in the study period. Although all had some improvement immediate post op, those with preserved EF and smaller left ventricles regardless of type of prostheses used, surgical techniques ( partial or full Sub-valvular Apparatus Preservation), had more sustained improvement after 3-4 years than those with lower EF and more dilation . It can be partially explained by more prevalence of aortic insufficiency in patients with pre op lower EF <50 and dilation ( average LVESD 49 mm vs 32 mm in EF >50). There are myocardial factors which also play a part , those with abnormal LV function have more extensive loss of myofibrils either due to disproportion of mitochondria-to-myofibril ratio or myofibrillar degeneration exhibiting the extent RHD involves myocardium. Structural adaptation may not all be just a result of hemodynamic abnormalities in these patients (1). The recommendation that surgical intervention should occur before the LV starts to dilate or EF drops is well founded and would be impactful in the developing world, an estimated 250,000 deaths occur annually worldwide and 10.5 million disability adjusted life years due to RHD, mostly in young people.