Martin S. Maron

TL;DR: Support is provided that abnormal MBF caused by microvascular dysfunction is responsible for myocardial ischemia-mediated myocyte death, and ultimately replacement fibrosis, providing support that interventional treatment strategies can be initiated earlier in the clinical course to mitigate ischemIA and beneficially alter the natural history of HCM.

TL;DR: CMR observations suggest that the cardiomyopathic process in HCM is more diffuse than previously regarded, extending beyond the LV myocardium to include thickening of the right ventricular wall as well as substantial morphologic diversity with regard to papillary muscles and mitral valve.

TL;DR: In a large longitudinally assessed adult HCM cohort, it is demonstrated that contemporary management strategies and treatment interventions, including ICDs for SD prevention, have significantly altered the clinical course, now resulting in a low disease-related mortality rate of 0.5%/year and an opportunity for extended longevity.

TL;DR: In a high-risk pediatric HCM cohort, ICD interventions terminating life-threatening ventricular tachyarrhythmias were frequent and extreme left ventricular hypertrophy was the most common risk factor present in patients experiencing primary prevention interventions.

TL;DR: Evidence has emerged from observational analyses in large patient cohorts that unequivocally supports subaortic pressure gradients (and obstruction) both as true impedance to LV outflow and independent determinants of disabling exertional symptoms and cardiovascular mortality.