Iconoclasts topple adaptive myocardial hypertrophy in aortic stenosis.

For more than 30 years, the development of concentric left ventricular (LV) hypertrophy in pressure overload was considered adaptive because the parallel deposition of new sarcomeres and the corresponding LV wall thickening succeeded in normalizing LV systolic wall stress despite the high intracavitary systolic pressure. In aortic stenosis, the validity of this paradigm was demonstrated by haemodynamic studies, which established an inverse relationship between LV systolic wall stress and LV ejection fraction (EF) and by clinical outcome studies, which demonstrated worse post-operative prognosis if LV performance fell below this inverse LV wall stress–LVEF relationship. This clinical paradigm of adaptive myocardial hypertrophy developing during progression of aortic stenosis clearly withstood the test of time despite the mounting epidemiological evidence of LV hypertrophy being associated with excess cardiac mortality and despite the ominous significance of LV hypertrophy in congenital aortic stenosis. Kupari et al. were the first to challenge the timehonoured concept of adaptive LV hypertrophy in aortic stenosis. In a carefully designed prospective study of patients with isolated aortic stenosis, they observed an inverse relationship between LV mass index and LVEF and a higher prevalence of LV hypertrophy in patients suffering of heart failure. They therefore concluded that the development of LV hypertrophy was actually promoting heart failure instead of preventing it.