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 adaptivebecause the parallel deposition of new sarcomeres and the correspondingLV wall thickening succeeded in normalizing LV systolic wallstress despite the high intracavitary systolic pressure.¹ Inaortic stenosis, the validity of this paradigm was demonstratedby haemodynamic studies, which established an inverse relationshipbetween LV systolic wall stress and LV ejection fraction (EF)and by clinical outcome studies, which demonstrated worse post-operativeprognosis if LV performance fell below this inverse LV wallstress–LVEF relationship.^2,3 This clinical paradigm ofadaptive myocardial hypertrophy developing during progressionof aortic stenosis clearly withstood the test of time despitethe mounting epidemiological evidence of LV hypertrophy beingassociated with excess cardiac mortality and despite the ominoussignificance of LV hypertrophy in congenital aortic stenosis. Kupari et al.⁴ were the first to challenge the time-honoured