Left ventricular mass regression after aortic valve replacement: Does size really matter?

Abstract

Since the initial conceptual description of prosthesis-patient mismatch by Rahimtoola in 1978, many studies have been published that have substantiated or called into question its clinical relevance among patients undergoing aortic valve replacement. Most of these studies have narrowly focused on seeking correlations among transprosthetic gradients, indexed effective orifice area, left ventricular (LV)mass regression, and postoperative survival. Conclusions have been inconsistent, suggesting that the determinants of survival after aortic valve replacement may be more complex than simple replacement of a stenotic native valve with a prosthetic that is often just less stenotic. With this notion as a backdrop, Helder and colleagues’ broader analysis of a wider array of factors that might affect LV mass regression prompts provocative questions pertaining to the relative impact of aortic valve replacement on survival, and the significant effects adjunctive therapeutics might exert. The authors quite reasonably analyzed each factor in the context of its effect on LV mass regression based on the well-established premise that LV hypertrophy (LVH) negatively affects postoperative survival after aortic valve replacement. Of most interest in this study were the findings that treatment with beta-blockers or calciumchannel blockers at discharge was independently associated with an increased probability of complete LV mass regression, whereas prosthesis-patient mismatch was not. These findings, coupled with the observation that there was no difference in 5-year survival rates or New York Heart Association functional status among patients with complete versus incomplete LV mass regression, suggest that the absolute extent of LVH reduction after aortic valve replacement may not affect survival rates or symptomatic status among patients undergoing aortic valve replacement as much as a physiologically meaningful and sustained reduction in ventricular afterload and wall stress afforded by the