Low Left Ventricular Mass in Aortic Stenosis: A Distinct Mode of Adaptation to Pressure Overload Associated with Better Contractility?

Abstract

Introduction About 10-30% of patients with severe aortic stenosis (AS) do not develop left ventricular hypertrophy (LVH). Intriguingly, the absence of LVH does not adversely affect outcome in AS, which challenges the classical notion of LVH as a beneficial compensatory response. Notably, only a few studies have attempted to characterize AS subjects with inadequately low LV mass (low-LVM) relative to afterload. We hypothesized that the low-LVM phenotype may be linked to myocardial function irrespective of AS severity. Aim: To assess relations between LV myocardial function and load in patients with low-LVM and moderate or severe AS. Methods We retrospectively analyzed hospital records of 227 patients with moderate or severe degenerative AS in sinus rhythm. Subjects with low-LVM were compared to those with appropriate or excessive LVM (ae-LVM), defined on the basis of the ratio of a measured LVM to the LVM predicted from an individual hemodynamic load. Circumferential end-systolic LV wall stress (cESS) and valvulo-arterial impedance (Zva), indices of LV afterload, were calculated from echocardiography and blood pressure. Assuming a constant LV wall volume during the cardiac cycle, we also computed LV midwall fractional shortening (mwFS), a better estimate of LV myocardial function than EF in concentric LV geometry. Results Patients with low-LVM and ae-LVM did not differ in aortic valve area, blood pressure, symptomatic status, prevalence of CAD or diabetes, end-diastolic LV diameter (a raw measure of LV preload), as well as Zva and cESS (estimates of LV afterload). Compared to ae-LVM, patients with low-LVM had higher mwFS (by 20−30%) in both moderate AS (p 0.5). Conclusions Subjects with low LVM maintain constant cESS during AS progression, probably due to higher LV contractility than in the majority of AS patients in whom the magnitude of LVH rises gradually over time. Thus, low LVM is associated with enhanced myocardial function, which may reflect a distinct mode of adaptation to chronic pressure overload, occurring already in less than severe AS. Whether better myocardial function contributes to favorable prognosis in AS without LVH, remains to be studied.