Better Myocardial Function in Aortic Stenosis with Low Left Ventricular Mass: A Mechanism of Protection against Heart Failure Regardless of Stenosis Severity?

Chyrchel Chyrchel,Nowak-Kępczyk Nowak-Kępczyk,Rożanowska Rożanowska,Kruszelnicka Kruszelnicka,Czestkowska Czestkowska,Długosz Długosz,Bolt Bolt,Surdacki Surdacki,Bałata Bałata,Urbańska Urbańska

doi:10.3390/jcm8111836

Abstract

About one-tenth to one-third of patients with severe aortic stenosis (AS) do not develop left ventricular hypertrophy (LVH). Intriguingly, the absence of LVH despite severe AS is associated with lower prevalence of heart failure (HF), which challenges the classical notion of LVH as a beneficial compensatory response. Notably, the few studies that have attempted to characterize AS subjects with inadequately low left ventricular (LV) mass relative to LV afterload (i-lowLVM) described better prognosis and enhanced LV performance in AS associated with i-lowLVM, but those reports were limited to severe AS. Our aim was to compare myocardial function between moderate and severe AS with i-lowLVM. We retrospectively analyzed in-hospital records of 225 clinically stable nondiabetic patients with isolated moderate or severe degenerative AS in sinus rhythm, free of coexistent diseases. Subjects with i-lowLVM were compared to those with appropriate or excessive LVM (a/e-LVM), defined on the basis of the ratio of a measured LVM to the LVM predicted from an individual hemodynamic load. Patients with i-lowLVM and a/e-LVM did not differ in aortic valve area, LV end-diastolic diameter (LVd, a measure of LV preload), and circumferential end-systolic LV wall stress (cESS), an estimate of LV afterload. Compared to a/e-LVM, patients with i-lowLVM had increased LV ejection fraction (EF) and especially higher LV midwall fractional shortening (a better index of LV myocardial function than EF in concentric LV geometry) (p < 0.001–0.01), in both moderate and severe AS. LVd and cESS were similar in the four subgroups of the study subjects, i.e., moderate AS with i-lowLVM, moderate AS with a/e-LVM, severe AS with i-lowLVM, and severe AS with a/e-LVM (p > 0.6). Among patients with i-lowLVM, LVM did not differ significantly between moderate and severe AS (p > 0.4), while in those with a/e-LVM, LVM was increased in severe versus moderate AS (p < 0.001). In conclusion, the association of the low-LVM phenotype with better myocardial contractility may already develop in moderate AS. Additionally, cESS appears to be a controlled variable, which is kept constant over AS progression irrespective of LVM category, but even when controlled (by increasing LVM), is not able to prevent deterioration of LV function. Whether improved myocardial performance contributes to favorable prognosis and the preventive effect against HF in AS without LVH, remains to be studied.

Highlights

About one-tenth to one-third of patients with severe aortic stenosis (AS) do not develop left ventricular hypertrophy (LVH) [1,2,3,4]
The absence of LVH despite severe AS was associated with better left ventricular (LV) systolic performance [1,2] and threefold lower prevalence of heart failure (HF) [2], which challenges the classical notion of LVH as an adaptive response to pressure overload, aimed at the preservation of LV systolic performance via the normalization of LV wall stress
Patients with moderate AS and i-lowLVM did not differ from their counterparts with moderate AS and appropriate or excessive left ventricular mass (LVM) (a/e-LVM) in terms of clinical (Table 1) and echocardiographic (Table 2) characteristics, except for higher ejection fraction (EF) (65 ± 7 vs. 58 ± 8%, p < 0.01) and midwall fractional shortening (mwFS) (18.9 ± 2.6 vs. 14.0 ± 3.3%, p < 0.001) (Table 2)

Summary

Introduction

About one-tenth to one-third of patients with severe aortic stenosis (AS) do not develop left ventricular hypertrophy (LVH) [1,2,3,4]. In hypertensives with a measured LVM below the 2.5th percentile of the distribution of the LVMpredicted from individual hemodynamic parameters and compared with a reference population, De Simone et al [5] described enhanced afterload-corrected LV myocardial function. With regard to severe AS, Cioffi et al [4] reported a reduced risk of adverse CV outcome in subjects in the lowest tertile of the observed-to-predicted LVM ratio, and we have recently observed an improved LV myocardial and chamber function despite comparable afterload in subjects with severe AS and i-lowLVM, defined as a LVM below the 23th percentile of the predicted LVM [6]

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Conclusion