Noninvasively estimated left ventricular stiffness >0.08 mL-1 at rest or during exercise predicted better clinical outcomes in asymptomatic patients with moderate to severe mitral regurgitation.
Cohort (n=143)
No
Does noninvasive estimation of left ventricular stiffness at rest and during exercise predict cardiac events in asymptomatic patients with moderate to severe mitral regurgitation?
Noninvasive evaluation of left ventricular stiffness at rest or during exercise provides independent prognostic value for mid-term risk stratification in asymptomatic patients with moderate to severe mitral regurgitation.
p-value: p=0.05
Abstract Background Adaptation to volume overload in mitral regurgitation (MR) decreases left ventricular (LV) chamber stiffness. Compromised diastolic function in MR may contribute to clinical decompensation. Purpose Aim of the study was to evaluate the effect of MR etiology on the noninvasively estimated LV stiffness both at rest (R) and supine exercise ergometry (Ex) and to interrogate potential implications for the outcome. Methods One hundred forty three asymptomatic subjects with moderate to severe MR (pts), followed up on valve clinic in a tertiary center (age 56±14), were referred for Ex. Fifty-three had myxomatous substrate (Myx), 57 fibroelastic deficiency (FD), 19 functional LV MR (LVfn) and 14 functional atrial MR (ATRfn). Cardiac events (independent decision for surgery, NYHA worsening) during a follow up of 34±25 months occurred in 24 pts. The following parameters (mean±SD) were estimated at R/Ex: Biplane LV enddiastolic volume (LVEDvol), ejection fraction, stroke volume, longitudinal strain, systolic tricuspid pressure gradient (TRPG), transmitral E/e, LV stiffness as the ratio E/e/LVEDvol (mL-1). The slope meanTRPG/cardiac output (CO) was estimated using R/Ex points. Results At R, LV stiffness was greater (thus implying decreased compliance) in ATRfn (0.21±0.16 vs 0.09±0.06 Myx/p0.001, 0.12±0.06 FD/p=0.005, 0.12±0.09 LVfn/p=0.03). During Ex, LVFn and ATRfn had similar stiffness (0.19±0.08 vs 0.16±0.09) and both continued to be greater than Myx(0.10±0.06,p0.001/=0.006 respectively). ATRfn remained also grater at Ex to FD (0.16±0.09, p=0.02). LV stiffness at Ex was related inversely with strain (r=-0.23 p=0.01). The meanTRpG/CO was related with LV stiffness both at R (r=0.4, p=0.001) and Ex (r=0.70, p=0.001) (figure 1). The relationship was also significant for separate analysis of Myx, FD and ATRfn. Pts with outcome events had decreased LV stiffness both at R (0.098±0.06 vs 0.13±0.06 p0.04) and at Ex (0.11±0.08 vs 0.14±0.08, p0.04). ROC analysis for outcome provided similar cut off for LV stiffness at R /Ex (=0.08 with area under curve 0.79/0.91,p=0.002/0.001, sensitivity: 73%/90%, specificity: 83%/83% respectively). Kaplan-Meier analysis using either LV stiffness R or Ex, predicted better outcome for values 0.08 mL-1 (R/Ex: log rank =3.6/6. p=0.05/0.01) overall. The evidence was more specific in the pts not increasing TRPG during Ex 55mmHg. The analysis remained with similar outcome when it was applied only in the degenerative/organic MR (R: log rank=3.3, p=0.05 figure 2). Conclusions LV stiffness differs according to the underlying pathophysiology in asymptomatic moderate to severe MR. Noninvasive evaluation of LV stiffness either at R or Ex may provide an independent contribution for the mid-term risk stratification in both organic and functional MR.
Armenis et al. (Thu,) conducted a cohort in Moderate to severe mitral regurgitation (n=143). Noninvasive left ventricular stiffness was evaluated on Cardiac events (independent decision for surgery, NYHA worsening) (p=0.05). Noninvasively estimated left ventricular stiffness >0.08 mL-1 at rest or during exercise predicted better clinical outcomes in asymptomatic patients with moderate to severe mitral regurgitation.