Early Recovery of Left Ventricular Systolic Function after Transcatheter Aortic Valve Implantation.

Background: A lot of studies have shown a positive effect of transcatheter aortic valve implantation (TAVI) on left ventricular ejection fraction (LVEF).

Objectives: We aimed to investigate the effect of TAVI on left ventricular function and correlate this phenomenon with hypertrophy degree in an early follow-up.

Materials and Methods: Between August 2015 and July 2016, 250 consecutive patients with symptomatic severe aortic stenosis (AS) underwent TAVI in our institution. Given the aim of this analysis, only patients with an LVEF <50%, no more than moderate mitral valve regurgitation, successful valve implantation, and 1-month follow-up available were included in the study ( n = 46). Patients were enrolled in a prospective database, with clinical and echocardiographic evaluations at 1 month after TAVI.

Results: All patients had severe symptomatic AS (mean transaortic pressure gradients: 44.1 ± 13.8 mmHg and mean aortic valve area: 0.66 ± 0.19 cm2 ). Mean baseline LVEF was 39.3 ± 8.8%. Significant hemodynamic improvement was observed after TAVI. Mean transvalvular aortic gradient decreased significantly from 44.1 ± 13.8 mmHg to 8.9 ± 4.2 mmHg ( P < 0.005). A statistically significant improvement in LVEF compared to baseline was observed in the 1st month of follow-up (39.3 ± 8.8% vs. 44.1 ± 10.1%, P < 0.019). Overall, 52.2% of patients showed an increase in LVEF, 32.6% had no change, while only 2.2% had a decrease in LVEF. Interestingly, we found a significant reverse correlation between LVEF improvement and ventricular hypertrophy measured as diastolic interventricular septum thickness (Pearson index r = -0.42). Patients showing greater improvement in LVEF were those with less than moderate hypertrophy.

Conclusions: Patients with depressed systolic function show a consistent and early LVEF recovery after TAVI. An impaired LVEF recovery is most likely among patients with more than moderate hypertrophy, probably responsible of left ventricular fibrosis that irremediably compromises systolic function.