Early post-surgery left ventricular changes helps to identify patients with residual valvular cardiomyopathy in primary valvular regurgitation

Background Left ventricular systolic dysfunction (LVSD) may occur transiently or persistently after surgical correction for valvular regurgitation, and persistent LVSD may represent a phenotype of residual valvular cardiomyopathy. While reductions in left ventricular ejection fraction (LVEF) and left ventricular size are recognized early postoperative changes following relief of chronic volume overload, their interaction and prognostic implications remain poorly defined. Purpose To characterize acute post-surgery dimensional and functional LV changes and identify predictors for chronic LV recovery in patients with early post-operative LVSD. Methods A prospective cohort study was conducted in which consecutive patients with acute post-operative LVSD (LVEF <50%) in 7-14 days after surgical correction for severe aortic and/or mitral regurgitation who were treated with guideline directed medical therapy (GDMT). LVEF and LV end-diastolic diameter (LVEDD) were assessed preoperatively, early postoperatively, and at 6-month follow-up. LV recovery was defined as the LVEDD < 50mm for women, <55mm for men and the LVEF≥50% at 6 months. Results A total of 215 patients (aged 57 ± 12 years, 79.5% males) were enrolled. Patients were stratified into two groups, i.e., new-onset LVSD (normal preoperative LVEF, n = 115) and persistent LVSD (LVEF <50% both pre- and postoperatively, n = 100). Both groups exhibited acute decreases in LVEDD and LVEF, with significant improvement at 6 months (Figure 1a). The new-onset LVSD group had smaller LVEDD and higher LVEF at baseline and early postoperatively, as well as greater early postoperative reductions in LVEDD and LVEF (∆LVEDD and ∆LVEF) (all P<0.05) (Figure 1a). Notably, ∆LVEDD and ∆LVEF were not correlated in either group (Figure 1b). Four distinct LV change patterns were defined according to ∆LVEDD and ∆LVEF thresholds, with significantly different distributions between the two groups (Figure 1b). LV recovery rates differed significantly across patterns in both groups (Figure 1c). Patients with ∆LVEDD ≥10 mm had higher LV recovery rates irrespective of ∆LVEF (new-onset LVSD: 68.8% vs. 50.0%, p=0.065; persistent LVSD: 54.3% vs. 29.6%, p=0.015). In contrast, ∆LVEF ≥10% vs. <10% was not associated with LV recovery, independent of ∆LVEDD (all P>0.05). Multivariable logistic regression demonstrated that greater ∆LVEDD, but not ∆LVEF, was an independent predictor of LV recovery in both groups (Figure 2). Conclusion This study demonstrates a distinct biphasic response after surgical correction of valvular regurgitation in patients with postoperative LVSD, that is, an initial phase of LV shrinkage and functional decline, followed by recovery under GDMT. Importantly, LV shrinkage did not correlate with LVEF reduction. Early reduction in LVEDD (∆LVEDD), but not ∆LVEF, indicated preserved ventricular adaptation to volume unloading and was a robust predictor of long-term LV recovery.