Left and right ventricular longitudinal systolic function following aortic valve replacement in the PARTNER 2 trial and registry.

Aims: Evaluation of left and right ventricular (RV) longitudinal systolic function may enhance risk stratification following aortic valve replacement (AVR). The study objective was to evaluate the changes in left and RV longitudinal systolic function and RV-pulmonary artery (RV-PA) coupling from baseline to 30 days and 1 year after AVR.
Methods and Results: Left ventricular (LV) longitudinal strain (LS), tricuspid annulus plane systolic excursion (TAPSE), and RV-PA coupling were evaluated in patients from the PARTNER 2A surgical AVR (SAVR) arm (n = 985) and from the PARTNER 2 SAPIEN 3 registry (n = 719). TAPSE and RV-PA coupling decreased significantly following SAVR, but remained stable following TAVR. Lower LV LS, TAPSE, or RV-PA coupling at baseline was associated with increased risk of the composite of death, hospitalization, and stroke at 5 years [adjusted hazard ratios (HRs) for LV LS < 15%: 1.24, 95% confidence interval (CI) 1.05-1.45, P = 0.001; TAPSE < 14 mm: 1.44, 95% CI 1.21-1.73, P < 0.001; RV-PA coupling < 0.55 mm/mmHg: 1.32, 95% CI 1.07-1.63, P = 0.011]. Reduced TAPSE at baseline was the most powerful predictor of the composite endpoint at 5 years. Patients with LV ejection fraction <50% at baseline had increased risk of the primary endpoint with SAVR (HR: 1.34, 95% CI 1.08-1.68, P = 0.009) but not with TAVR (HR: 1.12, 95% CI 0.88-1.42). Lower RV-PA coupling at 30 days showed the strongest association with cardiac mortality.
Conclusion: SAVR but not TAVR was associated with a marked deterioration in RV longitudinal systolic function and RV-PA coupling. Lower TAPSE and RV-PA coupling at 30 days were associated with inferior clinical outcomes at 5 years. In patients with LVEF < 50%, TAVR was associated with superior 5-year outcomes.
Competing Interests: Conflict of interest: J.T. is consultant for Abbott, Philips Healthcare, and General Electric. R.T.H. reports speaker fees from Abbott Structural, Baylis Medical, Edwards Lifesciences, Medtronic, and Philips Healthcare; she has institutional consulting contracts for which she receives no direct compensation with Abbott Structural, Edwards Lifesciences, Medtronic, and Novartis; she is Chief Scientific Officer for the Echocardiography Core Laboratory at the Cardiovascular Research Foundation for multiple industry-sponsored tricuspid valve trials, for which she receives no direct industry compensation. M.-A.C. has research grant with Medtronic and core laboratory contract with Edwards Lifesciences without direct compensation. W.J. is consultant for Boston Scientific and BridgeBio. F.M.A. and N.J.W. have institutional research grants as directors of an academic core lab from Edwards, Abbott, Medtronic, Boston Scientific, Biotronik, Corcyn, and Foldax. They have no personal disclosures. N.A. received speakers fees from Abbott Vascular, GE Healthcare, and Philips ultrasound and research grants from Alnylam and Pfizer. H.C.H. reports institutional research funding from Abbott, Boston Scientific, Edwards Lifesciences, Highlife, Medtronic, and WL Gore; consulting fees from Edwards Lifesciences, Medtronic, Wells Fargo, and WL Gore; and equity in Holistick Medical and Micro Interventional Devices. M.J.M. has served as a Co-Pi for clinical trials for Abbott and Edwards Lifesciences and as Study Chair for a trial for Medtronic. All roles were uncompensated. V.T. is consultant or researcher for Abbott Vascular, Boston Scientific, CryoLife, Edwards Lifesciences, Medtronic, and Shockwave. The other authors have nothing to disclose.
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