Atrial Secondary Tricuspid Regurgitation: Insights Into the EuroTR Registry.

Background: Atrial secondary tricuspid regurgitation (A-STR) has been proposed as an important etiologic subentity of secondary tricuspid regurgitation (STR). Patients with A-STR are frequently treated using transcatheter tricuspid valve edge-to-edge repair (T-TEER).
Objectives: The aims of this study were to evaluate prevalence and outcomes following T-TEER for severe A-STR and to compare the results to patients with nonatrial STR.
Methods: The study included patients from the EuroTR (European Registry of Transcatheter Repair for Tricuspid Regurgitation) registry who underwent T-TEER for STR from 2016 until 2022. A-STR was defined as a ratio of end-systolic right atrial area to right ventricular area ≥1.5 in the presence of preserved right ventricular function (tricuspid annular plane systolic excursion >17 mm). The primary study endpoint was 2-year survival free from heart failure hospitalization. Secondary endpoints were 2-year survival, tricuspid regurgitation (TR) reduction at discharge and 1-year follow-up as well as changes in NYHA functional class.
Results: This study included 641 patients (50% women) with a mean age of 79 ± 7 years. The overall prevalence of A-STR was 31% (n = 196). A-STR was associated with a higher prevalence of atrial fibrillation, less frequent comorbidities, better biventricular function, less leaflet tenting, and larger atria. Although TR severity was comparable at baseline, patients with A-STR had more effective procedural TR reduction (TR ≤2+ in 86.9% vs 80.4% of those with nonatrial STR; P = 0.005). Although NYHA functional class improved in both STR subetiologies, the symptomatic burden was lower in patients with A-STR at the latest available follow-up (NYHA functional class ≥III in 46% of patients with nonatrial STR vs 38% in those with A-STR; P = 0.033). Beyond that, A-STR was associated with higher 2-year survival rates free from heart failure hospitalization (66.3% [Q1-Q3: 58.2%-75.5%] vs 47.5% [Q1-Q3: 41.7%-54.7%] in patients with nonatrial STR; P < 0.001). Median survival follow-up was 379 days [Q1-Q3: 155-697 days].
Conclusions: A-STR is a common phenotype of STR and is associated with effective TR reduction and symptomatic reduction after T-TEER.
Competing Interests: Funding Support and Author Disclosures Dr Stolz has received speaker honoraria from Edwards Lifesciences. Dr Kresoja has received travel expenses from Edwards Lifesciences. Dr von Stein has received lecture honoraria from Edwards Lifesciences. Dr Rottbauer has received speaker honoraria Edwards Lifesciences and Abbott. Der Denti has served as a consultant for InnovHeart, Pi-Cardia, HVR, and Approxima; and has received speaker honoraria from Abbott and Edwards Lifesciences. Dr Rassaf has received speaker honoraria and consulting fees from AstraZeneca, Bayer, Pfizer, and Daiichi-Sankyo. Dr Barreiro-Perez has received speaker fees from Abbott Vascular, Edwards Lifesciences, and Venus Medtech. Dr Adamo has received consulting fees in the past 3 years from Abbott Structural Heart and Edwards Lifesciences. Dr von Bardeleben has received institutional grants from and served as a speaker for Abbott Vascular and Edwards Lifesciences. Dr Toggweiler has received personal honoraria from Medtronic, Boston Scientific, Biosensors, Abbott Vascular, Medira, Shockwave Medical, Teleflex, atHeart Medical, Cardiac Dimensions, Polares Medical, Amarin, Sanofi, AstraZeneca, ReCor Medical, and Daiichi-Sankyo; has received institutional research grants from Edwards Lifesciences, Boston Scientific, Fumedica, Novartis, and Boehringer Ingelheim; and holds equity in Hi-D Imaging. Dr Metra has received consulting fees in the past 3 years from Abbott Structural Heart, AstraZeneca, Bayer, Boehringer Ingelheim, Edwards Lifesciences, and Roche Diagnostics. Dr Geisler has received speaker honoraria and research grants from AstraZeneca, Bayer, Bristol Myers Squibb/Pfizer, Ferrer/Chiesi, Medtronic, and Edwards Lifesciences (all unrelated to this study). Dr Estévez-Loureiro has received speaker fees from Abbott Vascular, Edwards Lifesciences, Boston Scientific, and Venus Medtech. Dr Lüdike has received speaker honoraria and consulting fees from AstraZeneca, Bayer, Pfizer, and Edwards Lifesciences; and has received research honoraria from Edwards Lifesciences. Dr Maisano received grant and/or research institutional support from Abbott, Medtronic, Edwards Lifesciences, Biotronik, Boston Scientific, NVT, Terumo, and Venus Medtech; has received consulting fees and personal and institutional honoraria from Abbott, Medtronic, Edwards Lifesciences, Xeltis, Cardiovalve, Occlufit, Simulands, Mtex, Venus, Squadra, and Valgen; has received royalty income from and holds intellectual property rights with Edwards Lifesciences; and is a shareholder (including share options) in Magenta, Transseptal Solutions, and 4Tech. Dr Praz has received travel expenses from Edwards Lifesciences, Abbott Vascular, Polares Medical, Medira, and Siemens Healthineers. Dr Kessler has received speaker honoraria from Edwards Lifesciences and Abbott. Dr Kalbacher has received personal fees from Abbott Medical, Edwards Lifesciences, Pi-Cardia, and Medtronic. Dr Rudolph has received research grants from Abbott Medical, Boston Scientific, and Edwards Lifesciences. Dr Iliadis has received consultant fees and travel expenses from Abbott Medical and Edwards Lifesciences. Dr Lurz has received institutional grants from Edwards Lifesciences; and has received honoraria from Innoventrics. Dr Hausleiter has received research grant support and speaker honoraria from Edwards Lifesciences. Dr Sticchi has served on an advisory board for Edwards Lifesciences. Dr Tarantini has received speaker fees from Abbott Vascular and Edwards Lifesciences. Dr Karam has received consultant fees from Edwards Lifesciences, Boston Scientific, and Medtronic; and has received proctor fees from Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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