Background: Atrial fibrillation (AF) itself may lead to functional tricuspid regurgitation (FTR) through tricuspid annulus (TA) dilation. However, the pathophysiological determinants of TA enlargement in AF patients remain to be clarified. The objectives of this study were (1) to compare the TA size and function in AF patients versus healthy subjects; (2) to identify the determinants of TA remodeling in patients with AF and FTR;and (3) to assess the relationships among right heart structures and severity of FTR in AF patients.Methods: Eighty-three consecutive patients with long-term persistent AF and FTR (61 6 9.9 years, 67% women) were prospectively enrolled and compared with 83 sex and body surface area-matched healthy subjects. Heart chamber size and function and TA geometry were analyzed using three-dimensional echocardiography.Results: Among AF patients, 33%, 34%, and 33% had mild, moderate, and severe FTR, respectively. Right atrial (RA) dilation was detected in 93% of AF patients, while only 27% and 12% of them showed dilated or dysfunctional right ventricle (RV), respectively. End-diastolic TA area had the strongest correlation with the minimum volume of the RA (RAVmin r = 0.6981, P < .0001) but only mild correlation with RV end-diastolic volume and sex (r = 0.3405, P = .0019; r = 0.2914, P = .0075). At multivariable analysis, only RAVmin was independently associated with TA area in AF patients (r = 0.665, P < .0001). The RAVmin and TA area were the only predictors of FTR severity. Conclusions:In patients with AF, RA dilation seems to be more important than RV dilation to determine TA enlargement and subsequent FTR development. The RAVmin and TA area were directly correlated to FTR severity.

AimWe sought to evaluate the differences in prognosis between the atrial (A-STR) and the ventricular (V-STR) phenotypes of secondary tricuspid regurgitation.Materials and methodsConsecutive patients with moderate or severe STR referred for echocardiography were enrolled. A-STR and V-STR were defined according to the last ACC/AHA guidelines criteria. The primary endpoint was the composite of all-cause death and heart failure (HF) hospitalizations.ResultsA total of 211 patients were enrolled. The prevalence of A-STR in our cohort was 26%. Patients with A- STR were significantly older and with lower NYHA functional class than V-STR patients. The prevalence of severe STR was similar (28% in A-STR vs. 37% in V-STR, p = 0.291). A-STR patients had smaller tenting height (TH) (10 ± 4 mm vs. 12 ± 7 mm, p = 0.023), larger end-diastolic tricuspid annulus area (9 ± 2 cm2 vs. 7 ± 6 cm2/m2, p = 0.007), smaller right ventricular (RV) end-diastolic volumes (72 ± 27 ml/m2 vs. 92 ± 38 ml/m2; p = 0.001), and better RV longitudinal function (18 ± 7 mm vs. 16 ± 6 mm; p = 0.126 for TAPSE, and −21 ± 5% vs. −18 ± 5%; p = 0.006, for RV free-wall longitudinal strain, RVFWLS) than V-STR patients. Conversely, RV ejection fraction (RVEF, 48 ± 10% vs. 46 ± 11%, p = 0.257) and maximal right atrial volumes (64 ± 38 ml/m2 vs. 55 ± 23 ml/m2, p = 0.327) were similar between the two groups. After a median follow-up of 10 months, patients with V-STR had a 2.7-fold higher risk (HR: 2.7, 95% CI 95% = 1.3–5.7) of experiencing the combined endpoint than A-STR patients. The factors related to outcomes resulted different between the two STR phenotypes: TR-severity (HR: 5.8, CI 95% = 1, 4–25, P = 0.019) in A-STR patients; TR severity (HR 2.9, 95% CI 1.4–6.3, p = 0.005), RVEF (HR: 0.97, 95% CI 0.94–0.99, p = 0.044), and RVFWLS (HR: 0.93, 95% CI 0.85–0.98, p = 0.009) in V-STR.ConclusionAlmost one-third of patients referred to the echocardiography laboratory for significant STR have A-STR. A-STR patients had a lower incidence of the combined endpoint than V-STR patients. Moreover, while TR severity was the only independent factor associated to outcome in A-STR patients, TR severity and RV function were independently associated with outcome in V-STR patients.

Functional tricuspid regurgitation (FTR) is a strong and independent predictor of patient morbidity and mortality if left untreated. The development of transcatheter procedures to either repair or replace the tricuspid valve (TV) has fueled the interest in the pathophysiology, severity assessment, and clinical consequences of FTR. FTR has been considered to be secondary to tricuspid annulus (TA) dilation and leaflet tethering, associated to right ventricular (RV) dilation and/or dysfunction (the “classical”, ventricular form of FTR, V-FTR) for a long time. Atrial FTR (A-FTR) has recently emerged as a distinct pathophysiological entity. A-FTR typically occurs in patients with persistent/permanent atrial fibrillation, in whom an imbalance between the TA and leaflet areas results in leaflets malcoaptation, associated with the dilation and loss of the sphincter-like function of the TA, due to right atrium enlargement and dysfunction. According to its distinct pathophysiology, A-FTR poses different needs of clinical management, and the various interventional treatment options will likely have different outcomes than in V-FTR patients. This review aims to provide an insight into the anatomy of the TV, and the distinct pathophysiology of A-FTR, which are key concepts to understanding the objectives of therapy, the choice of transcatheter TV interventions, and to properly use pre-, intra-, and post-procedural imaging.