Impact of right ventricular dysfunction and dilation on tricuspid regurgitation development following pacemaker implantation

Background Tricuspid regurgitation (TR) is a common complication following pacemaker implantation (PMI). However, it is unclear whether right ventricular (RV) dysfunction or dilation, both of which may contribute to TR development, has a greater influence on TR development after PMI. Methods This single-center, retrospective study included patients undergoing PMI with no or mild TR at baseline echocardiography. Follow-up echocardiography was defined as the first showing significant TR (moderate or greater) or the last available in patients without TR development. RV dysfunction was assessed by tricuspid annular plane systolic excursion (TAPSE) < 17 mm, fractional area change (FAC) < 35%, and free wall strain (FWS) < 20% (absolute value), while RV dilation was defined as RV basal diameter > 41 mm. The primary endpoint was the development of significant TR, and the secondary endpoint was a composite of all-cause death or heart failure hospitalization. Results Among 455 patients included, 166 (37%) developed significant TR during a median follow-up of 4.0 years (IQR: 1.8-7.2). The prevalence of RV dysfunction at baseline was 32% when defined by TAPSE < 17 mm, 39% by FAC < 35%, and 46% by FWS < 20%, while RV dilation was observed in 14% of patients. Patients with baseline RV dysfunction, regardless of whether it was defined by TAPSE, FAC, or FWS, had a higher incidence of TR development (P <0.05 for all), whereas those with RV dilation did not (P=0.11). After adjusting for confounders, FAC < 35% and FWS < 20% at baseline were independently associated with significant TR development (HR [95% CI]: 1.46 [1.05-2.02], P=0.02, and 1.87 [1.31-2.67], P<0.001, respectively), while TAPSE < 17 mm and RV basal diameter > 41 mm were not (HR [95% CI]: 1.35 [0.95-1.93], P=0.09, and 1.53 [0.96-2.45], P=0.08, respectively) (Figure 1). Regardless of significant TR development, changes in RV function from baseline to follow-up were modest, with no significant interactions between TR development and any RV function parameter (TAPSE: P=0.79, FAC: P=0.90, and FWS: P=0.46). In contrast, RV diameter significantly increased at follow-up in patients with TR development but not in those without, resulting in a significant interaction between TR development and RV basal diameter (P<0.001) (Figure 2). The development of significant TR as a time-dependent covariate was independently associated with an increased risk of the secondary composite endpoint, regardless of RV function (each model adjusted for TAPSE, FAC, and FWS) or RV dilation. Conclusions In patients undergoing PMI, impaired FAC and FWS were significantly associated with TR development, whereas RV dilation was not. RV dysfunction, as assessed by FAC and FWS, may be useful for risk stratification of TR development, which is associated with worse outcomes. In contrast, RV dilation may occur as a secondary change related to TR development.