Impact of Right Ventricular Lead Position on Tricuspid Regurgitation and Right Ventricular Function Following Dual-Chamber Pacemaker Implantation

Abstract

Cardiovascular implantable electronic devices (CIEDs) have transformed the management of cardiac arrhythmias and represent one of the most significant advances in modern cardiovascular medicine. Permanent pacemakers remain indispensable in the treatment of bradyarrhythmias, improving cardiac hemodynamics, quality of life, and survival while becoming increasingly utilized worldwide owing to expanding indications and an aging population [1,2]. Despite these undeniable benefits, no cardiac intervention is without limitations. Conventional right ventricular pacing has been associated with adverse structural and functional cardiac remodeling, including left and right ventricular dysfunction, pacing-induced cardiomyopathy, and progressive tricuspid regurgitation (TR) [3,4]. These complications have prompted continued efforts to optimize pacing strategies in order to preserve physiological ventricular activation and improve long-term outcomes. The proposed mechanism underlying pacing-induced cardiac dysfunction is the dyssynchronous electrical activation produced by a lead positioned at the right ventricular apex (RVA). In normal physiology, ventricular depolarization proceeds rapidly through the His–Purkinje system in a coordinated base-to-apex sequence. Apical pacing disrupts this physiological activation pattern, producing electrical and mechanical dyssynchrony that contributes to ventricular remodeling, impaired systolic function, and chamber dilation. Progressive remodeling of the right ventricle and tricuspid annulus, together with the mechanical interaction between the pacing lead and tricuspid valve apparatus, is believed to promote the development and progression of TR [4]. To minimize these detrimental effects, alternative pacing strategies such as right ventricular septal (RVS) pacing and, more recently, conduction system pacing (CSP), have been advocated. These approaches more closely replicate physiological ventricular activation, thereby theoretically reducing ventricular dyssynchrony and limiting adverse remodeling [5]. The study by Morsy et al. investigates this important concept by comparing the short-term effects of RVA and RVS pacing on right ventricular structure, systolic function, and tricuspid valve competence. In this prospective observational study, 100 patients undergoing dual-chamber pacemaker implantation were equally assigned to RVA and RVS pacing groups. Comprehensive echocardiographic assessment, including conventional right ventricular functional indices and speckle-tracking strain imaging, was performed before implantation and repeated after three months. Right ventricular function, right atrial dimensions, and TR severity were systematically evaluated, and notably, complete follow-up was achieved for all enrolled participants [6]. Baseline demographic, clinical, and echocardiographic characteristics were well balanced between the two groups, minimizing baseline confounding. At three months, patients undergoing RVS pacing demonstrated significantly better preservation of right ventricular dimensions and systolic function compared with those receiving RVA pacing. Conventional measures, including tricuspid annular plane systolic excursion (TAPSE), right ventricular fractional area change (RV FAC), and tissue Doppler S′ velocity, together with speckle-tracking-derived right ventricular global longitudinal strain and free-wall longitudinal strain, consistently favored septal pacing, suggesting superior preservation of right ventricular mechanics. With respect to tricuspid valve function, several semi-quantitative echocardiographic markers—including TR jet area, peak velocity, and pressure gradient—favored the RVS group. However, the more objective quantitative parameter, vena contracta width, did not differ significantly between groups. The authors also observed a trend toward an association between increasing right ventricular longitudinal dimension and progression of TR. Although this relationship did not reach statistical significance, it provides an interesting mechanistic observation that merits further investigation in larger cohorts. The authors conclude that septal pacing is associated with reduced early right-sided chamber remodeling and better preservation of right ventricular systolic performance compared with apical pacing. These findings support the concept that pacing site influences early structural and functional cardiac adaptation and reinforce the growing body of evidence favoring more physiological pacing strategies. The study addresses an important and clinically relevant question by evaluating whether a relatively simple modification in lead positioning may reduce the adverse consequences of conventional pacing. Historically, RVA pacing has remained the preferred approach because of procedural simplicity, shorter fluoroscopy time, reproducible lead positioning, and excellent lead stability [7]. In contrast, RVS pacing more closely approximates the native conduction pathway and may partially recruit the intrinsic conduction system, thereby maintaining a more physiological sequence of ventricular activation. The most physiological approach currently available is conduction system pacing, including His bundle pacing and left bundle branch area pacing, which directly engage the native conduction system. However, these techniques require specialized expertise, longer procedural times, and greater financial resources. Consequently, particularly in resource-limited healthcare settings, RVS pacing may represent a practical and cost-effective alternative that offers many of the physiological benefits of CSP without substantially increasing procedural complexity. Although the study contributes valuable evidence, several methodological issues deserve consideration. First, the methodology used to confirm lead position was not clearly described. Fluoroscopic views alone may be insufficient to accurately distinguish septal from anterior or free-wall lead placement, and additional imaging modalities or standardized implantation criteria would strengthen confidence in group allocation. Second, the remarkably balanced baseline characteristics between the two groups are somewhat unexpected in a non-randomized observational study. Although this balance strengthens internal validity, greater clarification regarding patient allocation would help readers better assess the possibility of selection bias. Third, although the study appropriately focused on right-sided cardiac remodeling, complementary assessment of left ventricular mechanics—particularly left ventricular global longitudinal strain—would have provided a more comprehensive evaluation of pacing-induced ventricular dyssynchrony. Fourth, the statistical analysis primarily compared outcomes between groups at follow-up. Additional within-patient longitudinal analyses examining individual baseline-to-follow-up changes could have provided greater insight into the magnitude and trajectory of remodeling associated with each pacing strategy. Finally, although the authors appropriately acknowledge the relatively small sample size and short follow-up duration, inclusion of longitudinal clinical outcomes, biomarkers, heart failure symptoms, or device interrogation data would have strengthened the clinical relevance of the echocardiographic findings. Notwithstanding these methodological limitations, it is noteworthy that statistically significant differences in right ventricular remodeling and systolic function were detectable after only three months of follow-up. This observation suggests that pacing-induced adverse remodeling may begin considerably earlier than previously appreciated. Given the well-established association between right ventricular dysfunction and adverse cardiovascular outcomes, these findings may have important implications for future pacing practice. If confirmed in larger randomized studies with longer follow-up, a relatively modest modification in lead positioning may represent a practical strategy to reduce pacing-related cardiac remodeling, preserve right ventricular function, and improve long-term patient outcomes. References Richardson CJ, Prempeh J, Gordon KS, Poyser TA, Tiesenga F. Surgical Techniques, Complications, and Long-Term Health Effects of Cardiac Implantable Electronic Devices. Cureus. 2021;13(1):e13001. DOI: 10.7759/cureus.13001 Vijayaraman P, Longacre C, Kron J, Crossley GH. Clinical Outcomes of Right Ventricular Apical, Septal, and Conduction System Pacing in the Medicare Population. Circ Arrhythm Electrophysiol. 2025;18(9):e013940. DOI: 10.1161/CIRCEP.125.013940 Worsnick SA, Sharma PS, Vijayaraman P. Right Ventricular Septal Pacing: A Paradigm Shift. J Innov Card Rhythm Manag. 2018;9(5):3137-46. DOI: 10.19102/icrm.2018.090501 Chang JD, Manning WJ, Ebrille E, Zimetbaum PJ. Tricuspid Valve Dysfunction Following Pacemaker or Cardioverter-Defibrillator Implantation. J Am Coll Cardiol. 2017;69(18):2331-41. DOI: 10.1016/j.jacc.2017.02.055 Vijayaraman P, Longacre C, Kron J, Crossley GH. Clinical Outcomes of Right Ventricular Apical, Septal, and Conduction System Pacing in the Medicare Population. Circ Arrhythm Electrophysiol. 2025;18(9):e013940. DOI: 10.1161/CIRCEP.125.013940 Morsy AAZ, Salama MK, Haseeb WA, Elshaer OA, Abdelfattah ME. Impact of Right Ventricular Lead Position on Tricuspid Regurgitation and Right Ventricular Function Following Dual-Chamber Pacemaker Implantation: A Prospective Echocardiographic Study. Pak Heart J. 2026;59(04):945-952. DOI: 10.47144/phj.v59i4.3488 Dias-Frias A, Costa R, Campinas A, Alexandre A, Sá-Couto D, Sousa MJ, Roque C, Vieira P, Lagarto V, Reis H, Torres S. Right Ventricular Septal Versus Apical Pacing: Long-Term Incidence of Heart Failure and Survival. J Cardiovasc Dev Dis. 2022;9(12):444. DOI: 10.3390/jcdd9120444