Right Ventricular Mechanics and Dyssynchrony as Determinants of Tricuspid Regurgitation Progression After Permanent Pacemaker Implantation: A Speckle‐Tracking Echocardiography Study

ABSTRACT

Background

Tricuspid regurgitation (TR) progression is a recognized complication following permanent pacemaker (PPM) implantation with a significant impact on morbidity and mortality. The role of procedural aspects as well as advanced echocardiographic parameters in predicting TR progression remains incompletely defined.

Objective

To investigate procedural factors and echocardiographic parameters predicting progression to moderate‐to‐severe TR following PPM implantation.

Methods

Fifty‐two consecutive patients undergoing PPM implantation were prospectively included. Conventional echocardiography and speckle‐tracking echocardiography (STE) were performed at baseline, 3 months, and 6 months post‐implantation. Patients were classified according to the development of moderate‐to‐severe TR during follow‐up.

Results

Moderate‐to‐severe TR developed in 17 patients (32.7%) during follow‐up. Baseline clinical and echocardiographic parameters were largely comparable between groups, although patients with subsequent TR progression had mildly impaired baseline RV free wall longitudinal strain (RV‐FWLS) (p = 0.04). At 3 months, patients with TR progression demonstrated worse RV‐FWLS (p = 0.01), higher RV dyssynchrony index (p = 0.02), and larger tricuspid annular diameter (p = 0.04). On multivariable analysis, the direct trans‐tricuspid crossing technique (OR 5.42, 95% CI 1.01–29.12; p = 0.048), ventricular pacing burden (OR 1.39, 95% CI 1.05–1.86; p = 0.02), 3‐month RV‐FWLS (OR 1.47, 95% CI 1.01–2.15; p = 0.04) and 3‐month RV dyssynchrony index (OR 1.54, 95% CI 1.02–2.31; p = 0.03) could independently predicted TR progression. ROC analysis showed good predictive performance for RV dyssynchrony index (AUC 0.86) and RV‐FWLS (AUC 0.83).

Conclusions

Early abnormalities in RV strain and mechanical dyssynchrony were associated with subsequent TR progression following PPM implantation, highlighting the potential value of advanced echocardiographic assessment for early risk stratification.

Early abnormalities in RV strain and mechanical dyssynchrony were associated with subsequent TR progression following PPM implantation, highlighting the potential value of advanced echocardiographic assessment for early risk stratification.

Abbreviations

AF

Atrial fibrillation

AUC

Area under the curve

CI

Confidence interval

FAC

Fractional area change

LVEF

Left ventricular ejection fraction

OR

Odds ratio

PASP

Pulmonary artery systolic pressure

PPM

Permanent pacemaker

ROC

Receiver operating characteristic

RV

Right ventricle / right ventricular

RV‐FWLS

Right ventricular free wall longitudinal strain

RV‐GLS

Right ventricular global longitudinal strain

STE

Speckle‐tracking echocardiography

TAPSE

Tricuspid annular plane systolic excursion

TR

Tricuspid regurgitation

1. Introduction

Relevant (≥ moderate) tricuspid regurgitation (TR) has increasingly been viewed as a clinically significant valvular disorder associated with adverse cardiovascular outcomes, including right heart failure, reduced functional capacity, and increased mortality [1, 2].

The growing use of permanent pacemakers (PPMs) has introduced an important iatrogenic mechanism contributing to TR. Post‐PPM TR consists of new‐onset moderate‐to‐severe or worsening by ≥1 grade TR caused by the right ventricular (RV) lead, with a reported incidence ranging from 10% to 40% [3, 4, 5]. Depending on the underlying mechanism, it can be classified into primary or secondary. The primary mechanisms involve interference with leaflet coaptation, lead impingement on a leaflet, leaflet perforation, or distortion of the valvular apparatus; whereas the secondary mechanisms are related to RV dysfunction, dilatation, electromechanical dyssynchrony, or LV disease‐induced pulmonary hypertension [5, 6, 7]. Prior studies have focused on prediction of relevant post‐PPM TR using conventional echocardiographic parameters of RV function, namely tricuspid annular plane systolic excursion (TAPSE) and fractional area change. Recent evidence, however, has shown that speckle‐tracking echocardiography (STE) can adequately detect early or subtle changes in RV mechanics. In particular, RV free wall longitudinal strain and time‐to‐peak strain dispersion have gained increasing attention for early detection of pacemaker‐induced RV dysfunction [8, 9, 10, 11].

Post‐PPM TR progression has been associated with several procedural factors, particularly right ventricular apical pacing and higher right ventricular pacing burden. However, the role of trans‐tricuspid lead crossing technique in predicting subsequent TR progression remains incompletely understood [12, 13]. While these procedural factors as well as pacing‐induced RV dysfunction may represent complementary functional mechanisms contributing to TR progression. The relative contribution of these procedural and functional pathways remains incompletely defined.

Our study aimed to determine the incidence of moderate‐to‐severe tricuspid regurgitation following PPM implantation and to evaluate the predictive value of advanced STE‐derived parameters reflecting RV mechanical function and dyssynchrony, as well as the role of trans‐tricuspid crossing technique, for early identification of patients at risk for post‐pacing TR progression.

2. Patients and Methods

Study Population. This was a prospective observational cohort study conducted at Zagazig University hospitals. Consecutive patients ≥18 years who were candidates for permanent pacemaker (PPM) implantation were included. We excluded patients with pre‐existing moderate or severe TR, prior tricuspid valve surgery, congenital heart disease involving the tricuspid valve; or inadequate echocardiographic imaging quality. Informed consent was obtained from each patient and the study protocol was approved by institution's human research committee (ZU‐IRB #325/28‐4‐2024).

Clinical Assessment. Demographic data were collected (age, sex, and BMI). Pre‐implantation atrial fibrillation (AF) as well as other comorbidities (e.g. hypertension, diabetes mellitus, presence of coronary artery disease, presence of chronic kidney disease defined as estimated glomerular filtration rate < 60 mL/min/1.73 m2) were evaluated.

PPM Implantation. PPM implantation was performed using standard transvenous techniques. During implantation, 2 trans‐tricuspid crossing techniques were non‐randomly chosen, vis direct crossing and prolapsing techniques. In the direct crossing technique (26 patients), the distal tip of the lead directly traverses the tricuspid valve before entering the RV. In the prolapsing technique (26 patients), a pre‐shaped J stylet is used to create a loop configuration, allowing the body of the curved lead to prolapse across the tricuspid valve before advancement of the lead tip into the RV (Figure 1). Type of device (single vs dual chamber) and site of pacing (RV apical vs septal) were reported for each patient. Pacemaker interrogation was performed at follow‐up visits (at 3 months) using standard manufacturer‐specific programmers. Right ventricular pacing burden was defined as the cumulative percentage of ventricular paced beats relative to total ventricular beats during follow‐up [14] and was retrieved from device interrogation.

FIGURE 1.

Fluoroscopic demonstration of trans‐tricuspid lead crossing techniques during permanent pacemaker implantation.

(A) Direct crossing technique, in which the lead tip directly traverses the tricuspid valve into the right ventricle. (B) Prolapsing technique using a pre‐shaped J stylet, allowing the curved body of the lead to prolapse across the tricuspid valve before advancement into the right ventricle.

Transthoracic Echocardiography (TTE). Comprehensive two‐dimensional TTE was performed using a commercially available Vivid E9 ultrasound system (GE Healthcare Vingmed, Milwaukee, WI, USA) at baseline prior to PPM implantation, with follow‐up examinations repeated at 3 and 6 months post‐implantation. All measurements and image acquisition protocols were performed according to current recommendations of the American Society of Echocardiography [15]. Conventional two‐dimensional, M‐mode, and Doppler echocardiographic parameters were systematically evaluated. Echocardiographic examinations were performed under the prevailing rhythm at the time of image acquisition without intentional device reprogramming. Patients were categorized according to the occurrence of TR progression, defined as new‐onset moderate‐to‐severe TR or worsening of TR by at least one grade during follow‐up. Echocardiographic examinations were performed at baseline and repeated at 3 and 6 months after PPM implantation. Baseline and early follow‐up (3‐month) clinical and echocardiographic parameters were analyzed as candidate predictors of subsequent TR status, whereas the 6‐month examination was used for final assessment of the study endpoint.

Conventional Echocardiographic Parameters. in the apical four‐chamber view, tricuspid annular diameter, RV dimension (basal) and right atrial (RA) area at end‐systole were measured. RV systolic function was assessed using tricuspid annular plane systolic excursion (TAPSE) measured by M‐mode, RV fractional area change (FAC); and peak systolic velocity (S′) at the lateral tricuspid annulus using tissue Doppler imaging.

Assessment of TR. R severity was evaluated using an integrative multiparametric approach. Color Doppler imaging was used to assess TR jet area and jet direction from multiple acoustic windows. Continuous‐wave Doppler was utilized to evaluate TR jet density and contour. Additional semiquantitative parameters included vena contracta width and hepatic vein flow pattern. TR severity was graded as mild, moderate, or severe according to guideline‐recommended criteria. Mild TR was characterized by a small central jet with preserved systolic hepatic vein flow and vena contracta width <3 mm. Moderate TR was defined by intermediate Doppler findings not meeting criteria for mild or severe regurgitation. Severe TR was diagnosed in the presence of a large central jet or eccentric wall‐impinging jet, dense triangular continuous‐wave Doppler profile, systolic hepatic vein flow reversal, or vena contracta width ≥7 mm. Progression to relevant TR was defined as development of moderate‐to‐severe TR during follow‐up in patients without significant baseline TR. Pulmonary artery systolic pressure (PASP) was estimated from the peak TR jet velocity using the modified Bernoulli equation, with the addition of estimated right atrial pressure

Speckle‐Tracking Echocardiography (STE). STE was performed offline using dedicated software in accordance with current consensus recommendations [16, 17]. RV‐focused apical four‐chamber views were used to assess myocardial deformation. Frame rates were optimized between 60–90 frames per second. RV global longitudinal strain (RV‐GLS) and RV free wall longitudinal strain (RV‐FWLS) were calculated by averaging segmental strain values. Care was taken to exclude the interventricular septum when calculating RV‐FWLS. Strain values were expressed as negative percentages, with less negative values indicating impaired myocardial function. RV mechanical dyssynchrony was assessed using STE‐derived time‐to‐peak longitudinal strain as previously described [18]. Time intervals from the onset of the QRS complex to peak systolic strain were measured in RV free wall and septal segments. RV dyssynchrony index was defined as the absolute difference between the earliest and latest time‐to‐peak strain among analyzed segments. Higher values indicated greater mechanical dyssynchrony.

Intraobserver and Interobserver Variability Analysis. To assess the reproducibility of STE‐derived parameters, intraobserver and interobserver variability analyses were performed in a randomly selected subset of 20 patients. Measurements of RV‐FWLS, RV dyssynchrony index, and tricuspid annular diameter were repeated offline by the same observer after a 2‐week interval and independently by a second experienced echocardiographer blinded to the initial measurements and clinical outcomes. Agreement between measurements was assessed using the intraclass correlation coefficient and Bland–Altman analysis.

Statistical Analysis. Statistical analysis was performed using IBM SPSS Statistics version 26.0 (IBM Corp., Armonk, NY, USA). Continuous variables were tested for normality using the Shapiro–Wilk test and expressed as mean ± standard deviation or median (interquartile range), as appropriate. Categorical variables were presented as frequencies and percentages. Comparisons between patients with and without progression to moderate‐to‐severe tricuspid regurgitation (TR) were performed using the independent‐samples t‐test or Mann–Whitney U test for continuous variables and the chi‐ square test or Fisher's exact test for categorical variables, as appropriate. Multivariate regression analysis was done to detect independent predictors of TR progression. To avoid model overfitting given the limited number of outcome events, only clinically relevant variables with the strongest univariate association and minimal collinearity were entered into the multivariable logistic regression model. Odds ratios (ORs) with 95% confidence intervals (CIs) were reported. Receiver operating characteristic (ROC) curve analysis was performed to assess the predictive performance of significant echocardiographic parameters. Optimal cutoff values were determined using the Youden index. The area under the curve (AUC), sensitivity, specificity, and corresponding 95% confidence intervals were calculated. Comparisons between correlated ROC curves were performed using the DeLong method. A two‐sided p‐value <0.05 was considered statistically significant.

3. Results

A total of 52 patients who underwent PPM implantation were prospectively included in the study. Based on the occurrence of moderate‐to‐severe TR during follow‐up, 17 patients (32.7%) were classified as having TR progression and 35 patients (67.3%) as having no TR progression. Baseline clinical and procedural characteristics of the study population are summarized in Table 1. Significant differences between groups were present regarding trans‐tricuspid crossing technique (p = 0.04) and ventricular pacing burden (p < 0.001). Otherwise, both groups were comparable.

TABLE 1.

Baseline clinical and procedural characteristics.

Variable	No TR progression (n=35)	TR progression (n=17)	p value
Age, years	61.9 ± 11.1	64.7 ± 10.5	0.34
Male sex, n (%)	21 (60.0)	10 (58.8)	0.93
Hypertension, n (%)	18 (51.4)	10 (58.8)	0.62
Diabetes mellitus, n (%)	14 (40.0)	7 (41.2)	0.94
Atrial fibrillation, n (%)	5 (14.3)	5 (29.4)	0.18
Coronary artery disease, n (%)	8 (22.9)	5 (29.4)	0.61
Chronic kidney disease, n (%)	6 (17.1)	5 (29.4)	0.31
RV apical lead position, n (%)	15 (42.9)	11 (64.7)	0.13
Septal lead position, n (%)	20 (57.1)	6 (35.3)
Single‐chamber pacemaker	15 (42.9)	5 (29.4)	0.36
Dual‐chamber pacemaker	20 (57.1)	12 (70.6)
Direct crossing technique, n (%)	15 (42.9)	11 (64.7)	0.04
Prolapsing technique, n (%)	20 (57.1)	6 (35.3)
Ventricular pacing burden, %	48 ± 17	70 ± 15	<0.001
Fluoroscopy time, min	8.8 ± 2.5	9.6 ± 3.0	0.31

Data are presented as mean ± standard deviation or number (%). RV: right ventricle

Comparison Between Baseline and Follow‐Up Echocardiographic Characteristics Between Groups ( Table 2 ). Baseline conventional echocardiographic parameters were largely comparable between groups. Although no significant differences were observed in baseline RV basal dimension, RV FAC, RV dyssynchrony index, or tricuspid annular diameter patients with subsequent TR progression demonstrated subtly impaired RV‐FWLS (p = 0.04). At 3‐month follow‐up, patients with subsequent TR progression exhibited significantly larger tricuspid annular diameter (p = 0.04), worsening RV‐FWLS (p = 0.01), and increased RV dyssynchrony index (p = 0.02) compared to patients without TR progression. However, conventional RV systolic indices, including TAPSE and RV FAC, remained relatively preserved with only modest intergroup differences. At 6 months follow‐up, patients with TR progression demonstrated significantly lower TAPSE (p = 0.01), higher PASP (p = 0.003), larger tricuspid annular diameter (P< 0.001), worse RV‐FWLS (P< 0.001), and higher RV dyssynchrony index (P< 0.001).

TABLE 2.

Comparison between baseline and follow‐up echocardiographic characteristics.

Variable	No TR progression (n=35)	TR progression (n=17)	p value
Baseline echocardiography
LVEF, %	57.6 ± 6.9	55.9 ± 7.3	0.42
RV basal diameter, mm	35.1 ± 4.2	36.4 ± 4.5	0.31
Right atrial area, cm2	18.1 ± 3.1	19.0 ± 3.5	0.37
TAPSE, mm	21.2 ± 2.7	20.3 ± 2.9	0.26
RV FAC, %	43.8 ± 5.4	42.1 ± 5.8	0.29
Tricuspid annular S′ velocity, cm/s	11.8 ± 2.0	11.1 ± 2.2	0.24
PASP, mmHg	33.1 ± 6.7	35.0 ± 7.1	0.34
Tricuspid annular diameter, mm	34.5 ± 3.4	36.3 ± 3.8	0.08
TR grade	0.8 ± 0.4	0.9 ± 0.5	0.48
RV global longitudinal strain (%)	−21.4 ± 2.3	−20.1 ± 2.5	0.07
RV free wall longitudinal strain (%)	−23.0 ± 2.5	−21.1 ± 2.7	0.04
RV dyssynchrony index, ms	30.2 ± 11.1	36.8 ± 13.4	0.06
RV free wall time‐to‐peak strain, ms	382 ± 42	398 ± 49	0.18
Septal time‐to‐peak strain, ms	364 ± 39	378 ± 44	0.21
3‐Month follow‐up echocardiography
TAPSE, mm	20.8 ± 2.6	19.5 ± 2.9	0.12
RV FAC, %	43.1 ± 5.1	40.9 ± 5.5	0.15
PASP, mmHg	34.2 ± 7.0	37.1 ± 7.6	0.18
Tricuspid annular diameter, mm	35.1 ± 3.6	37.8 ± 4.0	0.04
TR grade	1.1 ± 0.4	1.7 ± 0.5	0.01
RV free wall strain (%)	−22.4 ± 2.4	−20.0 ± 2.6	0.01
RV dyssynchrony index, ms	32.5 ± 11.8	43.8 ± 14.6	0.02
6‐Month Follow‐Up Echocardiography
TAPSE, mm	20.2 ± 2.8	17.5 ± 3.2	0.01
PASP, mmHg	35.1 ± 7.3	42.6 ± 8.5	0.003
Tricuspid annular diameter, mm	35.8 ± 3.8	41.0 ± 4.7	<0.001
RV free wall strain (%)	−21.9 ± 2.6	−17.4 ± 3.0	<0.001
RV dyssynchrony index, ms	34.1 ± 12.2	61.8 ± 18.4	<0.001

Note: Data are presented as mean ± standard deviation or number (%).

Abbreviations: FAC: fractional area change; PASP: pulmonary artery systolic pressure; RV: right ventricle; TAPSE: tricuspid annular plane systolic excursion; TR: tricuspid regurgitation.

Predictors of Tricuspid Regurgitation progression ( Table 3 ). Univariable logistic regression analysis identified several procedural and echocardiographic parameters associated with the progression TR following PPM implantation vis direct crossing technique, ventricular pacing burden, 3‐month RV‐FWLS, 3‐month RV dyssynchrony index and 3‐ month tricuspid annular diameter. In the multivariable logistic regression model, the direct transtricuspid crossing technique remained an independent predictor of TR progression (OR 5.42, 95% CI 1.01–29.12; p = 0.048). Similarly, ventricular pacing burden could independently predict TR progression (OR 1.39, 95% CI 1.05–1.86; p = 0.02). Furthermore, 3‐month RV free wall strain and RV dyssynchrony index independently predicted TR progression after adjustment for other clinically relevant variables. Specifically, worsening RV free wall strain was associated with a 47% increase in the odds of significant TR for each 1% reduction in strain magnitude (OR 1.47, 95% CI 1.01–2.15; p = 0.04), while increasing RV dyssynchrony was associated with a 54% higher likelihood of TR progression per 10‐ms increase in dyssynchrony index (OR 1.54, 95% CI 1.02–2.31; p = 0.03).

TABLE 3.

Univariable and multivariable logistic regression analysis for predictors of tricuspid regurgitation progression following permanent pacemaker implantation.

Variable	Univariable OR (95% CI)	p‐value	Multivariable OR (95% CI)	p‐value
Age (per 1‐year increase)	1.03 (0.97–1.10)	0.28	—	—
Male sex	1.54 (0.46–5.10)	0.49	—	—
Atrial fibrillation	3.25 (0.95–11.02)	0.059	2.14 (0.54–8.47)	0.28
RV apical lead position	3.08 (0.84–11.29)	0.09	2.01 (0.46–8.73)	0.35
Direct transtricuspid crossing technique	7.08 (1.39–36.01)	0.019	5.42 (1.01–29.12)	0.048
Ventricular pacing burden (per 10% increase)	1.52 (1.16–2.01)	0.002	1.39 (1.05–1.86)	0.02
Baseline tricuspid annular diameter (per 1 mm increase)	1.13 (0.97–1.33)	0.11	—	—
Baseline RV free wall strain (per 1% less negative)	1.29 (0.99–1.69)	0.058	—	—
Baseline RV dyssynchrony index (per 10 ms increase)	1.36 (0.97–1.91)	0.07	—	—
3‐month RV free wall strain (per 1% less negative)	1.61 (1.13–2.30)	0.009	1.47 (1.01–2.15)	0.04
3‐month RV dyssynchrony index (per 10 ms increase)	1.69 (1.18–2.43)	0.005	1.54 (1.02–2.31)	0.03
3‐month tricuspid annular diameter (per 1 mm increase)	1.27 (1.04–1.56)	0.02	1.18 (0.93–1.51)	0.17

Abbreviations: CI: confidence interval; OR: odds ratio; RV: right ventricle

Receiver Operating Characteristic (ROC) Analysis ( Table 4 and Figure 2 ) was performed to evaluate the predictive performance of echocardiographic parameters for the development of moderate‐to‐severe tricuspid regurgitation following permanent pacemaker implantation. Among the evaluated variables, the 3‐month RV dyssynchrony index demonstrated the highest discriminatory performance, with an area under the curve (AUC) of 0.86 (95% CI 0.75–0.96; p<0.001). A cutoff value >45 ms predicted significant TR progression with 88.2% sensitivity and 74.3% specificity. Similarly, 3‐month RV free wall longitudinal strain showed good predictive accuracy (AUC 0.83, 95% CI 0.71–0.94; p = 0.001). An RV free wall strain value less negative than −19.5% predicted TR progression with 82.4% sensitivity and 77.1% specificity. Tricuspid annular diameter at 3 months also demonstrated significant predictive value (AUC 0.79, 95% CI 0.66–0.91; p = 0.003), with a cutoff >37 mm associated with subsequent development of moderate‐to‐severe TR. Comparison of ROC curves using the DeLong method demonstrated no statistically significant differences between the predictive performances of the evaluated echocardiographic parameters (Table 5). Although the 3‐month RV dyssynchrony index showed the numerically highest area under the curve (AUC = 0.86), its discriminatory performance was not significantly different from that of RV free wall longitudinal strain (AUC = 0.83; p = 0.58) or tricuspid annular diameter (AUC = 0.79; p = 0.21). Similarly, no significant difference was observed between RV free wall strain and tricuspid annular diameter (p = 0.44). These findings suggest that STE‐derived RV mechanical parameters and tricuspid annular remodeling provide complementary predictive information for identifying patients at risk of device‐related TR progression.

TABLE 4.

Receiver Operating Characteristic (ROC) analysis for prediction of tricuspid regurgitation progression.

Variable	AUC (95% CI)	p‐value	Optimal Cutoff	Sensitivity (%)	Specificity (%)
3‐month RV free wall strain (%)	0.83 (0.71–0.94)	0.001	> −19.5%	82.4	77.1
3‐month RV dyssynchrony index (ms)	0.86 (0.75–0.96)	<0.001	> 45 ms	88.2	74.3
3‐month tricuspid annular diameter (mm)	0.79 (0.66–0.91)	0.003	> 37 mm	76.5	71.4

Abbreviations: RV: right ventricle

FIGURE 2.

Receiver operating characteristic (ROC) curves for prediction of moderate‐to‐severe tricuspid regurgitation following permanent pacemaker implantation. ROC analysis demonstrating the predictive performance of 3‐month RV free wall longitudinal strain, RV dyssynchrony index, and tricuspid annular diameter for the development of moderate‐to‐severe tricuspid regurgitation during follow‐up. The RV dyssynchrony index showed the highest discriminatory ability (AUC = 0.86), followed by RV free wall strain (AUC = 0.83) and tricuspid annular diameter (AUC = 0.79). The dashed diagonal line represents the line of no discrimination (AUC = 0.50).

AUC: area under the curve; RV: right ventricle; ROC: receiver operating characteristic.

TABLE 5.

Comparison of areas under the ROC curves (AUCs).

Comparison of ROC curves	Difference in AUC	Standard error	p‐value
RV dyssynchrony index versus RV free wall strain	0.03	0.06	0.58
RV dyssynchrony index versus tricuspid annular diameter	0.07	0.05	0.21
RV free wall strain versus tricuspid annular diameter	0.04	0.05	0.44

Abbreviations: RV: right ventricle

4. Discussion

The present prospective study evaluated the incidence and echocardiographic predictors of progression of TR following PPM implantation using conventional and advanced echocardiographic assessment including STE. The principal findings of this study were:[1] moderate‐to‐severe TR developed in approximately one‐third of patients during 6‐month follow‐up;[2] baseline echocardiographic differences between groups were subtle, suggesting that significant TR progression was not merely attributable to pre‐existing RV dysfunction;[3] early deterioration in RV mechanical function and synchrony at 3 months preceded overt TR progression;[4] RV free wall longitudinal strain and RV dyssynchrony demonstrated significant predictive value for subsequent TR development; and [5] the direct transtricuspid crossing technique was associated with increased risk of device‐related TR. Taken together, these findings suggest that both procedural and pacing‐related functional factors may contribute to post‐PPM TR progression.

Device‐related TR has emerged as an increasingly recognized complication of transvenous cardiac implantable electronic devices. Previous studies have demonstrated that transvalvular leads may interfere with leaflet coaptation, alter valvular geometry, or contribute to progressive right‐sided chamber remodeling, ultimately leading to clinically significant TR and adverse cardiovascular outcomes. Lin et al. [3] demonstrated that worsening TR following device implantation was associated with increased mortality and heart failure hospitalization, highlighting the clinical relevance of early identification of high‐risk patients. Similarly, Kim et al. [4] reported that device‐related TR may occur even in patients without significant baseline structural heart disease, suggesting an important role for pacing‐induced RV remodeling and electromechanical alterations.

An important observation in the current study is that baseline conventional echocardiographic parameters were largely comparable between groups. Patients who subsequently developed moderate‐to‐severe TR showed only mildly impaired RV free wall strain and a comparable RV dyssynchrony at baseline. This finding strengthens the temporal association between PPM implantation and subsequent TR progression and reduces the likelihood that the observed TR worsening merely reflected pre‐existing advanced RV dysfunction. Moreover, conventional RV functional indices such as TAPSE and RV fractional area change were not significantly different at baseline, emphasizing the limited sensitivity of traditional echocardiographic parameters for detecting early subclinical RV dysfunction.

In contrast, STE‐derived RV mechanics demonstrated early divergence during follow‐up. At 3 months following implantation, patients who subsequently progressed to moderate‐to‐severe TR exhibited worsening RV free wall longitudinal strain and significantly higher RV dyssynchrony indices despite relatively preserved conventional RV systolic parameters. These findings suggest that pacing‐related electromechanical alterations may precede overt structural remodeling and clinically apparent TR progression.

RV longitudinal strain has been increasingly recognized as a sensitive marker of early myocardial dysfunction and has shown prognostic value in various right‐sided cardiac disorders [19, 20, 21].

The observed association between RV dyssynchrony and TR progression is physiologically plausible. Chronic RV pacing may induce heterogeneous ventricular activation patterns, impair coordinated RV contraction, and alter tricuspid annular dynamics. These changes may progressively impair leaflet coaptation and increase regurgitant severity over time [22, 23]. Our findings are consistent with previous reports suggesting that pacing‐induced RV dyssynchrony contributes to adverse RV remodeling and functional TR. Importantly, the current study extends these observations by demonstrating that STE‐derived dyssynchrony abnormalities may become evident before substantial deterioration in conventional RV systolic function occurs.

Another notable finding was the association between the direct transtricuspid crossing technique and subsequent TR progression. Patients undergoing direct lead crossing demonstrated significantly higher rates of moderate‐to‐severe TR compared with those implanted using the prolapsing technique. Although procedural variables have received less attention in prior device‐related TR studies, our findings suggest that lead traversal strategy may influence long‐term tricuspid valve function. A possible explanation is that direct trans‐tricuspid lead crossing may increase mechanical interaction between the pacing lead and tricuspid leaflets or chordae tendineae, thereby promoting progressive leaflet malcoaptation and subsequent TR progression. Accordingly, procedural lead‐related effects and pacing‐induced RV mechanical dysfunction should be viewed as complementary rather than mutually exclusive mechanisms of post‐PPM TR.

ROC analysis further demonstrated good discriminatory performance of STE‐derived parameters for prediction of clinically significant TR. The RV dyssynchrony index showed the highest predictive accuracy, followed closely by RV free wall longitudinal strain. These findings support the potential role of advanced echocardiographic assessment in identifying patients at increased risk for device‐related TR early during follow‐up. Importantly, tricuspid annular diameter also demonstrated reasonable predictive performance despite not remaining independently significant in multivariable analysis. This likely reflects the interrelated nature of annular remodeling, RV mechanical dysfunction, and pacing‐induced electromechanical alterations in the pathophysiology of TR progression.

4.1. Clinical Implications

The current study has several important clinical implications. First, routine post‐implantation echocardiographic surveillance may facilitate early identification of patients at risk for progressive device‐related TR before the onset of overt RV failure. Second, STE‐derived RV strain and dyssynchrony analysis may provide incremental value beyond conventional echocardiographic indices in this population. Third, procedural considerations such as trans‐tricuspid crossing technique and lead positioning may influence long‐term valvular outcomes and warrant further investigation. Early identification of high‐risk patients may potentially allow optimization of pacing strategies and closer clinical follow‐up. Although TR severity may be influenced by loading conditions, the principal predictors identified in the present study reflect RV mechanical function and procedural characteristics that are less likely to be substantially affected by transient variations in volume status.

4.2. Study Limitations

Several limitations should be acknowledged. This was a single‐center study with a relatively small sample size and limited number of clinical events, which may reduce statistical power and increase the risk of model overfitting. Follow‐up duration was limited to 6 months; therefore, longer‐term progression of TR and associated clinical outcomes could not be evaluated. In addition, advanced three‐dimensional echocardiographic assessment of lead—leaflet interaction was not systematically performed. Finally, although STE‐derived parameters demonstrated promising predictive performance, vendor‐related variability and technical limitations inherent to strain imaging should be considered.

5. Conclusions

In conclusion, moderate‐to‐severe TR developed in a substantial proportion of patients following PPM implantation. Impaired RV free wall longitudinal strain, increased RV mechanical dyssynchrony, higher ventricular pacing burden, and the direct trans‐tricuspid crossing technique were independently associated with the development of moderate‐to‐severe TR during follow‐up. These findings suggest that both pacing‐related RV mechanical dysfunction and procedural factors may contribute to post‐PPM TR progression. Advanced echocardiographic assessment using STE may facilitate early identification of patients at increased risk for device‐related TR following pacemaker implantation.

Conflicts of Interest

The authors declare no conflicts of interest.