Revised: July 5, 2026
Accepted: August 20, 2026
Published online: August 26, 2026
Processing time: 97 Days and 2.5 Hours
Transcatheter aortic valve replacement (TAVR) has become the standard treat
To synthesize evidence on baseline conduction abnormalities and their association with PPI after TAVR.
We conducted a systematic review and meta-analysis in accordance with PRISMA 2009 guidelines. We searched PubMed, Cochrane, and EMBASE for papers pub
Twenty studies comprising 15515 patients were included. The pooled incidence of new PPI was 18% (95%CI: 0.14-0.24). New-onset left bundle branch block (LBBB) occurred in a pooled proportion of 38% of patients (95%CI: 0.27-0.50) across 11 studies. New-onset RBBB was reported separately from new-onset LBBB in only two cohorts and could not be pooled. Pre-existing RBBB was the strongest pre
Baseline RBBB in particular demonstrated a strong and consistent association with PPI. These findings should inform preprocedural risk stratification, patient coun
Core Tip: Baseline right bundle branch block is associated with a 4.52-fold increased odds of permanent pacemaker im
- Citation: Fuchs TK, Jones C, Patterson JB. Impact of pre-existing conduction abnormalities on permanent pacemaker implantation after transcatheter aortic valve replacement: A meta-analysis. World J Cardiol 2026; 18(8): 123559
- URL: https://www.wjgnet.com/1949-8462/full/v18/i8/123559.htm
- DOI: https://dx.doi.org/10.4330/wjc.123559
Transcatheter aortic valve replacement (TAVR) has transformed the management of severe aortic stenosis, and its use has expanded from high-risk toward lower-risk populations worldwide[1,2]. With broader indications and rising procedural volumes, the balance of procedural benefit and device-related complications has become increasingly important for patient selection and perioperative planning[1,3]. Among the most frequent and clinically consequential complications are conduction distur
TAVR involves catheter-based delivery of a bioprosthetic valve, most commonly balloon-expandable or self-ex
A large synthesis of 108 studies comprising 77538 patients reported 14560 patients requiring PPI within 30 days after TAVR, illustrating substantial short-term event rates[5]. Prospective cohorts report PPI rates of roughly 10%-15% at one year, emphasizing persistent clinical relevance beyond the periprocedural window[6]. Valve type, im
Preexisting ECG conduction disease is a consistent and strong determinant of PPI after TAVR; key abnormalities include right bundle branch block (RBBB), existing AV block, hemiblocks, and bifascicular patterns[4,5,7]. Recognizing these baseline findings permits stratified counseling and procedural planning, which is critical. RBBB is markedly as
Baseline conduction disease influences not only the immediate need for pacing but also downstream outcomes, including pacing burden, heart failure progression, and device-related complications that may compromise long-term benefits of TAVR[8,9]. Despite several predictive models and single-center cohorts, prediction algorithms remain poor. Management techniques, such as timing of pacing, role of preventive pacemakers, and use of electrophysiological testing, continue to be debated[6,10,11]. This systematic review aims to synthesize contemporary evidence on baseline conduction abnormalities and their association with PPI after TAVR, clarify the magnitude of risk for specific ECG patterns, assess the impact on clinical outcomes, and evaluate gaps in prognostic tools. The objectives are to: (1) Quantify associations between predefined baseline conduction disorders and PPI after TAVR; (2) Evaluate downstream clinical consequences of PPI in these populations-including long-term pacing dependency, left ventricular ejection fraction (LVEF) trajectory, and mortality; and (3) Identify methodological and evidence gaps to inform future research and clinical guidance[4-6]. The present systematic review was undertaken to address three specific gaps not fully resolved in prior syntheses: (1) Prior meta-analyses have not incorporated studies reporting outcomes with contemporary balloon-expandable platforms (SAPIEN 3, SAPIEN 3 Ultra) or the newest self-expanding generations (Evolut FX, Navitor), which carry distinct con
We used the PRISMA 2009 guidelines and the ‘Population, Intervention, Comparison, Outcome, and Study design (PICOS)’ scheme to generate the eligibility criteria[12]. Studies were considered eligible for inclusion if they were pu
| Domain | Criteria |
| Population (P) | Adults (≥ 18 years) undergoing TAVR for aortic stenosis |
| Intervention/exposure (I) | Pre-existing conduction abnormalities on baseline ECG (e.g., RBBB, LBBB, first-degree AV block, bifascicular block, other baseline conduction disease) |
| Comparison (C) | TAVR patients without pre-existing conduction abnormalities (normal baseline ECG) |
| Outcomes (O) | Primary: Requirement for PPI after TAVR. Secondary (if reported): New-onset conduction disturbances, timing of pacemaker implantation, length of hospital stay, short-term mortality |
| Study design/setting (S) | RCTs, prospective and retrospective observational cohorts, and case series (n > 10) and registry analyses, published in English between January 1, 2010, and February 19, 2026 (inclusive); full text available |
Inclusion criteria: We included randomized controlled trials, cohort studies, and case series with more than 10 par
| Ref. | Study design | Study location | Population characteristics | Intervention | Primary outcomes | Key findings |
| Muntané-Carol et al[18] (2021) | Prospective multicenter | Canada, United States | TAVR recipients without prior pacemaker | Minimalist TAVR with 14-day AECG monitoring | Occurrence of delayed HAVB or CHB | 4.6% (21/459) developed delayed HAVB/CHB, leading to PPM in 81% |
| Pavlicek et al[19] (2023) | Prospective cohort | Germany | Severe AS; 54% male; mean age 80 | TAVR with SEV (n = 103) or BEV (n = 100) | HAVB requiring PPM within 30 days | 7% (15/203) required PPI; new LBBB (OR = 15.7) and diabetes (OR = 3.8) were predictors |
| Meduri et al[28] (2019) | RCT (REPRISE III) | United States, Germany | High/extreme surgical risk; mean age 83 | Lotus mechanically-expanded vs CoreValve SEV | PPM within 30 days and dependency at 1 year | PPM higher with Lotus (34%) vs CoreValve (18%); dependency was 43% at 30 days |
| Castro-Mejía et al[36] (2022) | Retrospective multicenter | Spain | Severe AS; 39% male; median age 83 | New-generation SEVs (Evolut, Acurate, Portico, Allegra) | Peri-procedural modification of AV conduction | 17.7% required PPI; valve recapture (OR = 2.8) and depth (OR = 1.9) were predictors |
| Auffret et al[22] (2017) | Multicenter registry | Global (Canada, France, Spain, etc.) | AS candidates; 50% male; mean age 82 | TAVR grouped by baseline RBBB | Cumulative all-cause mortality | Baseline RBBB in 10.3%; 30-day PPM in RBBB (40.1%) vs others (13.5%) |
| Bagur et al[23] (2012) | Case-matched cohort | Canada | Elderly AS; matched by baseline ECG | TAVI (Edwards) vs isolated SAVR | Complete AVB and PPM within 30 days | PPM higher in TAVI (7.3%) vs SAVR (3.4%); RBBB predicted TAVI PPM (OR = 8.6) |
| Wasim et al[30] (2025) | Prospective observational cohort | Norway | Severe AS; 50% male; mean age 80.6 | TAVI (various valves) over low vs high volume phases | New PPM ≤ 30 days and all-cause death | 31.6% total PPI rate; dropped from 45.8% to 23.9% with experience |
| Chen et al[25] (2024) | Registry analysis | United States, Canada | Intermediate/high risk PARTNER 2 S3 registries | TAVR with balloon-expandable SAPIEN 3 | New PPM within 30 days | 12.5% required PPI; RBBB (OR = 5.8) and depth > 6 mm (OR = 1.86) were predictors |
| Dizon et al[31] (2015) | RCT and registry analysis | United States, Canada | Inoperable/high-risk AS (PARTNER trial) | TAVI (Edwards SAPIEN) | 1-year all-cause mortality | New PPM (6.8%) and prior PPM (22.9%) independently predicted mortality |
| Natarajan et al[37] (2022) | Prospective cohort | Canada | Outpatient AS; mean age 81.8 | Routine 2-week pre/post rACM | Compliance to rACM and unplanned post-TAVI PPMI | 15.6% total PPMI rate; 12.5% rACM notifications; unplanned PPMI only 3.1% |
| Fraccaro et al[33] (2011) | Registry analysis | Italy | AS due to calcification; mean age 81 | TAVI with CoreValve system | Incidence/predictors of PPM | 39% required PPI; predictors were depth (P = 0.039) and pre-existing RBBB (P = 0.046) |
| Guetta et al[20] (2011) | Registry analysis | Israel | AS Israeli registry; mean age 83 | CoreValve TAVI | Development of HDAVB within 30 days | 36% developed HDAVB (40% total PPM); RBBB (OR = 43) and depth (OR = 22) were predictors |
| Husser et al[38] (2016) | Prospective cohort | Germany, Switzerland | High-risk AS; mean age 80-81. | SAPIEN 3 (n = 96) vs SAPIEN XT (n = 87) | New IVCA and PPM implantation | PPM rate 12.5% (S3) vs 12.6% (XT); S3 had more fascicular blocks (17% vs 5%) |
| Khawaja et al[27] (2011) | Retrospective multicenter | United Kingdom, Ireland | United Kingdom CoreValve Collaborative; mean age 81.3 | CoreValve TAVI | PPM within 30 days | 33.3% required PPI; predictors included peri-pro AVB (OR 6.29) and predilatation (OR 2.68) |
| Kooistra et al[24] (2020) | Retrospective multicenter | Netherlands, Spain | Multi-center European registry; median age 82 | TAVI (SEV vs BEV vs Other) | Timing of onset and predictors of late CDs | 12% PPM rate; 18% of these were late (> 48 hours); IVCD (OR = 3.3) and RBBB (OR = 2.6) predict late PPM |
| Kostopoulou et al[32] (2015) | Randomized prospective | Greece | NYHA II/III AS; mean age 81 | CoreValve TAVI with EPS vs ECG alone | Predictors of conduction abnormalities | 22% PPM within 1 month; baseline HV interval (cut-off 52 ms) was prognostic |
| Ledwoch et al[34] (2013) | Prospective registry (GARY) | Germany | German GARY registry; mean age 81.5 | TAVI (CoreValve vs Sapien) | Predictors of PPM up to 30 days | 33.7% PPM rate; independent predictors: CoreValve (OR = 2.86), porcelain aorta (OR = 1.64) |
| Naveh et al[21] (2017) | Prospective observational | Israel | AS at Hadassah center; mean age 80.7 | TAVI (CoreValve vs Sapien) | Predictors for long-term pacing dependency | 34.5% total PPI; 68.4% dependent; RBBB (OR = 18) and delta PR > 28 ms were predictors |
| Rampat et al[26] (2017) | Retrospective multicenter | United Kingdom | United Kingdom LOTUS experience; mean age 81.2 | LOTUS mechanically-expanded valve | PPM up to hospital discharge | 31.8% PPM rate; 55.2% new LBBB; pre-procedural block composite (OR = 2.54) and absence of valve calcification (OR = 0.55) were independent predictors |
| Van Gils et al[29] (2018) | Prospective cohort (CONDUCT) | Netherlands | Rotterdam cohort; mean age 79 | TAVI (various valves) with daily ECG monitoring. | QRS dynamics vs PPM requirement | 23% PPM rate; only persistent QRS prolongation led to PPM in normal baseline patients |
Exclusion criteria: We excluded cross-sectional studies, case reports, reviews, grey literature, non-English publications, studies with ≤ 10 participants, animal studies, and reports lacking data on baseline conduction status or post-TAVR pacemaker outcomes. Duplicate datasets were screened, and the most complete report was retained.
We searched through several digital databases to retrieve relevant literature. Among these are Cochrane, PubMed (MEDLINE), and EMBASE. Other resources, such as those from independent journals, were also included. The infor
The study methodology was developed based on a review of relevant peer-reviewed literature. Articles meeting the predefined inclusion criteria were appraised using the PICOS framework to ensure methodological strength. The screening and selection process was facilitated using Rayyan.ai, an evidence-based platform designed to streamline the review of primary and secondary sources[13]. Following this, a total of 20 studies were found to be appropriate for inclusion. Articles were excluded if they targeted a non-relevant population, used the wrong study design, failed to measure target outcomes, or exhibited a high risk of bias. In several cases, studies were excluded for more than one of these reasons. After finalizing the secondary screening process, we assessed the overall sample size (n = 20) of the selected literature. To create a PRISMA 2009 flow chart that follows the reporting standards of the PRISMA 2009, we used articles from reputable journals and other sources[14] (Figure 1).
We conducted a systematic analysis of patient demographics, the characteristics of the interventions, and the region of the study. For all the studies utilizing a randomized controlled design, we used the Cochrane Risk of Bias (ROBv2) tool to determine the bias in each study and across all domains[15]. The results of the risk assessment were represented as a ‘traffic lights’ plot, and the individual risk domains were summarized via a ‘summary plot’. For cohort studies, the Newcastle-Ottawa Scale (NOS) was used to summarize the risk across the included studies[16]. The NOS was applied using the cohort-specific version, which is appropriate for prospective and retrospective cohort studies rather than case-control designs; this dual-tool approach is consistent with Cochrane handbook recommendations for systematic reviews incorporating both randomized and non-randomized evidence. Domain-level abbreviations in Table 3 are as follows: Rep. Exposed = representativeness of the exposed cohort; Sel. non-exp. = selection of the non-exposed cohort; Ascert. exp. = ascertainment of exposure; Outcome absent = demonstration that outcome of interest was not present at start of study; Ctrl main = comparability on main confounders; Ctrl addit. = comparability on additional confounders; Assess. outcome = assessment of outcome; Follow-up dur. = adequacy of follow-up length; Adequacy FU = adequacy of follow-up of cohorts. Yes = criterion met; No = criterion not met.
| Ref. | Rep. exposed | Sel. non-exp. | Ascert. exp. | Outcome absent | Ctrl main | Ctrl addit. | Assess. outcome | Follow-up dur. | Adequacy FU | Total |
| Auffret et al[22] (2017) | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | 9 |
| Chen et al[25] (2024) | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | 9 |
| Dizon et al[31] (2015) | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | 9 |
| Kooistra et al[24] (2020) | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | No | 8 |
| Pavlicek et al[19] (2023) | Yes | Yes | Yes | Yes | Yes | No | Yes | Yes | Yes | 8 |
| Muntané-Carol et al[18] (2021) | Yes | Yes | Yes | Yes | Yes | No | Yes | Yes | Yes | 8 |
| Bagur et al[23] (2012) | No | Yes | Yes | Yes | Yes | Yes | Yes | Yes | Yes | 8 |
| Wasim et al[30] (2025) | Yes | Yes | Yes | Yes | Yes | No | Yes | Yes | Yes | 8 |
| Ledwoch et al[34] (2013) | Yes | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 7 |
| Naveh et al[21] (2017) | Yes | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 7 |
| Van Gils et al[29] (2018) | Yes | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 7 |
| Castro-Mejía et al[36] (2022) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | Yes | 7 |
| Husser et al[38] (2016) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | Yes | 7 |
| Natarajan et al[37] (2022) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 6 |
| Khawaja et al[27] (2011) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 6 |
| Rampat et al[26] (2017) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 6 |
| Guetta et al[20] (2011) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 6 |
| Fraccaro et al[33] (2011) | No | Yes | Yes | Yes | Yes | No | Yes | Yes | No | 6 |
All the data in the investigation were available as continuous and as dichotomous variables. Valve platform type (balloon-expandable, self-expanding, or mechanically expanded systems) was recorded when reported in the included studies to describe the overall distribution of device types across the pooled TAVR cohorts. The pre-test and post-test interventions were extracted for continuous outcomes. Due to a lack of paired t-test data, mean ± SD and n (%) were used independently in crossover studies. In the meta-analysis, several statistics were used to assess the heterogeneity of the included papers. The effect size varied amongst studies, as indicated by the tau square (τ2), which is an indication of the within-study variance. Degrees of freedom (df) represent the number of independent comparisons required to calculate the pooled effect size. If detected differences in effect sizes between studies were more than what would be expected by chance, it was determined by the χ2 test. If the χ2 value was significant, then heterogeneity was positive. The fraction of total variation that can be attributable to heterogeneity rather than random variation was assessed by the I2. Since the statistical heterogeneity was assessed using the I2 statistic, values above 50% were indicative of substantial heterogeneity. Elevated values suggested increased variability and disparity across research findings. Random-effects meta-analysis of pooled odds ratios (OR) was performed using restricted maximum likelihood (REML) estimation. Pooled proportions were estimated using a generalized linear mixed model (random-intercept logistic regression) on the logit scale, with the between-study variance estimated by maximum likelihood. The ‘forest plots’ were used to represent the analysis, with a null-effect line in the central axis, and the ‘diamond’ representing the combined effect of individual studies. The ‘meta’ and ‘metafor’ packages were employed to conduct the analysis via R Studio[17]. To explore sources of heterogeneity, subgroup analyses were performed stratifying the PPI incidence pool by valve platform (balloon-expandable, self-expanding, mechanically expanded, combined self-expanding and mechanically expanded, and mixed) and by study era (pre-2016 vs post-2016). For the primary OR analysis of baseline RBBB and PPI, a valve-type subgroup analysis was additionally conducted. Meta-regression of PPI rate on publication year was performed using a mixed-effects model. Sensitivity was assessed by leave-one-out analysis. Publication bias was evaluated using Egger’s test and visual inspection of funnel plot asymmetry. All title-and-abstract screening was performed independently by two reviewers (Tobias K Fuchs and Cameron Jones); discrepancies were resolved by consensus. Inter-rater agreement at the title-and-abstract screening stage was assessed using a Cohen’s kappa statistic (κ = 0.83), indicating strong inter-rater agreement.
A total of 362 records were identified through database searches, including 176 from PubMed, 128 from Cochrane, and 58 from EMBASE. Before screening, 86 records were removed (43 duplicates, 14 marked ineligible by automation tools, and 29 removed for other reasons), leaving 276 records for title and abstract screening. Of these, 73 were excluded, and 203 reports were sought for full-text retrieval. Two reports could not be retrieved, resulting in 201 full-text articles assessed for eligibility. Following full-text review, studies were excluded mainly due to wrong outcomes (n = 55), inappropriate study design (n = 54), or incorrect target population (n = 72). Ultimately, 20 studies met the inclusion criteria and were included in the systematic review. A summary of the literature search and study selection is provided in the PRISMA diagram below (Figure 1).
Out of 20, two used a randomized control design, and 18 were prospective or retrospective observational cohort studies. Figure 2 summarizes the risk assessment results through a ‘traffic light’ and a ‘summary’ plot. The randomized studies were assessed using the Cochrane ROB2 tool[15]. In contrast, the NOS was used to assess the risk of bias across the cohort studies[16] (Table 3).
A total of 20 studies were identified and included for analysis from the provided sources. The included research utilized various study designs, including randomized clinical trials, prospective cohorts, observational studies, case-matched cohorts, and retrospective multicenter registry or cohort analyses. These studies were conducted across diverse geo
| Ref. | n | Age | Male | Female | Population characteristics | Diagnosis |
| Muntané-Carol et al[18] (2021) | 459 | 79 ± 8 | 251 | 208 | Minimalist TAVR; SAPIEN 3 (85.6%) or Evolut (12.6%); hypertension (91.9%) | Severe aortic stenosis |
| Pavlicek et al[19] (2023) | 203 | 80 ± 6 | 106 | 97 | Symptomatic; EvolutR or SAPIEN 3; diabetes (37%), CAD (59%) | Degenerative severe aortic stenosis |
| Meduri et al[28] (2019) | 874 (baseline characteristics reported for 704 pacemaker-naive patients) | 82-83 (approx) | 345 | 359 | High/extreme surgical risk; Lotus vs CoreValve (Classic/EvolutR) | Symptomatic severe aortic stenosis |
| Castro-Mejía et al[36] (2022) | 344 | 83 (79-86) | 135 | 209 | New generation SEV (Evolut-R/Pro, Acurate-neo, Portico, Allegra) | Severe aortic stenosis |
| Auffret et al[22] (2017) | 3527 | 82 ± 8 | 1764 | 1763 | Baseline RBBB impact; 61% BEV; 39% SEV | Symptomatic severe aortic stenosis |
| Bagur et al[23] (2012) | 822 (411/group) | 81 ± 11 (TAVI); 80 ± 4 (SAVR) | 357 | 465 | Elderly; TAVI (Edwards) vs isolated SAVR; matched by baseline ECG | Symptomatic severe aortic stenosis |
| Wasim et al[30] (2025) | 548 | 80.6 ± 6.7 | 271 | 277 | Unselected cohort; various valves; AF (30%) | Severe aortic stenosis |
| Chen et al[25] (2024) | 857 | 82-83 (approx) | 501 | 356 | Intermediate/high risk; SAPIEN 3; annulus calcification highlighted | Symptomatic severe aortic stenosis |
| Dizon et al[31] (2015) | 2531 | 84.5 ± 7.2 | 1324 | 1207 | Inoperable/high-risk; Edwards SAPIEN valve | Severe aortic stenosis |
| Natarajan et al[37] (2022) | 192 | 81.8 ± 6.4 | 104 | 88 | Outpatient TAVI; 95.3% Sapien S3/ultra; remote monitoring | Symptomatic severe aortic stenosis |
| Fraccaro et al[33] (2011) | 64 | 80.97 ± 6.55 | 29 | 35 | Dystrophic calcification; CoreValve Revalving System | Aortic stenosis |
| Guetta et al[20] (2011) | 70 | 83 ± 4.6 | 26 | 44 | High risk or inoperable; CoreValve system | Symptomatic severe aortic stenosis |
| Husser et al[38] (2016) | 183 | 80-81 (approx) | 97 | 86 | High-risk; SAPIEN 3 vs SAPIEN XT | Symptomatic severe aortic stenosis |
| Khawaja et al[27] (2011) | 243 | 81.3 ± 6.7 | 123 | 120 | Very high/excessive surgical risk; CoreValve | Symptomatic severe aortic stenosis |
| Kooistra et al[24] (2020) | 2804 | 82 (77-85) | 1,248 | 1,556 | Elderly; SEV (37%) vs BEV (56%) vs Lotus (7%) | Severe aortic stenosis |
| Kostopoulou et al[32] (2015) | 45 | 81 ± 5 | 27 | 18 | NYHA II/III; normal/slightly impaired LV function; CoreValve | Severe aortic stenosis |
| Ledwoch et al[34] (2013) | 1147 | 81.5-82 (approx) | 468 | 679 | Elderly; high comorbidities; CoreValve or Sapien | Severe symptomatic aortic stenosis |
| Naveh et al[21] (2017) | 110 | 80.7 ± 6.5 | 51 | 59 | Symptomatic AS; Medtronic CoreValve or Edwards Sapien XT | Symptomatic aortic stenosis |
| Rampat et al[26] (2017) | 201 | 81.2 ± 7.7 | 102 | 99 | High surgical risk; LOTUS bioprosthesis | Degenerative aortic stenosis |
| Van Gils et al[29] (2018) | 291 | 79 ± 8 | 156 | 135 | Transarterial TAVI; CoreValve, Sapien XT/3, Lotus | Severe aortic stenosis |
Across the included TAVR cohorts (n = 15104), balloon-expandable valves accounted for 8609 patients (57.0%; note that this patient-level distribution differs from the study-level valve strata used in Figure 4, in which each study is assigned to a single platform category), self-expanding valves for 5316 patients (35.2%), and mechanically expanded or other valve platforms for 1158 patients (7.7%), with valve type not specified in 21 patients (0.1%). The overall study sample of 15515 patients includes one case-matched cohort study (Bagur et al[23]) that enrolled both transcatheter and surgical AV replacement recipients; the 411-patient TAVR subgroup from this study contributes to the PPI incidence meta-analysis pool (n = 15104), while the full matched cohort contributes to the total sample reported in the abstract. Valve platform distribution was calculated only for patients who underwent TAVR; accordingly, the denominator used for valve-type reporting (n = 15104) differs from the total enrolled study sample (n = 15515).
Need for new PPI: All the included studies reported on the primary outcome of PPI requirement following TAVR[18]. A total of 19/20 studies demonstrated a strong positive association between pre-existing conduction abnormalities and the subsequent need for PPI, while one study noted that baseline RBBB did not independently predict heart block, likely due to its very low prevalence in that specific cohort[19]; that study was accordingly not included in the pooled OR analysis. Pre-existing RBBB was consistently identified across the literature as the most potent predictor of procedural complications, with OR for PPI reaching 43.0 and 18.0 in specific centers[20,21]. These large effect estimates were derived from smaller single-center studies and should be interpreted with caution. Large-scale multicenter analyses revealed that patients with baseline RBBB faced PPI rates as high as 40.1%, compared to significantly lower rates in those with normal baseline conduction[22,23].
Furthermore, researchers found that the combination of baseline RBBB and increased valve implantation depth resulted in a 100% incidence of high-degree atrioventricular block[20]. Supplementary baseline factors, such as first-degree atrioventricular block and non-specific intraventricular conduction delays, demonstrated a strong collective association with both early- and late-onset pacing necessities[18,24]. A summary of reported associations between these other baseline conduction abnormalities and PPI across the included studies is provided in Table 5. Data from the PARTNER 2 registries indicate that the presence of the RBBB before the procedure significantly increased the likelihood of requiring a new device within 30 days, nearly sixfold[25]. Mechanically expanded valve systems, such as the Lotus device, were likewise associated with an elevated pacing requirement in patients with baseline conduction disease; in that cohort, a composite of pre-procedural conduction abnormalities was one of two independent predictors of the need for permanent pacing (OR = 2.54, 95%CI: 1.19-5.43, P = 0.048), the other being the absence of AV calcification[26].
| Ref. | n | Conduction abnormality | PPI rate in subgroup (%) | Adjusted effect estimate | Notes |
| Auffret et al[22] (2017) | 3527 | First-degree AV block | 18.5% | Not independently significant in MV model | Baseline PR > 200 ms associated with higher PPI rate; not significant on multivariate analysis |
| Kooistra et al[24] (2020) | 2804 | IVCD (non-RBBB) | OR 3.3 (95%CI: 1.7-6.3) | IVCD independently predicted late PPI (> 48 hours post-procedure) | |
| Rampat et al[26] (2017) | 201 | Pre-procedural block composite (1° AVB, hemiblock, BBB) | OR 2.54 (95%CI: 1.19-5.43) | Composite pre-procedural conduction disease was an independent predictor of PPI in the LOTUS cohort, alongside absence of aortic valve calcification (OR 0.55) | |
| Khawaja et al[27] (2011) | 243 | QRS duration > 120 ms (IVCD/hemiblock) | OR 2.1 (95%CI: 1.0-4.5) | Prolonged QRS independently predicted PPI in CoreValve cohort; not RBBB-specific | |
| Naveh et al[21] (2017) | 110 | PR interval prolongation (> 200 ms) | OR 4.7 (95%CI: 1.2-18.3) | Baseline delta PR > 28 ms independently predicted long-term pacing dependency at 6-12 months | |
| Van Gils et al[29] (2018) | 291 | Pre-existing conduction disease (non-RBBB) | Not reported | In Cohort A (normal baseline), new QRS prolongation (not pre-existing disease) drove PPI requirement | |
| Pavlicek et al[19] (2023) | 203 | New-onset LBBB after TAVR | OR 15.7 (CI not reported) | New-onset LBBB was the strongest predictor of high-degree AV block requiring PPI in this cohort | |
| Fraccaro et al[33] (2011) | 64 | Pre-existing RBBB + first-degree AVB combination | 100% | Not modelled separately | All patients with both RBBB and implant depth > 6 mm required PPI; no patients without both factors did |
Secondary outcomes, including new-onset conduction abnormalities and the timing of device installation, were reported across the included studies[26]. New-onset LBBB was the most frequent post-procedural conduction dis
The findings on short-term and mid-term mortality were inconsistent across studies; yet, the majority of research concluded that the insertion of a permanent pacemaker did not independently increase the risk of mortality[30]. However, the presence of baseline RBBB was independently associated with significantly increased all-cause and cardiovascular mortality at 30 days and during midterm follow-up[22]. In contrast, long-term data from the PARTNER study indicated that new chronic pacing was independently associated with increased 1-year mortality and significantly higher rehospitalization rates[31]. Patients requiring PPI typically experienced extended hospitalizations; the median duration increased from 3 to 4 days or longer when pacing was clinically indicated[25]. Available data suggest that right ventricular pacing may modestly attenuate LVEF recovery post-TAVR, though findings were heterogeneous across the three contributing studies (see next section). Secondary clinical outcomes such as stroke rates did not differ significantly between paced and non-paced patients[28]. Overall, these studies indicate that pacemakers address the immediate electrical risks; nonetheless, pre-existing conduction disease may identify a higher-risk patient population with reduced long-term survival[22,31] (Table 2).
A meta-analysis of pooled proportions was conducted to report the relative incidence of new PPI after TAVR, as reported across the literature. Due to heterogeneity in study design and reporting, pooled incidence results were interpreted with caution.
Need for new PPI: A total of 20 studies reported quantitative data on new PPI events in patients who received TAVR. The random effects model for the pooled proportion was found to be 0.18 (95%CI: 0.14-0.24). This indicates an 18% incidence of patients requiring new PPI post-procedure. The CI was large and signified between-study heterogeneity. The incidence varied from 4% to 40% across different studies[18,20,23]. Heterogeneity analysis revealed a significant variability in the pooled results (I2 = 97.7). The high heterogeneity likely reflected differences in valve generation, implantation depth, pacemaker implantation criteria, operator experience, and study era. Therefore, pooled incidence estimates should be interpreted cautiously. This difference arose mainly due to variations in patient characteristics, implantation depth, valve platform, and pacing criteria. For reference, the original pooled incidence forest plot is presented in Supplementary Figures 1, 2, 3 and 4, while an updated analysis is depicted in Figure 3. The associated funnel plot is provided in Supplementary Figure 5. Subgroup analysis by valve type demonstrated pooled PPI proportions of 9% (95%CI: 0.06-0.13) for balloon-expandable valves, 29% (95%CI: 0.22-0.38) for self-expanding valves, and 20% (95%CI: 0.13-0.29) for mixed-platform cohorts, with significant differences across subgroups (χ2 = 49.51, df = 4, P < 0.001; Figure 4). Stratification by study era (pre-2016 vs post-2016) yielded pooled proportions of 22% (95%CI: 0.13-0.36) and 17% (95%CI: 0.12-0.23), respectively, without a statistically significant between-group difference (χ2 = 0.79, df = 1, P = 0.374; Supple
Incidence of new-onset bundle branch block: New-onset LBBB was analyzed across 11 studies (n = 4907). The random-effects pooled proportion of new-onset LBBB was 38% (95%CI: 0.27-0.50; I2 = 98.4%, τ2 = 0.70), with individual study proportions ranging from 11% (Muntané-Carol et al[18]) to 71% (Van Gils et al[29]), reflecting marked variation attributable to valve platform and implantation technique (Figure 5). New-onset RBBB could not be pooled. Among the included cohorts, only Khawaja et al[27] (8/185, 4.3%) and Guetta et al[20] (3/70, 4.3%) reported new-onset RBBB separately from new-onset LBBB; the remaining cohorts reported new-onset LBBB alone. New-onset LBBB is therefore the predominant conduction disturbance after TAVR, and patients developing new bundle branch block require post-procedural monitoring, as a subset may progress to high-degree AV block and complete heart block.
Pooled analysis of four studies reporting OR for baseline RBBB and PPI yielded an OR of 4.52 (95%CI: 2.64-7.74; P < 0.001) using a random-effects REML model, with moderate heterogeneity (I2 = 50.3%, τ2 = 0.15) (Figure 6). Individual study ORs ranged from 2.23 (95%CI: 1.09-4.59) to 8.61 (95%CI: 3.14-23.67). These four estimates were not derived uniformly: One is an unadjusted estimate, the remaining three are adjusted for differing covariate sets, and the outcome was ascertained at hospital discharge in one study and at 30 days in the others. The pooled value should therefore be interpreted as a summary of heterogeneously derived associations rather than as a single adjusted effect. A fifth study previously included in this pool has been removed, because the OR entered for it was the multivariable estimate for any bundle branch block rather than for RBBB; that study reported a univariate RBBB OR of 0.99 (95%CI: 0.98-1.02) and identified RBBB as non-predictive in its cohort. A six-study pooled estimate reported in earlier versions of this analysis has been withdrawn in full following source verification of the underlying two-by-two counts. Leave-one-out sensitivity analysis yielded pooled ORs ranging from 3.92 to 5.76 across all omission scenarios (Supplementary Figure 2). A valve-type subgroup analysis demonstrated that the association between baseline RBBB and PPI was directionally consistent across balloon-expandable, self-expanding, and mixed platform subgroups (Supplementary Figure 3). Assessment of publication bias using Egger’s test did not identify significant asymmetry (t = 0.13, df = 2, P = 0.907), although with only four contributing studies this assessment has very limited power, and visual inspection of the funnel plot was similarly unremarkable (Supplementary Figure 1). Pre-existing RBBB represents one of the strongest and most consistently reported predictors of PPI requirement after TAVR across the included studies.
Only three studies examined the comparative change in LVEF post-TAVR in 4262 patients. The random effects model produced a mean difference of -1.60 (95%CI: -4.99-1.80). The negative mean difference indicates that patients necessitating PPI exhibited marginally lower LVEF values relative to those not requiring PPI. The heterogeneity in the analysis was significant (I2 = 94.3%, τ2 = 8.5116), indicating a non-linear association between TAVR and LVEF. No consistent asso
Nine studies reported long-term pacing dependency data following PPI after TAVR (Table 6). Pacing dependency rates varied considerably across studies and follow-up durations, reflecting differences in patient population, valve type, and pacing indication criteria. The highest dependency rate was reported by Naveh et al[21], in which 68.4% of implanted patients remained pacing-dependent at 6-12 months of follow-up. Van Gils et al[29] reported 61% dependency (defined as > 20% ventricular pacing) at six months[29], while Meduri et al[28] documented 50% dependency at one year in the REPRISE III trial, with 83% of patients who were dependent at 30 days remaining so at one year. Conversely, Kosto
| Ref. | n (PPM) | Follow-up | Dependency rate | Definition/notes |
| Naveh et al[21] (2017) | 38 | 6-12 months | 68.4% | Long-term pacing dependency |
| Van Gils et al[29] (2018) | 66 | 6 months | 61% | > 20% ventricular pacing |
| Meduri et al[28] (2019) | 245 | 1 year | 50% | 83% of 30-day dependent remained so at 1 year |
| Dizon et al[31] (2015) | 173 | 1 year | 51% paced ECGs | 95% RV-paced morphology |
| Wasim et al[30] (2025) | 173 | Follow-up visits | 38% | PM dependency during follow-up |
| Guetta et al[20] (2011) | 28 | 3 months | 40% | HDAVB persisting at 3-month check |
| Fraccaro et al[33] (2011) | 25 | 6 months | 23.5% | > 95% pacing; mean burden 19% in remainder |
| Kostopoulou et al[32] (2015) | 10 | 24 months | 40% | 60% recovered endogenous rhythm by 1 month |
| Bagur et al[23] (2012) | 30 | Discharge | 80% paced rhythm | Long-term dependency not formally reported |
This systematic review synthesized available observational and cohort data to quantify how baseline conduction ab
The differential mortality associations observed across studies may be explained by the underlying temporal and mechanistic context. In-hospital and 30-day PPI does not appear to independently increase short-term mortality in the majority of registry analyses included in this review; pacing requirements in this period predominantly reflect acute transient conduction injury from mechanical compression of the conduction system during valve deployment rather than primary myocardial disease. By contrast, long-term pacing dependency, particularly high-burden right ventricular pacing, has been associated in registry data with pacing-induced ventricular dyssynchrony, attenuated LVEF recovery, and worse clinical outcomes at one year[31]. These observations are further confounded by baseline left ventricular dysfunction, comorbidity burden, and hemodynamic effects of the index TAVR procedure itself, which preclude direct causal interpretation of the mortality associations reported across the included observational studies.
Differences in valve platform likely contributed to the heterogeneity observed across studies. Self-expanding valve systems have generally been associated with higher PPI rates compared with balloon-expandable valves, as demonstrated in registry analyses where device type independently predicted pacing requirement[34]. Because our pooled analysis included mixed device types and generations, variability in reported event rates should be interpreted within this context.
The present review was undertaken to address several gaps identified in prior work. Hosseini Mohammadi et al[5] pooled data from 108 studies and 77538 patients using a network meta-analysis framework to rank conduction and procedural predictors of PPI, but did not perform subgroup analyses stratified by valve platform or study era, leave-one-out sensitivity analysis, or formal publication bias assessment using Egger’s test. Peng et al[2] examined perioperative risk factors for PPI without synthesizing data on long-term pacing dependency, LVEF trajectory, or mortality. The present review contributes updated REML-based random-effects analysis, valve-type and study-era subgroup analyses, meta-regression of PPI rate over time, leave-one-out sensitivity analysis, Egger’s test for publication bias, a descriptive synthesis of long-term pacing dependency across nine studies, and a structured summary of associations between non-RBBB conduction abnormalities and PPI (Table 5). A comparison of the present review with prior meta-analyses is provided in Table 7.
| Ref. | Study design | Included studies/patients | Search period | OR for RBBB predicting PPI | REML random-effects analysis | Subgroup analysis by valve type | Subgroup analysis by study era | Meta-regression on publication year | Leave-one-out sensitivity analysis | Egger test for publication bias | Long-term pacing dependency synthesis | Summary of non-RBBB conduction abnormalities |
| Present study | Systematic review and meta-analysis | 20/15515 | 2010-2026 | 4.52 (95%CI 2.64-7.74) | Yes | Yes (Figure 4; Supplementary Figure 3) | Yes (Supplementary Figure 6) | Yes (Supplementary Figure 7) | Yes (Supplementary Figure 2) | Yes (P = 0.907) | Yes (Table 6, 9 studies) | Yes (Table 5) |
| Mohammadi et al[5] (2025) | Systematic review and network meta-analysis | 108/77538 | Not reported | RR approx. 3.20 | No | No | No | No | No | No | No | No |
| Peng et al[2] (2025) | Systematic review and meta-analysis | Not reported separately | Systematic | Not computed | No | No | No | No | No | No | No | No |
| Sultan et al[3] (2024) | Prospective subanalysis (Navitor IDE) | Prospective cohort | Prospective | Device-specific analysis | No | Yes | No | No | No | No | No | No |
A recent network meta-analysis and systematic review that pooled more than 77000 patients ranked RBBB among several conduction predictors and reported a pooled relative risk for PPI after TAVR of approximately 3.20 for baseline RBBB, with multiple conduction and procedural factors contributing to PPI risk[5]. Single-center derived risk models and validation cohorts have emphasized the outsized effect of baseline RBBB; the RITMO risk score found baseline RBBB to be a key predictor and reported an OR exceeding six for high-score patients in a validation cohort, underscoring heterogeneity in effect estimates across designs and valve platforms[7]. Large prospective device-specific analyses, such as the Navitor IDE sub-analysis, illustrate that pre-existing conduction abnormalities remain important determinants of 30-day new PPI across contemporary valve platforms, while also highlighting procedural and device-related modifiers of risk[3].
The observed PPI rate of 18% and the association between baseline RBBB and PPI should be interpreted in the context of the surgical risk profile of the study populations. The included studies enrolled predominantly high-risk and intermediate-risk patients, populations in which the benefit-risk balance of TAVR has been evaluated in randomized trials. Generalizability of these conduction complication rates to lower-risk populations, in whom TAVR is increasingly performed, may be limited given differences in baseline comorbidity burden, valve morphology, and device generations used across study eras. The temporal decline in pooled PPI rates suggested by meta-regression (slope = -0.06 per year, P = 0.118, not statistically significant) and reported in individual cohort data may reflect concurrent changes in valve technology, implantation technique, and institutional experience, though these factors were not independently assessed in the available studies.
TAVR has been evaluated across the full spectrum of surgical risk in landmark randomized trials. In high-risk populations (PARTNER 1, CoreValve High Risk trial), TAVR demonstrated non-inferiority to surgical AV replacement with respect to all-cause mortality at one year, establishing the foundational evidence base for its adoption[5]. Extension to intermediate-risk patients (PARTNER 2, SURTAVI trial) and subsequently to low-risk populations (PARTNER 3, Evolut Low Risk trial) demonstrated consistent survival benefit with acceptable procedural complication rates. However, the risk-benefit balance differs across strata: Lower-risk patients face a longer expected valve lifespan and are therefore subject to cumulative risks from structural valve deterioration and valve-in-valve reintervention, whereas higher-risk patients derive greater near-term benefit from avoiding open surgery. Within this broader adverse event spectrum, which includes paravalvular leakage, stroke, vascular access complications, and acute kidney injury-PPI represents one of the most frequent device-related complications, occurring in approximately 10%-20% of patients across contemporary series. The temporal decline in PPI rates with increasing institutional volume and device iteration, as suggested by meta-regression in the present analysis, is consistent with broader observations that procedural learning curves and prosthesis design iteration reduce conduction injury rates over time.
The pooled findings suggest several actionable steps for clinicians involved in TAVR care, spanning pre-procedural counseling to post-procedural monitoring and procedural planning. Discuss with patients the elevated baseline probability of needing a PPI (approximate pooled risk 18%) and explain that pre-existing RBBB substantially increases that risk, which may influence patient preferences and informed consent. Because most pacemaker implantations occurred during the index hospitalization and typically within the first week after TAVR, extended telemetry monitoring should be strongly considered in patients with baseline RBBB or evolving conduction changes. The integration of baseline ECG (specifically presence of RBBB, bifascicular block, and hemiblocks) with anatomical metrics and device choice is important. Centers may adopt validated scores (for example, RITMO or other two-step tools) to individualize risk estimates and plan follow-up[8]. Valve selection and implantation depth strategies that minimize conduction system trauma and have a low threshold for intraprocedural electrophysiology consultation or monitoring should also be considered[35-38]. Programs performing TAVR should ensure availability of pacing services and pathways for rapid PPI implantation, particularly for cohorts enriched for baseline conduction disease[9].
This review has several important strengths. By pooling data from multiple cohorts and registries, it included a large, aggregated sample, improving the precision of estimates for PPI after TAVR and for the effect of baseline conduction abnormalities. The analysis also focused on clinically relevant predictors, particularly the increased risk associated with RBBB, providing information that may assist clinicians in risk stratification and procedural planning. In addition, the inclusion of both broad registry data and device-specific studies increases the applicability of the findings across different TAVR platforms and clinical settings. Several limitations need discussion. There was significant variability between studies. This was mainly because of differences in valve types, implantation techniques, causes for pacemaker im
Sex and gender disaggregation was not consistently reported across the included studies, precluding sex-stratified analysis; this represents a recognized methodological gap that future prospective studies should address. Asian and non-Western patient cohorts were underrepresented in the included literature, limiting the generalizability of findings to non-European or non-North American TAVR populations. Pacing dependency definitions and follow-up durations varied substantially across the nine studies contributing dependency data, precluding formal pooled synthesis; these data are therefore reported descriptively. The temporal decline in PPI rates suggested by meta-regression and the single-cohort volume analysis should be interpreted cautiously, as concurrent changes in valve technology, patient selection, and implantation technique may confound this trend. The primary updated OR meta-analysis included four studies, reflecting the limited number of eligible reports with extractable comparative data for baseline RBBB and PPI. The moderate heterogeneity observed in the updated analysis (I2 = 48.4%) likely reflects differences in valve platform, pacing thresholds, and patient-level confounders. As pooled estimates were derived from observational data with variable degrees of multivariable adjustment, residual confounding by implantation depth, valve oversizing, and membranous septum length cannot be excluded. A pooled estimate of new-onset RBBB incidence could not be generated. Among the included cohorts, only two reported new-onset RBBB separately from new-onset LBBB, and the remainder reported new-onset LBBB alone; the incidence of new-onset RBBB after TAVR therefore could not be quantified from the available literature and is not reported here.
Baseline RBBB demonstrated a strong and consistent association with PPI after TAVR. The pooled estimates from this review indicate an 18% PPI incidence, 38% new-onset LBBB occurrence, and a pooled OR of 4.52 (95%CI: 2.64-7.74) for the association between baseline RBBB and PPI in the updated analysis. Beyond the acute pacing decision, a substantial proportion of implanted patients develop long-term pacing dependency, ranging from 23.5% to 68.4% among studies applying a formal dependency definition (nine studies contributed dependency data), with implications for pacing-induced cardiomyopathy and long-term ventricular function. A temporal reduction in PPI rates with increasing institutional volume further suggests that operator experience is a modifiable determinant of this burden. Collectively, these observational findings are consistent with baseline RBBB serving as a risk marker that may inform preprocedural counseling, risk stratification, and postprocedural monitoring protocols for TAVR candidates, pending prospective validation. Future prospective, standardized studies with uniform dependency definitions and device-specific ran
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