Structural Heart 9 (2025) 100428Articles and Issues Available at ScienceDirect
Structural Heart
journal homepage: www.structuralheartjournal.orgOriginal ResearchConduction Disorders After Transcatheter Aortic Valve Implantation:
Evolution Over Time and Association With Long-Term Outcomes
Aileen Paula Chua, MD a , Rinchyenkhand Myagmardorj, MD a, Takeru Nabeta, MD a,
Jurrien H. Kuneman, MD a , Frank van der Kley, MD, PhD a , Jeroen J. Bax, MD, PhD a,b,
Nina Ajmone Marsan, MD, PhD a,*
a Department of Cardiology, Heart Lung Center, Leiden University Medical Center, Leiden, The Netherlands
b Department of Cardiology, Turku Heart Center, University of Turku and Turku University Hospital, Turku, FinlandA R T I C L E I N F O
Article history:
Submitted 20 June 2024
Revised 30 January 2025
Accepted 12 February 2025
Available online 17 February 2025
Keywords:
Conduction disorders post-TAVI
Left bundle branch block
Long-term outcomes
Permanent pacemaker* Address correspondence to: Nina Ajmone Mars
Leiden 2333 ZA, The Netherlands.
E-mail address: n.ajmone@lumc.nl (N. Ajmone M
https://doi.org/10.1016/j.shj.2025.100428
2474-8706/© 2025 The Author(s). Published by Els
(http://creativecommons.org/licenses/by/4.0/).A B S T R A C T
Background: Expanding indications for transcatheter aortic valve implantation (TAVI) highlighted the importance
of complications such as new left bundle branch block (LBBB) or permanent pacemaker (PPM) implantation.
However, studies on the long-term outcomes of these conduction abnormalities (CA) are limited. This study aims
to examine the progression of CA within the first year after TAVI and their long-term prognostic value.
Methods: TAVI patients were divided into 1) PPM implantation within the first year, 2) post-TAVI LBBB persisting
until 1 year (permanent LBBB), and 3) no-CA. Endpoint was all-cause mortality after 1 year.
Results: Among 794 patients initially included, 30% developed new LBBB, which persisted in 17% until discharge;
12% received a PPM during the hospitalization. One-year follow-up was available in 502 patients: 11% were
classified as permanent LBBB (n ¼ 56), 18% as PPM (n ¼ 89), and the rest as no-CA (n ¼ 357). Baseline char-
acteristics were comparable, except for valve type, with self-expanding more common among the PPM group. At
1-year follow-up, lower left ventricular ejection fraction and global longitudinal strain were observed in the PPM
and permanent LBBB groups compared to the no-CA group (55%  9% and 15%  4% vs. 54%  11% and 15% 
4% vs. 58%  9% and 17%  4%, respectively, p < 0.001). At long-term follow-up (median: 4 [interquartile
range: 3-6] years), higher mortality was observed in the PPM group (χ2 ¼ 10.168, p ¼ 0.006). In addition, PPM
implantation (hazard ratio: 1.654, p ¼ 0.011) and global longitudinal strain at 1 year (hazard ratio: 0.950, p ¼
0.027), as well as pre-TAVI EuroSCORE II and New York Heart Association III-IV at 1 year, were independently
associated with the outcome.
Conclusions: Post-TAVI CAs are dynamic within the first year. Patients who needed PPM implantation did not
show significant improvement in left ventricular function after TAVI and had higher long-term mortality.A B B R E V I A T I O N S AS, aortic stenosis; CAs, conduction abnormalities; ECG, electrocardiogram; EF, ejection fraction; GLS, global
longitudinal strain; HAVB, high-grade atrioventricular block; IVCD, intraventricular conduction defect; LBBB, left
bundle branch block; LV, left ventricle; LVMI, left ventricular mass index; PPM, permanent pacemaker; RV, right
ventricle; TAVI, transcatheter aortic valve implantation.Introduction
Transcatheter aortic valve implantation (TAVI) is an effective treatment
option for patients with severe aortic stenosis (AS), not only for high- and
intermediate-risk patients but also for those with lower surgical risk.1
Optimization of procedural aspects and valve prosthesis design has greatlyan, MD, PhD, Department of Car
arsan).
evier Inc. on behalf of Cardiovascimproved patient outcomes, especially in the first year after TAVI im-
plantation.2,3 Now, attention is given to the complications that affect
long-term outcomes, especially in low-risk patients with longer life ex-
pectancies. Conduction abnormalities (CA) are still relatively common after
TAVI, including high-grade atrioventricular block (HAVB), left bundle
branch block (LBBB), and the need for a permanent pacemaker (PPM).diology, Heart Lung Center, Leiden University Medical Center; Albinusdreef 2,
ular Research Foundation. This is an open access article under the CC BY license
A.P. Chua et al. Structural Heart 9 (2025) 100428Numerous studies have evaluated the factors associated with the
development of CA and their impact on outcomes after TAVI, but results
are inconsistent, and follow-up duration is limited to the first 1 to 2
years.4 In addition, most studies investigated the occurrence of CA
immediately post-TAVI without considering the progression or persis-
tence of electrocardiographic changes during follow-up. Therefore, the
current study aims to 1) examine the progression of significant CA within
the first year post-TAVI in a large patient cohort; 2) investigate the
impact of PPM implantation and permanent LBBB on outcomes, starting
from the first year after TAVI; and 3) identify additional factors at
follow-up that may be associated with long-term mortality. Since these
patients are often referred back to their primary care physician at 1 year
after TAVI, understanding the clinical relevance of these complications
may help guide risk stratification and monitoring of these patients for the
subsequent years.
Materials and Methods
Study Population
Patients with severe AS who underwent TAVI between 2007 and
2019 at the Leiden University Medical Center (the Netherlands) were
included in the study. Patients with cardiac implantable electronic de-
vices (either PPM or implantable cardiac defibrillator) and preexisting
LBBB were excluded. Patients were assessed before the procedure, after
the procedure (immediately after and before discharge), and at 1-year
follow-up. Long-term analysis was performed only on patients with
complete data at 1-year follow-up. These patients were then divided into
3 groups: 1) those who underwent PPM implantation within the first year
(PPM group), 2) those who developed LBBB during the post-TAVI hos-
pitalization and persisted until 1-year follow-up (permanent LBBB
group), and 3) those without new LBBB or PPM (no-CA group).
The decision to perform TAVI was taken by a multidisciplinary heart
team. Clinical data, including demographics, cardiovascular risk factors,
medications, and procedural information, were retrospectively collected
from the departmental Cardiology Information system (EPD-Vision;
Leiden University Medical Center, the Netherlands). Indications for PPM
implantation were in accordance with guidelines.5 The institutional re-
view board of the Leiden University Medical Center approved the
retrospective analysis of the clinically acquired data and waived the need
for written informed consent.Electrocardiographic Variables
Twelve-lead electrocardiograms (ECGs) were collected at baseline,
post-TAVI (immediately after TAVI until discharge), and at 1-year follow-
up. ECG calibration was set at 0.1 mV/mm and the paper speed at 25
mm/s. Heart rate and rhythm, PR interval, and QRS duration were
recorded. New CA, specifically atrioventricular blocks, LBBB, right
bundle branch block, and nonspecific intraventricular conduction defects
(IVCDs), were analyzed. The criteria defining conduction disturbances
were adopted from the third Valve Academic Research Consortium and
the American Heart Association/American College of Cardiology/Heart
Rhythm Society recommendations.6,7Echocardiographic Variables
Transthoracic echocardiography was performed both at pre-proced-
ure and at 1-year follow-up using commercially available ultrasound
systems (Vivid7, VividE9 and E95; GE Healthcare, Horten, Norway)
equipped with 3.5 MHz or M5S-D transducers. Parasternal, apical, sub-
costal, and suprasternal views were obtained according to current rec-
ommendations.8 Data were digitally stored in cine-loop format for offline
analysis using commercially available software (EchoPac 204; GE Med-
ical Systems, Horten, Norway) and were retrospectively analyzed.2From the apical three- or five-chamber views, continuous wave
Doppler recordings were measured to estimate peak aortic jet velocity,
and the mean transvalvular pressure gradient was calculated using the
Bernoulli equation. Aortic valve area was derived from the left ventric-
ular (LV) outflow tract diameter and the velocity-time integrals of the
aortic valve (AV) and outflow tract. LV dimensions were measured from
the parasternal long-axis view and used to calculate LV mass index
(LVMI). The apical four- and two-chamber views provided LV end-
systolic and end-diastolic volumes, and ejection fraction (EF) was
derived using biplane Simpson’s method. Right ventricular (RV)
dysfunction was defined as tricuspid annular plane systolic excursion
<17 mm. The presence of significant regurgitation of the aortic, mitral,
and/or tricuspid valves was assessed by a multiparametric approach
based on current guidelines.8,9
LV strain was measured using speckle-tracking imaging (EchoPac204;
GE, Horten, Norway). The analysis was performed from the apical two-,
three-, and four-chamber views with a frame rate >40 frames/sec. The
region of interest was determined automatically but manually adjusted
when necessary. Global longitudinal strain (GLS) was calculated from the
average peak strain of the 17 LV segments and reported as absolute (i.e.,
positive) values.
Clinical Endpoint
The study endpoint was all-cause mortality starting from the 1-year
follow-up after TAVI. Data were obtained through the departmental
Cardiology Information System, which is linked to the governmental
death registry database.
Statistical Analysis
Continuous variables are expressed as means SDs or as medians and
interquartile ranges and were compared between the 3 groups using
Analysis of Variance (ANOVA) or the Kruskal-Wallis test, as appropriate.
Categorical variables are expressed as numbers and percentages andwere
compared using the chi-square test or Fisher exact test. The Bonferroni
method was used to correct for multiplicity. For the comparison of
echocardiographic parameters between baseline and follow-up, paired
sample t-test for 2 related samples was used.
The survival rate was estimated using Kaplan-Meier analysis and the
log-rank test. Analysis was started 12 months after TAVI until the
endpoint was reached. To investigate the association between clinical,
electrocardiographic, and echocardiographic parameters with all-cause
mortality, univariable and multivariable Cox proportional hazards
regression analyses were performed. Variables at 1-year follow-up, which
were statistically significant on univariable analysis, were included in the
multivariable regression. Only EuroSCORE II was included from the
baseline characteristics, and the clinical variables comprising the score
were excluded in the model to avoid collinearity. ECG parameters after
TAVI were likewise not included since these are inherent to the definition
of the subgroups. From the variables at the 1-year follow-up, New York
Heart Association (NYHA) functional class was selected as a measure of
clinical status, while among the echocardiographic parameters, GLS was
selected as a measure of LV function, and LVMI as a measure of size, since
LV hypertrophy in patients undergoing TAVI has been associated with
mortality.10 Hazard ratios and 95% CIs were calculated.
All analyses were performed using SPSS for Windows, version 25
(SPSS, Armonk, NY). A p-value <0.05 was considered statistically
significant.
Results
Progression of Conduction Abnormalities After TAVI
The progression of CA according to the different time points is illus-
trated in Figure 1.
Figure 1. Progression of CA over time. This Sankey diagram illustrates the progression of CA assessed in this study at 3 time points: immediately postprocedure, at
discharge, and at 1-year follow-up. (Image made in Sankeymatic.com).
Abbreviations: CA, conduction abnormality; LBBB, left bundle branch block; PPM, permanent pacemaker; TAVI, transcatheter aortic valve implantation.
A.P. Chua et al. Structural Heart 9 (2025) 100428CA Immediately Post-TAVI and at Discharge
An initial group of 794 patients who underwent TAVI and fulfilled
the inclusion criteria abovementioned were examined for the pre-
liminary analysis. From these patients, 30% (n ¼ 237) presented with
new-onset LBBB immediately post-TAVI, but only 17% still showed
LBBB at discharge (n ¼ 137, “persistent LBBB”; in 100 patients, LBBB
resolved), while 6% (n ¼ 51) underwent PPM implantation during
hospitalization. Of the 70% (n ¼ 557) of patients who did not developFigure 2. Timing of PPM implantation from the day of TAVI. This histogram dis
after TAVI.
Abbreviations: PPM, permanent pacemaker; TAVI, transcatheter aortic valve implan
3LBBB after TAVI, 8% (n ¼ 46) needed a PPM during the hospital stay,
while the remaining patients (n ¼ 549, 62%) did not have either LBBB
or PPM at discharge.
CA at 1-Year Follow-Up
At 1 year, 205 patients did not have follow-up, and 87 patients died.
Therefore, 502 patients who had follow-up ECG 1 year after TAVI were
included in the long-term analysis.plays the frequency of time to PPM implantation, with a median time of 4 days
tation.
Table 1
Baseline (pre-TAVI) clinical and echocardiographic characteristics according to the subgroups of CA
Variables No-CA (n ¼ 357) PPM (n ¼ 89) Permanent LBBB (n ¼ 56) p-value
Age (years) 80  7 80  7 79  6 0.724
Sex, male n (%) 185 (52) 55 (62) 25 (45) 0.104
BMI (kg/m2) 26.5  4.1 26.3  4.2 28.3  6.1*,y 0.010
EuroSCORE II (%) 2.95 (1.94-5.06) 3.07 (1.86-4.73) 3.45 (2.08-5.14) 0.535
NYHA, n (%)
I-II 145 (41) 39 (44) 19 (34) 0.493
III-IV 212 (59) 50 (56) 37 (66)
Comorbidities
Hypertension, n (%) 266 (75) 68 (76) 47 (84) 0.307
Dyslipidemia, n (%) 231 (65) 58 (65) 39 (70) 0.770
Diabetes mellitus, n (%) 94 (26) 21 (24) 21 (38) 0.155
Coronary artery disease, n (%) 207 (58) 57 (64) 32 (57) 0.558
Previous MI, n (%) 71 (20) 19 (21) 8 (14) 0.550
Stroke, n (%) 64 (23) 10 (16) 12 (26) 0.388
PAD, n (%) 110 (31) 15 (17)* 19 (34) 0.022
Atrial fibrillation, n (%) 91 (26) 26 (29) 15 (27) 0.772
Previous valve procedures, n (%) 22 (6) 4 (5) 4 (7) 0.777
Smoking, n (%) 80 (22) 13 (15) 12 (21) 0.268
COPD, n (%) 56 (16) 15 (17) 14 (25) 0.225
eGFR (mL/min/1.73 m2) 65  22 64  20 63  22 0.925
Procedural factors
TAVI approach, n (%)
Transfemoral 266 (74) 77 (86) 44 (79) 0.053
Transapical and subclavian 91 (26) 12 (14) 12 (21) 0.053
Valve type, n (%)
Balloon expandable 305 (85) 53 (60)* 42 (75) <0.001
Self-expanding 52 (15) 36 (40)* 14 (25) <0.001
ECG
Sinus rhythm, n (%) 281 (8) 66 (74) 44 (79) 0.646
Atrial fibrillation, n (%) 76 (21) 23 (26) 12 (21)
PR interval (ms) 180  32 196  41* 185  30 0.002
QRS duration (ms) 101 (92-112) 109 (98-138)* 93 (87-104)*,y <0.001
First degree AVB, n (%) 60 (21) 31 (46)* 10 (23)y <0.001
RBBB, n (%) 28 (8) 23 (26) - <0.001
IVCD, n (%) 102 (29) 42 (47)* 6 (11)*,y <0.001
Echocardiography
AV peak velocity (m/s) 4.0  0.8 4.1  0.8 3.9  0.9 0.439
AV mean gradient (mmHg) 42  17 43  17 42  21 0.831
Aortic valve area (cm2) 0.83  0.30 0.82  0.27 0.82  0.31 0.944
LV mass index (g/m2) 121  37 127  36 113  36 0.087
LVEDV (mL) 95  41 94  36 86  37 0.295
LVESV (mL) 47  30 46  25 44  31 0.742
LV EF (%) 53  11 53  11 52  13 0.658
LV GLS (|%|) 14.2  4.2 14.5  3.7 15.1  3.4 0.339
RV dysfunction, n (%) 104 (31) 25 (29) 15 (29) 0.919
Significant AR, n (%) 69 (19) 19 (21) 9 (16) 0.736
Significant MR, n (%) 64 (18) 16 (18) 5 (9) 0.236
Significant TR, n (%) 48 (14) 22 (25)* 9 (16) 0.029
Notes. Values are mean  SD, median (interquartile range), or n (%). p-values <0.05 were considered statistically significant and are shown in bold.
Abbreviations: AR, aortic regurgitation; AV, aortic valve; AVB, atrioventricular block; BMI, body mass index; CA, conduction abnormality; COPD, chronic obstructive
pulmonary disease; ECG, electrocardiogram; eGFR, estimated glomerular filtration rate; GLS, global longitudinal strain; IVCD, intraventricular conduction delay; LBBB,
left bundle branch block; LV EF, left ventricular ejection fraction; LV, left ventricle; LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular end-systolic
volume; MI, myocardial infarction; MR, mitral regurgitation; NYHA, New York Heart Association; PAD, peripheral artery disease; PPM, permanent pacemaker; RBBB,
right bundle branch block; RV, right ventricular; TAVI, transcatheter aortic valve implantation; TR, tricuspid regurgitation.
* p < 0.05 on Bonferroni correction vs. no-CA group.
y p < 0.05 on Bonferroni correction vs. new PPM group.
A.P. Chua et al. Structural Heart 9 (2025) 100428Of the patients with LBBB at discharge (94 patients), only 56 still
presented LBBB at 1-year follow-up, comprising the permanent LBBB
group (since no patients developed new LBBB at 1 year). In 35 patients,
LBBB resolved, and they were considered as no-CA, while 3 needed a
PPM implantation and were included in the PPM group.
From the 549 patients who did not develop CA at discharge, 16 pa-
tients needed a PPM within the first year post-TAVI and were included in
the PPM group.
Therefore, when examining the patients at the 1-year follow-up, the
PPM group consists of 89 patients (18%) who received a pacemaker
within the first year following TAVI. The median time of PPM implan-
tation was 4 days after TAVI, with an interquartile range of 3 to 6 days4(Figure 2). Although less common, 21% of patients (n ¼ 19) received the
PPM after the first week.
Regarding the type of PPM, dual chamber pacing was most common
(54%), followed by single-chamber pacing (32%). In 10% of patients, an
implantable cardiac defibrillator or cardiac resynchronization therapy
was implanted. Indications for the PPMwere high-grade AV block in 73%
and sinoatrial node disease in 17%.
Percentage of pacing was assessed at baseline and at follow-up. At
implantation, 54% of patients were paced >40% of the time, 16% paced
1% to 40%, while 19% had <1% pacing. At the 1-year follow-up, pacing
frequency was slightly reduced, with 45% paced >40% of the time, 29%
paced 1% to 40% of the time, and 17% had <1% pacing.
Table 2
One-year follow-up clinical and echocardiographic characteristics according to the subgroups of CA
Variables No-CA PPM Permanent LBBB p-value
(n ¼ 357) (n ¼ 89) (n ¼ 56)
NYHA at 1 year, n (%) 0.039
I-II 328 (97) 82 (94) 50 (89)
III-IV 11 (3) 5 (6) 6 (11)*
ECG at 1-year
Sinus rhythm, n (%) 277 (78) 29 (32) 42 (75) <0.001
Atrial fibrillation, n (%) 80 (22) 7 (8) 14 (25)
Paced rhythm, n (%) - 53 (60) -
PR interval (ms) 186  32 209  50* 199  29 <0.001
QRS duration (ms) 105 (96-116) 131 (107-156)* 147 (138-156)* <0.001
First degree AVB, n (%) 78 (28) 14 (48) 19 (45) 0.012
Echocardiography at 1-year
AV mean gradient (mmHg) 10  5 10  6 10  4 0.742
LV mass index (g/m2) 96  26 100  24 96  28 0.554
LV EDV (mL) 79  30 86  30 88  30 0.025
LV ESV (mL) 34  19 41  19* 42  22* <0.001
LVEF (%) 58  9 54  8* 54  11* <0.001
LV GLS (|%|) 17.1  3.7 15.1  3.5* 15.3  4.3* <0.001
Significant AR, n (%) 47 (14) 10 (12) 7 (13) 0.872
Significant MR, n (%) 68 (20) 33 (38)* 16 (29) 0.001
Significant TR, n (%) 64 (19) 32 (37)* 10 (18) 0.001
Notes. Values are mean  SD, median (interquartile range), or n (%). p-values <0.05 were considered statistically significant and are shown in bold.
Abbreviations: AR, aortic regurgitation; AV, aortic valve; AVB, atrioventricular block; CA, conduction abnormality; ECG, electrocardiogram; GLS, global longitudinal
strain; LBBB, left bundle branch block; LV EF, left ventricular ejection fraction; LV, left ventricle; LVEDV, left ventricular end-diastolic volume; LVESV, left ventricular
end-systolic volume; MR, mitral regurgitation; NYHA, New York Heart Association; PPM, permanent pacemaker; TAVI, transcatheter aortic valve implantation; TR,
tricuspid regurgitation.
* p < 0.05 on Bonferroni correction vs. no-CA group.
A.P. Chua et al. Structural Heart 9 (2025) 100428Long-Term Analysis
Baseline Patient Population Characteristics
Since outcomes were explored from 1-year after TAVI, long-term
analysis only included the 502 patients with follow-up ECG. Compared
to the patients who were excluded (n¼ 292; Supplementary Table 1), the
study population had higher median EuroSCORE II and more frequent
history of coronary artery disease and dyslipidemia. In terms of echo-
cardiographic parameters, end-diastolic and end-systolic volumes were
lower, but EF was not significantly different from those who were
excluded. GLS was higher in the patients with follow-up.
The study population for long-term analysis was divided into the PPM
group (n ¼ 89), permanent LBBB group (n ¼ 56), and no-CA group (n ¼
357). When comparing the groups (Table 1), preexisting comorbiditiesTable 3
Changes in LV echocardiographic parameters over time for the overall popula-
tion and stratified according to the 3 subgroups
Pre-TAVI 1-year follow-up p-value
LV mass index (g/m2)
Overall population 121  37 97  26 <0.001
No-CA 121  37 97  26 <0.001
PPM 128  36 99  24 <0.001
Permanent LBBB 113  36 96  28 <0.001
LV ejection fraction (%)
Overall population 52  11 57  9 <0.001
No-CA 53  11 58  9 <0.001
PPM 52  11 54  8 0.072
Permanent LBBB 52  13 54  11 0.171
LV GLS (|%|)
Overall population 14.4  4.0 16.6  3.9 <0.001
No-CA 14.3  4.1 17.2  3.7 <0.001
PPM 14.5  3.7 15.1  3.5 0.110
Permanent LBBB 15.0  3.4 15.4  4.4 0.483
p-values <0.05 were considered statistically significant and are shown in bold.
Abbreviations: CA, conduction abnormality; GLS, global longitudinal strain;
LBBB, left bundle branch block; LV, left ventricle; LVEF, left ventricular ejection
fraction; PPM, permanent pacemaker; TAVI, transcatheter aortic valve
implantation.
5were for the most part comparable, except for the presence of peripheral
artery disease, which was less frequent in the PPM group relative to the
no-CA group. As for the procedural characteristics, the percentage of
patients who underwent TAVI using the transfemoral or transapical/
subclavian approach was similar. However, valve type significantly
differed, with self-expanding valves more frequent among the PPM group
compared to the no-CA group (40 vs. 15%, p < 0.001).
For the preprocedural ECG, the initial rhythm was more often
sinus (79%), without significant difference between the groups.
The PPM group had a longer PR interval and consequently first-
degree AV block, a longer QRS duration, and more frequent
IVCD vs. patients in the no-CA group. As for echocardiographic
characteristics, AS severity, LV function, and RV function did not
differ between the groups. Only tricuspid regurgitation varied, as it
was more frequent in the PPM group as compared to the no-CA
group (25% vs. 14%, p ¼ 0.029).
One-Year Follow-Up Characteristics
Table 2 compares the clinical and echocardiographic characteristics
at 1-year follow-up among the groups. Significant symptoms (NYHA III-
IV) at follow-up were more common in the PPM group and in the per-
manent LBBB group compared to the no-CA group (11 vs. 3%, p¼ 0.029).
For ECG characteristics, more than half (60%) of patients who received a
PPMwithin 1 year had paced rhythm. When it was possible to measure in
the follow-up ECG (non-paced rhythm), the PR interval was longer for
the PPM group compared to the no-CA group, and QRS duration was
significantly longer for both the PPM and permanent LBBB groups
compared to the no-CA group (p < 0.001).
In terms of echocardiographic findings at 1 year, left ventricular
ejection fraction (LVEF) of patients with PPM and LBBB were lower
compared to the no-CA group (54% and 54% vs. 58%, p< 0.01), and GLS
was likewise lower in both groups as compared to the no-CA group (15%
and 15% vs. 17%, p< 0.01). For valvular regurgitation, significant mitral
regurgitation and tricuspid regurgitation were more common in the PPM
group (38% and 37%, respectively, p ¼ 0.01).
When comparing the changes in LV echocardiographic parameters
pre-TAVI and at 1-year follow-up, LVMI, LVEF, and GLS all significantly
Figure 3. Change in LV function from baseline to 1-year
follow-up. Graphs illustrate the change in (a) LV ejection
fraction and (b) global longitudinal strain from baseline to
1-year follow-up according to the subgroups.
Abbreviations: CA, conduction abnormality; EF, ejection
fraction; GLS, global longitudinal strain; LBBB, left bundle
branch block; LV, left ventricle; PPM, permanent pace-
maker; TAVI, transcatheter aortic valve implantation.
A.P. Chua et al. Structural Heart 9 (2025) 100428improved at follow-up (Table 3). However, when stratifying according to
the CA groups, several differences were depicted: although the decrease
in LV mass was similar across the subgroups, the change (improvement)
in LVEF and GLS was significant only for the no-CA group and not for the
PPM and permanent LBBB groups (Figure 3).
Association of CA and Outcome
During a median follow-up of 49 months from the first-year follow-
up after TAVI (interquartile range: 34-74 months), a total of 166 events
were recorded. The Kaplan-Meier curves showed a significant differ-
ence in all-cause mortality (χ2 ¼ 10.168, p ¼ 0.006), specifically
between patients who received a PPM as compared to those without CA
(p ¼ 0.001, Figure 4).
The univariable Cox regression analysis is presented in Table 4.
Among the 3 subgroups, the PPM group was significantly associated with
worse outcome as compared to the no-CA group. Other factors with
significant hazard ratios were baseline EuroSCORE II, baseline QRS
duration, and right bundle branch block or IVCD. Of the 1-year follow-up
variables, NYHA class, QRS duration, and some echocardiographic pa-
rameters including GLS were also significantly associated with the
outcome. Significant variables at the univariate analysis were included in
the multivariable analysis (Table 4), but parameters at 1-year follow-up
were prioritized (see also Statistical Methods). The analysis showed
that the PPM group (hazard ratio [HR]: 1.626, p ¼ 0.015), baseline
EuroSCORE II (HR: 1.073, p ¼ 0.002), worse NYHA class at 1 yearFigure 4. Long-term outcomes of CA post-TAVI. Kaplan-Meier survival curves sta
over time in the 3 CA groups used in the study.
Abbreviations: CA, conduction abnormality; LBBB, left bundle branch block; PPM, p
6(HR: 4.461, p< 0.001), and LV GLS at 1 year (HR: 0.951, p¼ 0.034) were
independently associated with all-cause mortality.
Discussion
The main findings of this study can be summarized as follows: 1) New
CA after TAVI are dynamic within the first year after intervention, with a
notable decrease in the prevalence of LBBB; 2) LV function, as assessed by
both EF and GLS, improves 1 year after TAVI, but the change is significant
only in patients with no-CA group; and 3) PPM implantation, but not
permanent LBBB, is independently associated with worse outcome
beyond the first year, together with increased EuroSCORE II, more
symptoms, and reduced LV GLS.
CA Changes Over Time After TAVI
Conduction disturbances remain a relatively frequent complication
after TAVI. The rates of PPM implantation vary according to different
studies from 3% to 36%, while new-onset LBBB varies from 4% to 65%.4
These rates, however, reflect only patients who experience CA immedi-
ately postprocedure or within the first 48 hours. Despite the awareness
that in a significant number of patients, CA can improve over time with
the resolution of the inflammation,4 most studies focused on the impact
of CA developed acutely after TAVI regardless of their persistence. A
different approach is applied in the current study by assessing how theserting at 1-year follow-up after TAVI showing a difference in all-cause mortality
ermanent pacemaker; TAVI, transcatheter aortic valve implantation.
Table 4
Univariable and multivariable Cox proportional hazard model for prediction of all-cause mortality
Univariate analysis Multivariable analysis
Hazard ratio (95% CI) p-value Hazard ratio (95% CI) p-value
Age (y) 0.986 (0.966-1.007) 0.183
Gender 1.334 (0.980-1.816) 0.067
BMI (kg/m2) 1.004 (0.970-1.038) 0.829
EuroSCORE II 1.083 (1.043-1.125) <0.001 1.073 (1.026-1.121) 0.002
TAVI valve type
Balloon expandable 1.482 (0.961-2.285) 0.075
Self-expanding 0.675 (0.438-1.041) 0.075
Baseline ECG
First degree AVB 1.282 (0.871-1.886) 0.207
RBBB 1.907 (1.262-2.881) 0.002
IVCD 1.685 (1.236-2.298) 0.001
PR interval 1.003 (0.998-1.008) 0.230
QRS duration 1.011 (1.005-1.017) <0.001
Baseline echocardiography
AV mean gradient 0.997 (0.988-1.006) 0.484
Aortic valve area (cm2) 0.905 (0.542-1.511) 0.703
LV mass index 1.000 (0.996-1.004) 0.999
LVEF 0.993 (0.981-1.006) 0.316
LV GLS 0.984 (0.947-1.022) 0.407
CA subgroup at 1 y
No-CA Reference 0.007 Reference 0.040
PPM 1.775 (1.240-2.539) 0.002 1.626 (1.098-2.409) 0.015
Permanent LBBB 1.155 (0.701-1.904) 0.572 0.991 (0.584-1.680) 0.973
At 1 y
NYHA III-IV 4.210 (2.501-7.086) <0.001 4.461 (2.610-7.626) <0.001
QRS duration 1.010 (1.004-1.017) 0.002
Echocardiography at 1 y
AV mean gradient 1022 (0.994-1.051) 0.126
LV mass index 1.008 (1.002-1.013) 0.009 1.000 (0.993-1.007) 0.957
LVEDV 1.007 (1.002-1.011) 0.008
LVESV 1.009 (1.002-1.016) 0.013
LVEF 0.987 (0.971-1.003) 0.103
LV GLS 0.933 (0.897-0.971) <0.001 0.951 (0.907-0.996) 0.034
Significant AR 1.378 (0.922-2.059) 0.118
Significant MR 1.183 (0.837-1.672) 0.341
Significant TR 1.053 (0.727-1.525) 0.784
Pacing percentage at 1 y
<0% Reference 0.259
1%-40% 2.081 (0.745-5.812) 0.162
>40% 2.262 (0.847-6.045) 0.104
p-Values <0.05 were considered statistically significant and are shown in bold.
Abbreviations: AR, aortic regurgitation; AV, aortic valve; AVB, atrioventricular block; BMI, body mass index; CA, conduction abnormality; ECG, electrocardiogram; GLS,
global longitudinal strain; IVCD, intraventricular conduction delay; LV, left ventricle; LVEDV, left ventricular end-diastolic volume; LVEF, left ventricular ejection
fraction; LVESV, left ventricular end-systolic volume; MR, mitral regurgitation; NYHA, New York Heart Association; PPM, permanent pacemaker; RBBB, right bundle
branch block; RV, right ventricle; TAVI, transcatheter aortic valve implantation; TR, tricuspid regurgitation.
A.P. Chua et al. Structural Heart 9 (2025) 100428CA change within the first year and evaluating how the persistence of
these disturbances relates to outcomes. In line with previous studies,4
PPM implantation at discharge was 12% and new-onset LBBB was 17%.
Interestingly, at the 1-year follow-up, there were 18% with PPM, while
only 11% with permanent LBBB.
The CA dynamic may be explained by mechanical manipulation
during the AV procedure causing inflammation, edema, or ischemia of
the His bundle or the left bundle branch, which traverse close to the
aortic annulus.4 If and when these local damages resolve is unpredict-
able, and therefore, the onset and/or resolution of CA are variable as
well.
When patients develop LBBB after TAVI, 85% to 94% of these LBBB
occur already periprocedurally, but only 44% to 65% persist until
discharge or 30 days.11 The prevalence of LBBB after 30 days has not
been evaluated extensively, and little is known about its impact on
long-term outcomes. The current study showed that a third of patients
demonstrate LBBB recovery, with 37% labeled initially as persistent
LBBB moving to the no-CA group at 1 year. This is in agreement with the
findings of Faroux et al., who noted a 33% recovery of LBBB at 1 year but
in a small patient cohort (n ¼ 153) with new-onset LBBB12; however, the
authors did not report the impact of LBBB recovery on outcomes. LBBB
can also progress toward HAVB and eventually require a PPM in 5% to714% of patients.11 For the current study’s cohort, 7% of those with LBBB
postprocedure received a pacemaker before discharge, while 2% of those
discharged with LBBB received a PPM within 1 year. Given this low
likelihood for patients with LBBB to need a PPM, guidelines recommend
electrophysiologic testing or long-term monitoring instead of immediate
PPM implantation.13
Similar to LBBB, HAVB occurs primarily periprocedurally, which in
60% to 96% of patients is within the first 24 hours, and 85% to 90%
receive a PPM within 7 days.11 The course after that is likewise seldom
assessed. In the study by De-Torres-Alba et al., 22% (n ¼ 17) of CA
requiring PPM implantation occurred after 48 hours, and 10% (n ¼ 8)
after 5 days; among the patients who developed CA requiring PPM after
48 hours, 24% had no prior CA.14 However, this study limited the
observation to the first week postprocedure. Our study in turn docu-
mented that 21% received a PPM after the first week from TAVI—a
sizable number that should still be studied when examining long-term
outcomes.
The current study was also able to demonstrate that pacing percent-
age tended to decrease over time, in concordance with previous studies.
In our cohort, 45% of patients had>40% pacing at 1 year, as compared to
54% at discharge. A literature review by Ravaux et al. determined that up
to 50% of patients with PPM did not show PPM dependency at 1 year,15
A.P. Chua et al. Structural Heart 9 (2025) 100428while Costa et al.16 showed an even smaller percentage of 33%. This
decrease in PPM dependency, along with the unclear association of PPM
with mortality, has led to stricter recommendations in PPM implantation
post-TAVI.13
Impact of CA on LV Function and Long-Term Outcomes
The dynamicity of these CA over time and the different definitions of
LBBB and PPM implantation post-TAVI have created conflicting evidence
on their impact on mortality. Data are particularly scarce regarding long-
term follow-up of patients with CA (especially LBBB), since most studies
limited the analysis to 1 or 2 years after TAVI. Among the studies with
longer follow-up time, Costa et al. demonstrated in patients with PPM an
increase in all-cause mortality at 6 years,16 while Chamandi et al. did not
show an effect of PPM on mortality for a follow-up of 4 years17; still, both
studies included patients who received PPM only within 30 days.
Regarding the impact of LBBB on long-term outcomes, similar conflicting
results are reported. Chamandi et al. did not find a significant association
between new-onset LBBB at discharge with mortality at 3 years of fol-
low-up,18 while Houthuizen et al. noted a higher all-cause mortality in
patients who developed LBBBwithin 7 days post-TAVI within a follow-up
of 450 days.19
The current study tried to clarify this aspect by including a large
patient population and defining CA at a landmark point of 1 year after
TAVI. Similar findings to the study of Costa et al.16 were observed as
patients who received a PPM were found to have a higher mortality risk
compared to patients with no-CA or permanent LBBB, within a follow-up
of 4 years (therefore 5 years after TAVI). Previous studies have already
suggested that the association between PPM and mortality occurs
through cardiac dyssynchrony secondary to RV pacing, which causes a
reduction in cardiac output and myocardial perfusion, including sym-
pathetic activation and endothelial dysfunction, referred to as “pacin-
g-induced heart disease.”20 Cardiac dyssynchrony also hampers
postprocedural normalization of cardiac function and may even induce
further decline.20 However, it is also possible that the association be-
tween PPM and mortality may have other causes, such as the ischemic
injury to the conduction system itself, rather than being induced by
pacing.20
In addition, the current study showed that permanent LBBB post-TAVI
was not significantly associated with mortality, which is in concordance
with the findings of Chamandi et al.18 Unlike most studies that focused
on the presence of LBBB within the first week, we assessed the effect of
LBBB persistence at 1 year on long-term outcomes. Other studies that
identified an association between LBBB and mortality explained this
relationship by possible progression to HAVB or by cardiac dyssynch-
rony19—mechanisms that may have resolved at 1 year.
Finally, this study evaluated the impact of CA post-TAVI on LV
function in the first year after intervention. Dolci et al. demonstrated that
EF improved after TAVI for the overall population, but significantly only
in patients without CA.21 However, follow-up duration was restricted to 6
months, and only EF was used to assess LV function. Similarly, but by
using both EF and GLS, the current study showed that both parameters
improved for the entire population 1 year after TAVI. However, the
improvement was significant only for patients without CA. These results
may partially explain the difference in outcomes among the subgroups,
especially since a significant association was demonstrated between GLS
at 1 year and mortality.
The findings of the current study support and expand existing
knowledge on the significant impact of CA, particularly when leading to
PPM implantation, on long-term outcome after TAVI. Monitoring CA up
to 1 year after the procedure becomes, therefore, important, as CA may
change as compared to immediately post-TAVI. In addition, when in-
dications for PPM implantation present, these patients may require closer
follow-up, including LV function assessment and particularly using GLS
as the most reflective of subclinical changes and independently associ-
ated with mortality. These findings also support current efforts to8improve devices and implantation techniques in order to prevent the
development of CA after TAVI and to minimize the impact of pacing in
patients who still develop these CA. These observations are particularly
important to be taken into account when considering TAVI in low-risk or
asymptomatic patients.Study Limitations
As a retrospective single-center study, there are limitations imposed
by the study design, particularly on generalizability of results. Larger
prospective studies are needed to confirm these findings and establish
more definitive causalities. Second, in order to ensure a large number of
included patients and sufficient long-term follow-up, the inclusion period
was long and relatively dated (2007 to 2019) and may therefore repre-
sent a limitation in terms of applicability of the results to the new gen-
eration of TAVI prosthesis. Also, guidelines for TAVI indication,
procedure specifications, and PPM implantation have changed and could
have an impact on patient selection and outcomes. Third, the study
investigated outcomes beyond the first year, which caused 292 patients
to be excluded at the landmark point of 1 year, with a potential selection
bias. However, as presented in the Supplemental File, no substantial
differences were observed between patients included and excluded in the
long-term analyses. Lastly, missing data could not be completely avoided
and could have had some effect on the results.
Conclusion
After TAVI, CAs remain relatively frequent but with a dynamic na-
ture, which necessitates regular ECG follow-up, especially within the first
year. PPM implantation is associated with less or no improvement in LV
function after TAVI and increased risk for long-termmortality, suggesting
the need for a closer follow-up of these patients, potentially using GLS to
monitor LV function.
ORCIDs
Aileen Paula Chua https://orcid.org/0000-0003-4183-2893
Jurrien H. Kuneman https://orcid.org/0000-0003-2162-2768
Frank van der Kley https://orcid.org/0000-0003-4521-8698
Nina Ajmone Marsan https://orcid.org/0000-0001-7208-5769
Ethics Statement
This research was performed in accordance to relevant research
ethical guidelines and received approval from the Leiden University
Medical Center Institutional Review Board as a retrospective study.
Funding
This research received a study grant from Edwards Lifesciences
(Irvine, California).Disclosure Statement
The Department of Cardiology of Leiden University Medical Center
received research grants from Abbott Vascular, Alnylam, Bayer, Bio-
tronik, Bioventrix, Boston Scientific, Edwards Lifesciences, GE Health-
care, Medtronic, Pie Medical, Medis, Pfizer, and Novartis. A. P. Chua, R.
Myagmardorj, and T. Nabeta received research grants from Turku PET
Centre. N. Ajmone Marsan received speaker fees from Abbott Vascular,
Philips Ultrasound, Omron, Pfizer, and GE Healthcare. J. J. Bax received
speaker fees from Abbott Vascular, Edwards Lifesciences, and Omron.
The other authors had no conflicts to declare.
A.P. Chua et al. Structural Heart 9 (2025) 100428Supplementary Data
Supplemental data for this article can be accessed on the publisher's
website.
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