Incidence rate and predictors of permanent pacemakerimplantation after transcatheter aortic valve implantationwith self-expanding CoreValve prosthesis

Valeria Calvi & Sergio Conti & Giusi Paola Pruiti & Davide Capodanno &

Euglena Puzzangara & Donatella Tempio & Angelo Di Grazia & Gian Paolo Ussia &

Corrado Tamburino

Received: 27 July 2011 /Accepted: 14 October 2011 /Published online: 26 November 2011# Springer Science+Business Media, LLC 2011

AbstractBackground Conduction disorders and permanent pace-maker (PPM) implantation are common complications inpatients undergoing transcatheter aortic valve implantation(TAVI). Previous studies, evaluating small populations,have identified several different predictors of PPM implan-tation after TAVI. The aim of this study was to assess theincidence rate of conduction disorders and the predictors ofpostoperative PPM requirement in a large series of patientsundergoing TAVI.Methods Data were analyzed from 181 consecutive patientsat high-risk surgery who underwent TAVI at our institutebetween July 2007 and April 2011. All patients underwentimplantation of the third-generation percutaneous self-expanding CoreValve® prosthesis (CoreValve, Inc., Irvine,CA, USA). In all patients, a 12-lead electrocardiogram anda 24-h holter monitoring was recorded before and after theprocedure in order to assess the presence of conductiondisorders. Clinical data, preoperative conduction disorders,echocardiographic patterns, and procedural data were testedas predictors of PPM implantation after TAVI.Results Left bundle branch block (LBBB) was the mostcommon conduction disorder, with an incidence of 50.3%at discharge. Fifty-two (32.1%) patients developed apersistent complete AVB requiring PPM implantation.

PPM implantation was strongly correlated with the pres-ence of preoperative right bundle branch block (RBBB)which was found to be the only independent predictor ofPPM implantation (HR 16.5, CI 3.3–82.3, p<0.001).Conclusions LBBB and PPM implantation requirementafter TAVI are common occurrences using the self-expanding CoreValve prosthesis. In this large series ofconsecutive patients, only RBBB was found to be a strongpredictor of PPM requirement.

Keywords Transcatheter aortic valve implantation .

Pacemaker implantation . Predictors . Completeatrioventricular block . Right bundle branch block

1 Introduction

Transcatheter aortic valve implantation (TAVI) is becominga viable alternative to open heart surgery in high-riskpatients with aortic stenosis [1–6]. Despite long-term dataon TAVI outcomes remain limited, the procedure isassociated to early functional class improvement, with anoverall success rate ranging from 74% to 100% [7, 8].However, conduction disorders necessitating a permanentpacemaker (PPM) implantation are frequent complicationsassociated to the procedure [9–15]. In particular, the needfor PPM implantation following TAVI ranges from 5.7% to39% depending on the type of percutaneous prosthesis used[10–16]. Studies assessing predictors of PPM implantationin the TAVI setting identified a number of candidatevariables but were limited by the small sample size.Therefore, a re-assessment of predictors of PPM implanta-tion in a larger population may be of added utility. The aimof this study was to identify the predictors of post-

V. Calvi : S. Conti (*) :G. P. Pruiti :D. Capodanno :E. Puzzangara :D. Tempio :A. Di Grazia :G. P. Ussia :C. TamburinoCardiology Department, Ferrarotto Hospital,University of Catania,via Citelli 1,Catania 95100( Sicily, Italye-mail: sergioconti.md@gmail.com

J Interv Card Electrophysiol (2012) 34:189–195DOI 10.1007/s10840-011-9634-5

procedural PPM implantation in patients undergoing per-cutaneous implantation of the third-generation CoreValveprosthesis.

2 Methods

2.1 Patient population

Between June 2007 and April 2011, consecutive patientsundergoing TAVI were prospectively enrolled at FerrarottoHospital (Catania, Italy). All patients received the third-generation percutaneous self-expanding CoreValve® prosthesis(CoreValve, Inc., Irvine, CA, USA). The inclusion andexclusion criteria for the procedure have been reportedelsewhere [17]. The study was conducted according to theDeclaration of Helsinki. The local hospital ethics committeeapproved the protocol and a written informed consent wasobtained from all patients or their closest relatives.

2.2 Procedure and post-procedural management

The technique of TAVI has been described extensivelyelsewhere [6, 17]. Briefly, a retrograde transfemoraltechnique was utilized. In all patients, a temporarypacemaker was placed in the right ventricle by trans-venous access. Burst rapid pacing at 180–220 beats/minwas used to reduce cardiac motion and transvalvular flowduring balloon dilatation. After balloon valvuloplasty, therelease system was positioned across the native valve andwith the aid of repeated contrast media injections andunder fluoroscopy guidance, deployed in a stepwisemanner. Once the final release was obtained, finalaortography was performed in order to assess the implanteffectiveness. Before the procedure, a 12-lead electrocar-diogram (ECG) and a 24-h Holter monitoring wereobtained in all patients. After implantation, all patientswere transferred to the intensive care unit for the first 48 hand continuously monitored. Temporary pacing was leftfor 24 h with multiple check of spontaneous rhythmturning down the pacing rate. Before discharge, patientsunderwent a new 12-lead ECG and a 24-h Holtermonitoring. To assess prosthesis performance and leftventricular function, transthoracic echocardiography wasperformed after the procedure and every 24 h thereafteruntil hospital discharge. Follow-up was scheduled for eachpatient at 1, 6, and 12 months after TAVI. At each visit, allpatients underwent cardiology evaluation, 12-lead ECGand 24-h Holter monitoring. Mean follow-up for the studypopulation was 13.6±8 months. Type of device and pacingwas chosen according to the latest guidelines of TheEuropean Society of Cardiology on Cardiac Pacingpublished in 2007 [18].

2.3 Statistical analysis

Continuous data are reported as means±standard deviationand compared by using independent sample Student’s t test.Categorical variables are reported as counts and percen-tages and compared using the chi-square or Fisher’s exacttests, as appropriate. All preoperative variables were firsttested individually by univariate analysis to evaluate theirassociation with the need for PPM implantation. Factorstested as potentially related to PPM implantation includedclinical condition (age, sex, hypertension, hypercholester-olemia, previous myocardial infarction, stroke, percutane-ous coronary intervention, or cardiac surgery); preoperativeconduction disorders as first-degree atrioventricular block(AVB), left bundle branch block (LBBB), right bundlebranch block (RBBB), or left anterior hemiblock; echocar-diographic patterns (biplane ejection fraction, annulusdiameter, septal dimensions in end diastole on parasternallong axis views, systolic pulmonary arterial pressure), andprocedural factors (distance in millimeters from the loweredge of the non-coronary cusp to the lower portion of theframe) evaluated using angiographic techniques. A Coxmultivariate analysis was performed including all thevariables which were significant at p<0.20 in the univariateanalysis and those deemed clinically important. Variablesfinally entered in the multivariate model were age,hypertension, peripheral vascular disease, prior aorticvalvuloplasty, New York Heart Association (NYHA II),prior RBBB, atrial fibrillation. PPM-free survival curveswere generated by the Kaplan–Meier method and comparedwith the log-rank test. A p value<0.05 was consideredstatistically significant. All statistical tests were performedby using SPSS 15.0 (SPSS, Inc., Chicago, IL, USA).

3 Results

A total of 181 consecutive patients were enrolled. Nineteen(10.5%) patients were excluded from the present analysison the basis of one or more of the following: presence of apreoperative PPM (16 patients, 8.8%), unsuccessful implantfor instability of the prosthesis during the release (2patients, 1.1%), death during the procedure (1 patient,0.5%). Finally, 162 patients were included. Baseline clinicalcharacteristics of these patients are summarized in Table 1.Overall, mean age was 80.5±4.9 years and 98 patients(60.5%) were women. Before the procedure 135 (83.3%)patients were in sinus rhythm and 27 patients (16.7%) werein atrial fibrillation. Mean hospital stay after TAVI was 5±1 days.

Overall mortality during hospital stay was 4.4% (8/181).One patient with complete AVB died because of cardiactamponade during monitoring in intensive care unit after

190 J Interv Card Electrophysiol (2012) 34:189–195

24 h from the procedure as a consequence of a temporaryPM electrocatheter malpositioning. One patient with noECG modification after TAVI died suddenly during thehospital stay whereas three patients died because of non-cardiac reasons.

ECG abnormalities Immediately after the procedure, newonset of LBBB was documented in 76 (47%) patients. Seven(4.3%) of them showed a first-degree AVB in association.Three patients developed a new isolated first-degree AVB(1.8%). A new onset of RBBBwas documented in one (0.6%)patient. Twenty-eight patients (17.3%) developed a completeAVB; one of them (0.6%) developed a transient AVB which

was not detected after 24 h. During hospital stay, the rate ofconduction disorders changed: in ten (6.2%) patients, LBBBprogressed to complete AVB, 17 (10.5%) patients with LBBBdeveloped a first-degree AVB in association, while in five(3.1%) patients, the abnormality was temporary and there wasa return to a normal intraventricular conduction pattern atdischarge. In the same period, a new onset conductiondisorders was documented in nine (7.8%) patients: completeAVB in five (3.1%) patients and LBBB in three (1.8%)patients, one of these with an associated first-degree AVB.

These data in aggregate indicate that LBBB was presentin 3.1% of patients before TAVI and in 39.5% at discharge(p<0.001). LBBB was associated with a first-degree AVB

Table 1 Baseline clinical characteristics of patients

Overall (162) No PPM (n=110) PPM implanted (n=52) P value

Age (years), mean±SD 80.5±4.9 80.3±5.4 81±3.8 0.14

Female, n (%) 98 (60.5%) 68 (61.8) 30 (57.7) 0.52

Hypertension, n (%) 138 (85%) 90 (81.8) 48 (92.3) 0.20

Smoke, n (%) 48 (29.6%) 31 (28.7) 17 (32.7) 0.64

Dyslipidemia, n (%) 94 (58%) 63 (57.3) 31 (59.6) 0.84

Diabetes, n (%) 50 (31%) 31 (28.2) 19 (36.5) 0.71

Pulmonary hypertension, n (%) 83 (51.2%) 57 (51.8) 26 (50) 0.70

Prior myocardial infarction, n (%) 44 (27.2%) 32 (29.1) 12 (23.1) 0.66

Prior percutaneous coronary interventions, n (%) 51 (31.5%) 35 (31.8) 16 (30.5) 0.74

Prior coronary artery bypass, n (%) 28 (17.3%) 20 (18.2) 8 (15.4) 0.31

Prior stroke, n (%) 26 (16%) 19 (17.3) 7 (13.5) 0.44

Prior aortic valvuloplasty, n (%) 82 (51%) 60 (54.5) 22 (42.3) 0.14

Logistic euroscore, mean±SD 28±15

New York Heart Association, n (%)

I 3 (1.8%) 2 (1.8) 1 (1.9) 0.59

II 52 (32%) 43 (39.1) 12 (23.1) 0.16

III 85 (52.5%) 52 (47.3) 33 (63.5) 0.77

IV 19 (11.7%) 13 (11.8) 6 (11.5) 0.65

Left ventricular ejection fraction, mean±SD 50±11.3 50.1±12.2 49.9±9.3 0.67

Mean pressure gradient (mmHg), mean±SD 58±17.6 57.6±19 58.8±14.3 0.38

Aortic valve area (cm2), mean±SD 0.58±0.24 0.57±0.21 0.61±0.29 0.37

Annulus, mean±SD 21.3±2.2 21.2±2.2 21.4±2.2 0.95

End-diastolic interventricular septal dimension (mm), mean±SD 13.9±1.7 14±1.9 13.7±1.4 0.46

Depth of prosthesis (mm), mean±SDa 10.5±4.1 9.9±3.9 10.7±0.2 0.41

Sinus rhythm, n (%) 135 (83.3%) 94 (85.5) 41 (78.8) 0.30

Atrial fibrillation, n (%) 27 (16.7%) 16 (14.5) 11 (21.2) 0.08

Left anterior hemiblock, n (%) 4 (2.5%) 3 (2.7) 1 (1.9) 0.89

Left bundle branch block, n (%) 5 (3.1%) 3 (2.7) 2 (3.8) 0.40

Right bundle branch block+left anterior hemiblock, n (%) 18 (11.1%) 3 (2.7) 15 (28.8) <0.0001

First-degree atrioventricular block, n (%) 11 (6.8%) 6 (5.5) 5 (9.6) 0.77

Peripheral vascular disease is defined by a history of symptomatic claudication or angiographic evidence of peripheral vascular disease. Renaldysfunction=estimated glomerular filtration rate <60 mL/min. Chronic obstructive pulmonary disease=history of respiratory problems associatedwith inhaled bronchodilator therapya Depth=distance in millimeters from the lower edge of the non-coronary cusp to the lower portion of frame, evaluated using angiographictechniques

J Interv Card Electrophysiol (2012) 34:189–195 191

in 13% at discharge (p<0.001). Persistent complete AVB,requiring PPM implantation, was found in 26% of patients(42/162) at discharge. Table 2 displays the incidence of newconduction disorders during hospital stay. The incidence ofLBBB was 50.3%, whereas the incidence of complete AVBrequiring PPM implantation was 26%.

Nine patients developed late conduction disorders: fivepatients developed a new complete AVB 30 days followingthe procedure; between 6 and 12 months, one patient withno post-procedural conduction disorders and four patientswith post-procedural LBBB developed a complete AVB. APPM was implanted in all these cases. Clinical andelectrocardiographic characteristics of these patients aregiven in Table 3.

Therefore, during the whole study period, includinghospital stay and follow up, 52 (32.1%) patients developeda persistent complete AVB, and a PPM implantation wasimplanted in 51 cases.

3.1 Predictors of PPM implantation and long-term survival

Preoperative clinical data revealed no demographic, clini-cal, and electrocardiographic differences between patientswho underwent PPM implantation (n=52) and those whodid not (n=110), except that patients who required PPMimplantation had more RBBB (3, 2.7% vs. 15, 28.8%, p<0.001) (Table 1). At multivariate Cox regression analysis,RBBB (HR 16.5, 95% CI 3.3–82.3, p<0.001) was selectedas the only independent predictor of PPM implantation. TheKaplan–Meier survival analysis confirmed a significantdifference in freedom from PPM implantation after TAVIbetween patients with RBBB compared with patientswithout RBBB (Fig. 1). After 1 year from the procedure,the probability of PPM-free survival was lower in patients

with prior RBBB compared with patients with otherconduction disorders.

4 Discussion

TAVI provides an alternative for patient with high surgicalrisk, who is not a candidate to open heart surgery. Thesafety and feasibility of the procedure has been demon-strated in several studies [4, 6, 19]. The main complicationrelated to the procedure is complete AVB and subsequentneed for PPM implantation [9–15, 20]. These complicationsmay affect significantly the outcome of the patient, increasehospital stay, and overall cost and may be associated withan increased risk of sudden death [21].

Several studies have evaluated the possible predictors forimplant of PPM after conventional aortic valve surgery[22–26]. Fukuda et al. demonstrated that histologicalabnormalities of the conduction system such as degenera-tive disease age-related or fibrous thickening of the leftventricular endocardium correlate to aortic valve diseaseand aortic regurgitation, may cause degeneration of theunderlying conduction fibers, predisposing to injury ofconduction tissue after surgical aortic valve replacement[27]. In 2003, Koplan et al. developed a simple risk score topredict postoperative PPM need after surgery, showing thatpreoperative RBBB was the strongest independent predictorof PPM implant, but LBBB and previous PR interval>200 ms were associated to an increased risk of PPM aswell [28]. Other proposed clinical factors predicting theneed for a post-surgical implantation of a PPM are aorticregurgitation, myocardial infarction, pulmonary hyperten-sion, and postoperative electrolyte imbalance [23]. A role isalso played by systemic hypertension, whereas the admin-istration of drugs is still disputed [25].

The reported incidence of AVB requiring PPM afterCoreValve implant ranges from 18% to 39% while theincidence of LBBB is about 50% [9, 10, 12–16]. New onsetconduction disorders and requirement of a PPM afterimplantation of an Edwards Sapien aortic bioprosthesisare infrequent (incidence of PPM 4.3%). The EdwardsSapien prosthesis was specifically designed to respectnearby anatomic structures. Indeed, the lower limit of theEdwards valve should not reach the upper part of theinterventricular septum and in contrast to the nithinolCoreValve’s self-expandable frame, the stainless-steel stentused with the Edwards model does not keep expandingafter valve deployment, thus decreasing the risk of delayedconduction disturbance [29]. A few studies sought toidentify clinical and procedural predictors of PPM implan-tation following TAVI. These are summarized in Table 3.Unfortunately, the majority of these studies were limited bythe small number of patients enrolled. Therefore, re-

Table 2 Incidence of new electrocardiographic abnormalities duringhospital stay

Percent (%)

RBBB 1/144 0.7

LAH 0/153 0

LBBB 79/157 50.3

I degree AV block 22/151 14.6

II degree AV block 0/162 0

Complete heart block or needfor PPM implantation

42/162 26

Incidence was calculated as (number of cases/number of patientswithout PPM or the considered ECG abnormality before TAVI)×100

RBBB Right bundle branch block, LBBB left bundle branch block,LAH left anterior hemiblock, PPM permanent pacemaker, AVatrioventricular

192 J Interv Card Electrophysiol (2012) 34:189–195

assessment of clinical, electrocardiographic, and echocar-diographic predictors in a larger population is of interest.

We observed a relatively high incidence of new onsetLBBB (50.3%). This could be explained by the anatomy ofthe aortic cusp, its relationship with the conduction system,and the prosthesis’ characteristics. The valvular leaflets areattached across the ventriculoarterial junction in crown-likefashion running onto either the muscle of the ventricularseptum or the mitral valve. The left bundle branch (LBB)emerges at the junction of the membranous septum andright fibrous trigone at the base of the interleaflet trianglebetween the right and non-coronary leaflets. In patientswith aortic stenosis (AS), the valvular attachment changeswith fusion of the leaflets. It becomes more annular and liesclose to the ventriculoarterial junction. Therefore, in thesetting of AS the valvular leaflets are directly close to theLBB. The CoreValve aortic bioprosthesis is placed acrossthe annulus and the lower edge of the frame will lieadjacent to the LBB. Therefore, the His bundle may beinvolved during the expansion of the prosthesis. The highradial force of the self-expandable CoreValve prosthesismight damage the cardiac conduction tissue with a traumacorrelated by direct compression and/or edema. Probably,the transient conduction disorders are related to theformation of intra-tissue edema secondary to irritation dueto manipulation and release of the valve. After the edemaresolution, the conduction system functions may recover.The persistent conduction disorders are due to the destruc-tion of the conduction system. In our study, a preoperativeRBBB was found to be the only strong independent riskfactor for PPM implant (HR 16.5, CI 3.3–82.3, p<0.001).Previous studies from Piazza et al. and Ferriera et al.reported prior RBBB as a possible predictor of completeT

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Fig. 1 The Kaplan–Meier survival analysis confirmed a significantdifference in freedom from PPM implantation after TAVI betweenpatients with RBBB compared with patients without RBBB

J Interv Card Electrophysiol (2012) 34:189–195 193

AVB, but these finding was not statistically significant [10,15]. Ferreira et al. identified as a predictor of new onsetcomplete AVB a deeper implantation of CoreValve pros-thesis within the outflow. However, among eight patientsthat had developed a complete AVB in this study, about50% had a pre-procedural RBBB. A role of RBBB could beexplained by considering the possibility of damaging theLBB during the procedure, which would result in completeAVB in presence of preoperative RBBB.

In the series from Bleiziffer et al. (n=126), pre-procedural conduction disorders were not identified as riskfactors for complete AV block. However, the incidence ofpreoperative RBBB was quite small compared to our series,thus not allowing a trustworthy evaluation of this factor. Onthe other hand, in the study from Jilaihawi et al. [12] (n=34), severe septal hypertrophy (defined as end-diastolicseptal dimension >17 mm) and LBBB were found asindependent predictors of PPM implantation. Unfortunately,in our population, we did not have patients with this severegrade of hypertrophy. However, as noted above, cautionshould be applied when interpreting multivariate analysesfrom small-scale studies.

4.1 Study limitations

This study reports a single-center experience. Our findingsseem to suggest that the damage to the conduction system isbelow the AV node, thus reflecting the finding of RBBB asthe only predictor of PPM following TAVI. However, animportant limitation of this study was the lack ofelectrophysiology study to assess the level of the AV blockand its relationship with the technique of the implantespecially in patients with preexisting bundle branch block.

5 Conclusions

PPM implantation is a common complication after TAVIusing the CoreValve prosthesis. This large series providesevidence that preexisting RBBB is the key predictor forPPM implantation after CoreValve implant. Therefore,these patients should be carefully monitored and thelikelihood of PPM implantation should be discussedpreoperatively with the patient.

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