Tricuspid valve repair in the presence of a permanent ventricular pacemaker lead

Abstract

Objective: Few studies have focussed on the outcomes of tricuspid valve (TV) repair in patients with a right ventricular permanent pacemaker lead (PPL) and tricuspid regurgitation (TR). Methods: Retrospective analysis of all patients with a PPL undergoing TV repair (annuloplasty ring in 83 patients and De Vega annuloplasty in 33 patients) between April 2001 and May 2008 (n = 116) was performed. The mean patient age was 71 ± 8.8 years; 59.8% were female, and the average European System for Cardiac Operative Risk Evaluation (EuroSCORE) was 16.4 ± 14.5%. Follow-up was 100% complete with a mean duration of 19.4 ± 20.3 months. Results: In addition to annular dilatation, leaflet injury secondary to PPL was observed in eight patients (7%). Isolated ring implantation or De Vega annuloplasty was performed in all patients, including five of the eight patients with leaflet injury. In the remaining three patients, the PPL was removed and an epicardial lead was implanted. A 30-day mortality was 14.6% and a 5-year survival 45% (95% confidence interval (CI): 29.4–61.6%). Four patients underwent TV re-operation resulting in a 5-year freedom of 93.4% from TV-related re-operation (95% CI: 88.2–97.7). Two of the four re-operated patients had PPL-related leaflet injury at the time of the initial operation and the PPL was left in situ. Conclusions: Patients with a pre-existing PPL, who require TV surgery for significant TR, however without evidence of PPL-induced TR, can undergo TV repair without removal of the PPL. In patients with evidence of PPL-related TR, we suggest PPL removal followed by insertion of an epicardal or transcoronary sinus lead.

1 Introduction

Patients who undergo permanent ventricular pacemaker lead (PPL) implantation can develop haemodynamically significant tricuspid regurgitation (TR) thereafter. Whether the PPL should be explanted and replaced with an epicardial lead or whether it should be left in situ at the time of subsequent tricuspid valve (TV) surgery is not known. This is due to the relative paucity of publications in the literature on this subject. In addition, the few published studies have revealed contradictory results for this uncommon, but vexing problem. Lin et al. [1] reported 41 patients with definitive PPL-related TR, in which all PPL’s were left in situ during TV surgery. On the other hand, McCarthy et al. [2] have recommended explantation of the PPL and placement of a new epicardial lead in such patients.

The most common cause of TR is tricuspid annular dilation secondary to increased right ventricular pressure and/or volume, frequently in the presence of mitral valve disease. Significant TR in patients with a pacemaker could therefore be secondary to left heart or lung pathology and the presence of a PPL could be coincidental. It may be important to try to determine the cause of TR in such patients, to decide which PPL management strategy should be used. The aim of this study was to therefore describe TR pathology in patients who have a PPL, as well as the medium-term postoperative outcomes, including recurrent TR, following TV surgery.

2 Patients and methods

Between April 2001 and May 2008, a total of 116 patients with a previously implanted intraventricular PPL and significant TR underwent TV surgery at our institution. Indications for isolated TV surgery were symptomatic severe tricuspid regurgitation (TR), Indications for TV surgery were symptomatic severe TR alone or at least mild-to-moderate TR with marked tricuspidal annular dilation in echocardiography (> 4.0 cm) in patients with other indications for cardiac surgery. Patients with infective endocarditis or organic disease of the tricuspid valve (i.e., rheumatic, Ebstein’s or carcinoid disease) were excluded from the current study.

Pre-, intra- and postoperative parameters of all patients were prospectively incorporated into the hospital’s patient data management system and then retrospectively analysed. In addition, further chart review and information from operative and echocardiography reports were gathered and analysed.

The mean duration for which the PPL had been implanted before TV surgery was 5.4 ± 4.6 years. Mean patient age was 71 ± 8.8 years. There were 46 male and 70 female patients. The mean preoperative New York Heart Association (NYHA) class was 2.9 ± 0.5. The logistic European System for Cardiac Operative Risk Evaluation (EuroSCORE)-predicted risk of perioperative mortality was 16.4 ± 14.5%. The mean left ventricular ejection fraction (LVEF) was 43.3 ± 16.1%, the mean grade of TR was 2.7, and the mean pulmonary artery pressure (PAP) was 46.3 ± 17 mmHg. Elective surgery was performed in 78 patients (67%), while 38 patients (33%) required urgent or emergent surgery.

The re-operation was performed in 18 patients and re-re-operation in two patients. A sternotomy was performed in 92 patients (79%), while 24 patients (21%) underwent minimal invasive surgery through a right lateral minithoracotomy with femoral cannulation for cardiopulmonary bypass (CPB).

TV repair was performed using well-established techniques including bicaval cannulation and mild hypothermic CPB. The type of TV repair performed was at the discretion of the operating surgeon. A De Vega or Kay suture annuloplasty was performed in 33 patients (28%), a semi-rigid ring was implanted in 45 patients (39%), and, in 38 patients (33%), a flexible band was implanted (Table 1 ). Eight patients were observed to have restricted TV leaflet motion due to the PPL. In three of these eight patients, the PPL was explanted and a right ventricular epicardial pacing lead was placed. The PPL was left in situ in the other five patients.

Concomitant surgical procedures were performed in all patients: coronary bypass in 35 patients (30%), mitral valve (MV) reconstruction in 60 patients (52%), MV replacement in 46 patients (40%), aortic valve (AV) replacement in 41 patients (35%), replacement of the ascending aorta in three patients (3%), cryoablation for atrial fibrillation in 28 patients (24%), and closure of a patent foramen ovale in eight patients (7%) (procedures not mutually exclusive and therefore total more than 100%).

2.1 Follow-up

Patients were contacted individually by sending questionnaires annually after the operation. Patients who did not respond were contacted by telephone. However, if no further information about the patients was available, the family physicians were contacted. Follow-up results were available for all 116 patients. Follow-up was 100% complete with a mean follow-up time of 19.4 ± 20.3 months (range 0.1–6.6 years).

2.2 Statistical evaluation

Results are displayed in the standard format with continuous variables expressed as mean ± standard deviation and categorical data as proportions.

Cumulative survival was calculated by Kaplan–Meier methods and differences in follow-up were calculated with 95% confidence limits and compared by the log rank (Mantel-Cox) test.

All statistical analyses were performed using the Statistical Package for Social Sciences (SPSS) statistical package 15.0 (SPSS Corp., Birmingham, AL, USA). A p-value less than 0.05 was considered to be statistically significant.

3 Results

Tricuspid annular dilatation was found to be a principal cause of TR in all patients. In addition, perforation of the anterior TV leaflet due to the PPL was found in one patient (0.8%) and catched TV chordae of the anterior leaflet due to the PPL in another (0.8%). In six patients (4.9%), the PPL was thought to be contributory to the TR because of secondary restricted leaflet motion (n = 2) or because of PPL fixation to the tricuspid valve leaflets (n = 4).

In three of these eight patients, the PPL was explanted and a right ventricular epicardial pacing lead was placed. This affected the patient with perforation of the anterior TV leaflet due to the PPL, the patient with catched TV chordae of the anterior leaflet due to the PPL and one patient with massive adhesions of the PPL with the TV. The PPL was left in situ in the other five patients with PPL-related TV.

The mean total operation time was 226.3 ± 69.1 min, the mean duration of CPB was 146.6 ± 50.6 min and the mean aortic clamping time was 90.5 ± 30.2 min, principally as a result of the concomitant procedures.

Four patients (4%) had to undergo re-exploration due to excessive postoperative bleeding. A total of 26 patients (21.4%) developed low cardiac output syndrome requiring intra-aortic balloon pump (IABP) insertion in 17 patients and extracorporeal membrane oxygenation (ECMO) support in two patients.

The mean hospital stay duration was 18.9 ± 13.6 days. The overall 30-day mortality was 14.6% (17 patients). The 5-year survival was 45% (95% confidence interval (CI) 29.4–61.6%, see Fig. 1 ) and 5-year freedom from TV-related re-operation was 93.4% (95% CI 88.2–97.7%, see Fig. 2 ).

The echocardiographic findings of the TR, preoperative and postoperative, are summarised in Fig. 3(A) and (B). Fig. 4 shows the echocardiographic results after TV repair of the affected patients with PPL-related TR, differentiated in the patients with removed PPL versus PPL in place.

During follow-up, four patients were re-operated upon because of recurrent severe TR. In two cases, the reason for recurrent TR was not PPL-related (one patient had a retracted TV leaflet after radiotherapy for Hodgkin’s disease; and one patient had progressive central TR following De Vega’s annuloplasty with concomitant mechanical aortic and mitral valve replacement). In two patients, TV re-operation was performed because of PPL-related TR. These two patients were from the group of five patients who were originally operated on for pacemaker-related TR, in which the PPL was left in situ at the first operation. The TV re-operation was performed 2 weeks and 3 months after the first operation. In the first patient, the anterior leaflet was being displaced by the PPL and the Carpentier–Edwards ring was partially separated from the annulus. During the second operation, the ring was reattached to the annulus and the PPL was explanted and replaced with an epicardial lead. In the second patient, the PPL was fixed to the posterior leaflet of the TV, and the Cosgrove band that was implanted at the first operation did not seem to give enough stability to the repair. The flexible Cosgrove band was therefore excised and a rigid Carpentier–Edwards Classic ring was implanted. The PPL was left in situ after separating it from the leaflet.

4 Discussion

Severe TR is associated with a poor prognosis independent of patient age, biventricular systolic function, right ventricular size, as well as dilation of the inferior vena cava. Nath et al. reported a 1-year survival of only 63.9% for such patients [3]. TR following permanent pacemaker implantation is not uncommon. Klutstein et al. [4] have reported a worsening of TR by more than two grades in 18% of 410 patients after PPL implantation. Existence of a PPL has also been previously shown to be a significant risk factor for late recurrent TR after TV repair [2]. Because of these findings, McCarthy et al. [2] concluded that trans-tricuspid pacing leads should be explanted and replaced with epicardial leads during TV repair surgery. However, details of the specific TV pathology were not recorded in this study, making interpretation of the results somewhat challenging.

There have been few case reports of PPL-related TR published in the literature [5–8] showing that this pathology is due to various mechanisms.

Loupy et al. [5] reported an unusual case of severe TR that developed a few weeks after aortic valve replacement (AVR) in a patient with previous permanent pacemaker (PPM) implantation. The mechanism of severe TR was due to leaflet malcoaptation and they hypothesised that the AV surgery was responsible for the conformational changes between cardiac chambers, TV and the PPLs, causing severe TR. The other mechanisms reported are either immobilisation or perforation of the anterior tricuspid leaflet or entrapment of the lead shaft in the fused septal and posterior tricuspid leaflets [6–8].

Lin et al. [1] published a report of 41 patients with PPL-related TR. They found perforation of the TV leaflet by the PPL in seven patients, and lead entanglement, impingement and adherence to the TV in four, 16 and 14 patients, respectively. A total of 22 patients in this study underwent TV replacement, while TV repair without explantation of the PPL was performed in the remaining 19 patients. The investigators observed no re-operations for recurrent TR after a mean follow-up of 8.2 years. Echocardiographic data regarding postoperative residual or recurrent TR, however, were not presented.

It is frequently a challenge to determine the exact mechanism of TR by two-dimensional (2D)-echocardiography. Real-time three-dimensional (3D) echocardiography can give the surgeon additional information about the mechanism of TR and may improve the chances of a successful TV repair, but experience with this imaging modality for TR remains limited [6,7].

In our study, isolated tricuspid annular dilatation was the cause for TR in the vast majority of patients. PPL-related TR was found to be present in only eight patients (7%), which was somewhat surprising given the long period that the PPL was in place (average 5.4 years). Such a finding supports the clinical impression that PPLs are well tolerated in the majority of patients without development of significant TR.

TV re-operation for recurrent TR in our patient collective was required in only 4 of 116 patients (3.4%) after a mean follow-up period of 19.4 ± 20.3 months. Our observed 5-year freedom from the TV-re-operation rate was a very acceptable 93.4%, particularly considering that the PPL was left in situ in 113 of 116 patients (97%). On the other hand, we must also keep in mind the relatively short period of follow-up in the current study and the fact that TV re-operation may be avoided in some patients because of their known poor prognosis. TV re-operation has been reported by Bernal et al. to have a hospital mortality of 35% and a late mortality of 40% [9].

However, we observed recurrent TR in two of five patients (40%), who underwent surgery for pacemaker-related TR in whom the PPL was kept in place during their initial TV operation. In both cases, the PPL hindered the free movement of the TV leaflets. In the first case, the rigid Carpentier–Edwards ring was partially separated from the annulus; in the second case, the flexible Cosgrove band did not give enough stability to the repair. This relatively high re-operation rate (40%) in patients with PPL-related TR leads us to recommend PPL removal and the placement of an epicardial lead in such patients.

In patients who require TV replacement, removal of the PPL with the placement of an epicardial lead is routinely recommended. However, a disadvantage of the epicardial leads is the requirement of relatively high stimulation thresholds with the necessity of frequent battery changes.

Another possibility for TV replacement surgery is to place the pre-existing PPL between the native annulus and the sewing ring of the TV prosthesis [10]. Such a recommendation could also be applied in the case of patients undergoing TV repair with a flexible or rigid ring. However, such a technique will lead to a more difficult lead removal in the future, if lead removal is required.

Another option for patients undergoing TV replacement with a bioprosthesis is the transvenous placement of a new PPL directly through the prosthesis [11], although this is not routinely recommended. The transvenous placement of a new lead directly through a TV that was previously repaired, however, is a commonly accepted practice. Although PPL placement across a previously repaired TV usually proceeds uneventfully, the risk always exists that the TV can be damaged during PPL insertion leading to recurrent TR. A very good alternative solution for such patients is the transvenous placement of a PPL into the coronary sinus with advancement into the lateral cardiac vein. Although this technique is more technically challenging than normal right ventricular PPL placement, it has the added benefit of pacing of the left ventricular chamber rather than the right ventricle [12,13]. Such a technique is also possible through a right lateral minithoracotomy in patients in whom transvenous coronary sinus intubation is too difficult [14].

We can conclude from the current study that patients with a pre-existing PPL who require TV surgery and who do not have evidence of PPL-induced TR can undergo simple TV repair without removal of the PPL. In TV repair patients with evidence of PPL-related TR, however, we suggest PPL removal followed by insertion of an epicardial or transcoronary sinus lead. In addition, we also suggest that the function of the reconstructed TV should be assessed under beating-heart conditions before closure of the right atrium, so as to confirm that the PPL is anchored and fixed to the right ventricle in a way that does not restrict the movement of the TV leaflet.

References