Long‐term results of tricuspid valve transcatheter edge‐to‐edge repair in patients with cardiac implantable electronic devices

Abstract

Tricuspid valve transcatheter edge-to-edge repair (T-TEER) is an increasingly used treatment tool for patients with severe tricuspid regurgitation (TR) which has been shown to effectively and safely reduce TR and improve quality of life.¹ TR is a heterogeneous disease entity comprising primary, secondary and cardiac implantable electronic device (CIED)-related phenotypes.² Patients with CIED-related TR represent a continuous spectrum reaching from patients with transtricuspid leads as the main cause of TR to leads without relevant contribution.³ Previous studies suggest a CIED prevalence of approximately 20–25% in patients undergoing T-TEER.^{4, 5} Those data also hint at a comparable TR reduction at discharge and 30-day follow-up as well as comparable 1-year survival rates in patients with versus without transtricuspid leads.⁵ However, more recent data from the PASTE registry with echocardiographic core laboratory supervision identified transvalvular CIED leads to be independently associated with relevant post-procedural TR.⁶ Depending on the attempted T-TEER strategy and lead location, interventional TR treatment potentially interferes with CIED leads and might have an impact on device performance. Until today, information regarding CIED function before and after T-TEER is scarce. One single-centre study including 33 CIED patients found no significant change in lead function from baseline to immediate device follow-up 1 day after the procedure.⁷ To expand the respective body of evidence, the present study aimed at not only confirming the safety and effectiveness of T-TEER in patients with CIEDs in a larger multicentre setting, but also at evaluating potential changes in CIED function from baseline to post-procedural and over the course of follow-up.

The study included CIED patients with at least one transtricuspid lead from two European centres (LMU University hospital Munich, Clinic for General and Interventional Cardiology/Angiology Bad Oeynhausen) who underwent T-TEER for symptomatic TR between 2016 and 2022. Prior to T-TEER a multidisciplinary heart team involving interventional cardiologists, cardiac surgeons, heart failure specialists and electrophysiologists opted for T-TEER as primary treatment approach. With respect to the study objectives, echocardiographic evaluation included assessment of lead position before and after the procedure (anteroseptal, posteroseptal, posteroanterior, central, anterior leaflet body, posterior leaflet body, septal leaflet body), origin of the main TR jet (anteroseptal, posteroseptal, anteroposterior, central) and contribution of the lead to TR (none, partially, main aetiology). Device interrogation was performed prior and after the procedure, as well as at latest available follow-up. Evaluation of long-term CIED function included threshold amplitude, threshold duration, sensing and impedance for the respective leads depending on the type of implanted device.

Data were depicted using means and standard deviation. Differences of two independent samples were evaluated using the Mann–Whitney U test. Dependent samples were compared by applying the Wilcoxon test. The level of statistical significance was set to a two-sided p-value <0.05. All analyses were performed using R (version 4.0.4) and SPSS (version 25, IBM, Armonk, NY, USA).

The study included 155 patients at a mean age of 79.0 ± 8.1 years (40.6% women). TR was torrential in 11.0% of patients, massive in 36.8% of patients and severe in 50.3% of patients (mean effective regurgitant orifice area 21.8 ± 32.7 cm²; regurgitant volume 48.3 ± 21.9 ml). Left and right ventricular function were borderline (left ventricular ejection fraction 49.0 ± 13% and tricuspid annular plane systolic excursion 17.2 ± 4.7 mm). The most frequently implanted CIEDs were one- and two-chamber pacemakers (30.3% and 31.6%, respectively) as well as cardiac resynchronization therapy with defibrillator systems (20.0%). A broad variety of CIED lead types were observed (Biotronik Solea 20%, Medtronic CapSureFix 13.3%, SJM Durata 8.9%, SJM Tendril 8.9%, Biotronik Linox Smart 4.4%, Biotronik ProMRI 4.4%). While the majority of leads partially contributed to TR (49.4%) or showed no relevant leaflet interaction (36.3%), leads were observed to be the main cause of TR in 14.4% of patients. Before T-TEER, most leads were located in the posteroseptal commissure of the valve (38.7%), followed by the posterior leaflet body (18.7%) and the centre of the valve (12.7%). Among patients with transvalvular leads as main mechanism of TR, the majority of leads were located in the posteroseptal commissure (43.5%) or at the posterior leaflet body (34.8%). Main TR jets originated anteroseptal in 42.5%, posteroseptal in 37.5% and central in 16.3%. Posteroanterior jets were rarely encountered (3.8%). A one-, two- and three-device strategy was chosen in 22.1%, 63.6% and 14.8% of patients, respectively. TR was reduced to ≤2+ and to ≤1+ in 89.7% and 56.1%, respectively. Residual TR ≥3+ was observed in 16 patients (10.3%) at discharge. Among those, leads were primarily located in the posteroseptal commissure (56.3%). In 37.5% of cases with relevant residual TR, leads contributed partially to TR and in 31.3% of patients leads were the main cause of TR prior to the procedure. After T-TEER, lead position changed in 28% of patients leading to the following distribution of device positioning: posteroseptal 45.9%, posterior leaflet body (17.1%), central (12.3%) and anteroseptal (12.3%). TR severity at baseline and discharge were comparable in patients with implantable cardioverter-defibrillator versus pacemaker leads (baseline p = 0.316, discharge p = 0.326). TR was ≥3+ in 20 patients (12.9%) at latest available follow-up. In all patients at least one device was successfully implanted. Again, in those patients CIED leads were predominately located in the posteroseptal commissure (40%) or at the posterior tricuspid valve leaflet body (30%).

Data on CIED function prior to T-TEER were available in a subset of 131 (84.5%). From baseline (15 [4–46] days prior to T-TEER) to immediate post-procedural device interrogation (2 [1–5] days after T-TEER, available in 133 patients, 113 paired samples) no significant changes in right atrial or left ventricular lead function were noted. In contrast, we observed a significant increase in right ventricular (RV) sensing (9.22 ± 5.28 mV to 9.92 ± 5.26 mV, p = 0.015) and a significant decrease in RV impedance (488.2 ± 161.3 Ω to 482.5 ± 160.0 Ω, p = 0.018). Of note, a decrease in RV impedance was only observed in patients with CIED leads contributing to TR (patients with CIED lead as main TR aetiology or partial contribution to TR). In a subset of patients with available long-term follow-up (338 [116–731] days after TEER, 73 patients, 60 paired samples), apart from a slight increase in RV impedance (54 paired patients; 481.1 ± 172.2 Ω to 502.2 ± 179.7 Ω, p = 0.024), no changes in CIED function were observed (Figure 1). Notably, RV pacing burden increased from baseline to follow-up (69.0 ± 35.3% to 76.0 ± 35.2%, p = 0.049). Pacing mode was changed only in a minority of patients (n = 5 from baseline to discharge and n = 9 from baseline to follow-up). No cases of lead dislodgement, fracture or other types of CIED malfunction which required surgical revision were observed. Of note, antiarrhythmic medication remained stable over the course of follow-up (baseline vs. follow-up: beta-blocker 91.0% vs. 91.1%, p = 0.705; amiodarone 7.1% vs. 6.5%, p = 0.317; flecainide 0.6% vs. 0.8%, p = 1.000; digoxin 5.8% vs. 5.7%, p = 0.317; ivabradine 1.3% vs. 1.6%, p = 1.000; verapamil 1.3% vs. 1.6%, p = 1.000 and sotalol 0.6 vs. 1.6%, p = 0.564). TR reduction was sustained at 30 days with 82.9% of patients having moderate or less residual TR and 47.9% having mild or no TR. No major differences in device function were observed when comparing patients with versus without change of CIED lead position.

Figure 1

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Outlines types of implanted cardiac implantable electronic devices (CIEDs), lead position before and after tricuspid valve transcatheter edge-to-edge repair (T-TEER), lead contribution to tricuspid regurgitation (TR) and CIED function. A, anterior; CRT-D, cardiac resynchronization therapy-defibrillator; CRT-P, cardiac resynchronization therapy-pacemaker; P, posterior; PM, pacemaker; RA, right atrium; RV, right ventricle; S, septal.

This study for the first time presents follow-up data on CIED function after T-TEER beyond immediate post-procedural device interrogation. Additionally, it provides detailed insights into lead positioning and contribution of CIED leads to TR in a real-world T-TEER population from two experienced European centres.

First and foremost, T-TEER significantly reduced TR in the vast majority of patients (≤1+ and ≤2+ in 56.1% and 89.7% of patients) with good durability (≤2 + in 80% of patients at latest available follow-up). TR reduction rates to ≤2+ in this population were lower compared to the TRILUMINATE trial (89% TR ≤2+) but comparable to real-world data (75–80% TR ≤2+).^8-10 CIEDs are usually implanted without echocardiographic guidance and hence position of the lead and their contribution to TR is variable.¹¹ Retrospective data from T-TEER treated TR patients identified the posteroseptal commissure as the most common lead location.^{5, 7} These findings were confirmed in our study, with posteroseptal being the most commonly observed lead position (38.7%) followed by the posterior leaflet body (18.7%) and the centre of the valve (12.7%). Given the overall low rate of patients with residual TR ≥3+, no statistically valid statement regarding potential predictors (lead position, contribution of lead to TR, main jet location) for persistent TR can be made in this study. Overall, we observed a slight increase in RV impendence from baseline to latest available follow-up at approximately 1 year. Given the lack of clinical consequences and a relatively small numerical effect, the results appear to be of limited clinical relevance. However, these results require validation in a larger and potentially prospective study cohort. As stated above, no significant differences in device function were observed when comparing patients with versus without change of CIED lead position. One might hypothesize that changes could have happened by procedural interaction of the device and the lead even without a respective change in lead position. Though, these findings once again emphasize the need of integrating dedicated electrophysiologists into the interdisciplinary heart team. Against the background of an increasing evidence and more patients being treated using transcatheter tricuspid valve replacement this becomes even more important. Beyond that, patients with alterations of device function over the course of follow-up should closely be monitored. Although this study is limited to certain limitations due to its retrospective nature (no core laboratory supervision, patients lost to follow-up), it provides important insights into T-TEER in patients with CIED. Of note, no data regarding potential conduction disturbances after TEER were available for the present analysis. Whether differences in exact RV pacing sites might have had an impact on changes in pacing thresholds during follow-up cannot be excluded since the respective information is not available within the study cohort. As demonstrated above, T-TEER is a safe and effective treatment option for with relevant TR. Close cooperation between interventionalists and cardiologists ensuring continuous monitoring of CIED function before and after treatment as well as over the course of follow-up is highly recommended.