Device-related tricuspid regurgitation

Article written and reviewed by Dr Luca Moretti

Device-related tricuspid regurgitation is new or worsened regurgitation in which a pacemaker, implantable cardioverter-defibrillator, or another cardiac implantable electronic device truly contributes to loss of coaptation. It is not synonymous with the mere presence of a lead in the right ventricle: many leads cross the tricuspid valve without restricting leaflet motion, while atrial fibrillation, left-sided heart disease, pulmonary hypertension, and right-heart remodeling can independently explain regurgitation. Demonstrating causality is the step that turns an echocardiographic finding into an electrophysiologic and valvular decision.

This entity therefore requires terminology and a pathway distinct from tricuspid regurgitation considered as a whole and from secondary regurgitation caused by annular or ventricular dilation. A lead may compress the septal leaflet from the time of implantation, adhere to it over the years, injure it during extraction, or act indirectly through dyssynchrony and ventricular dysfunction. In late disease these mechanisms overlap, and the condition may not regress even after device removal.

Modern management requires integration of three-dimensional imaging, CIED interrogation, expertise in transvenous extraction, and structural heart therapy. It is not enough to establish how severe the jet is: the course of the lead must be reconstructed, any restricted structure identified, implant duration and pacing dependence determined, and the consequences for the system of repair or replacement anticipated. This analysis leads to an individualized strategy ranging from surveillance or early lead revision to TEER, TTVR, or surgery.

Definition, nomenclature, and clinical relevance

Terminology distinguishes CIED-associated TR, in which the device and regurgitation coexist without evidence of causation, from CIED-related or lead-related TR, in which the temporal relationship and imaging demonstrate or make a causal role highly likely. “Lead-induced” is appropriate when mechanical interference is unequivocal; “pacing-related” instead describes deterioration mediated by electrical activation and remodeling. Indiscriminate use of “pacemaker-induced” assigns to the lead a disease that may actually be atrial, ventricular, or pulmonary in origin.

Causality is strong when a previous examination documented a competent valve, regurgitation appears after implantation, and echocardiography shows impingement, adherence, perforation, or entanglement; it becomes probable when the jet location and restriction correspond to the lead course even without perfect images. It is weak when the lead is mobile within a commissure and distant from the orifice while annular dilation, global tethering, and elevated pulmonary pressure predominate, because chronology alone is insufficient in patients who already have a high prevalence of structural heart disease.

Studies report widely varying frequencies, partly because they compare a one-grade increase, new regurgitation of at least moderate severity, or mechanically confirmed diagnoses at different time points. In cohorts, worsening after implantation is observed in approximately one fifth of patients, whereas the overall reported association ranges from 7% to 30%. These figures do not represent a single true incidence: they depend on the quality of the baseline examination, device type, duration of follow-up, and how competing causes are controlled.

The presence of a transvalvular lead is not prognostically neutral, however, when it accompanies significant regurgitation. In a large analysis of approximately 18,800 pacemaker recipients, moderate or severe regurgitation was more frequent than in controls, 23.8% versus 7.7%, and the combination of a device and significant TR identified higher adjusted mortality. The association does not prove that extracting every lead improves survival, but it justifies surveillance, etiologic diagnosis, and timely referral before advanced right-sided heart failure develops.

The natural history includes an early potentially reversible phase and a late composite phase. Focal contact creates an eccentric jet; volume overload dilates the atrium, annulus, and ventricle, increases the coaptation gap, and produces tethering. At that point the lead may no longer be the sole determinant, but it remains the event that initiated the cascade. This mechanism-to-remodeling transition explains why early revision may correct the defect, whereas isolated extraction after years may leave autonomous secondary regurgitation.

Symptoms mainly reflect systemic congestion and reduced effective forward output, with edema, weight gain, abdominal distension, ascites, early satiety, asthenia, and reduced exercise tolerance. Elevated jugular venous pressure, v waves, a pulsatile liver, and systolic backflow in the hepatic veins document the hemodynamic consequences but do not distinguish the etiology; effective diuretic therapy may therefore reduce signs without resolving the mechanical conflict between the lead and leaflet.

Risk is not distributed uniformly. Multiple leads, greater diameter and stiffness, excessive slack, ICD systems, previous procedures, atrial fibrillation, annular and ventricular dilation, and elevated pulmonary pressures increase the likelihood of regurgitation or amplify its effect. Longer dwell time favors fibrosis and adherence, although important impingement may appear immediately. Neither an apical nor septal tip position alone identifies a safe course through the valve.

Anatomical mechanisms and pacing-related pathophysiology

With impingement, the lead remains mobile in diastole but during systole becomes interposed in closure or pushes a leaflet away from the coaptation plane. The septal leaflet is frequently involved because of its relationship with the septum and the lead trajectory toward the ventricle, but the anterior and posterior leaflets may also be compressed. Echocardiography shows diastolic separation between the lead and tissue followed by systolic apposition and restriction, with a jet arising from the defect created by contact.

Fibrous adherence differs from simple contact. Fibrotic tissue incorporates the lead and binds it to a leaflet or the subvalvular apparatus; the lead and structure move together throughout the cardiac cycle. Fibrosis increases with implant duration, endocardial reactions, and repeated procedures, may be underestimated by echocardiography, and makes extraction more hazardous. Apparently mild traction may avulse tissue or rupture chordae when the relationship is not recognized before the procedure.

Perforation traverses the leaflet body and creates an orifice separate from the coaptation line; laceration produces a flail edge or a larger defect. It may occur during implantation, through chronic erosion, or during manipulation and extraction. Color Doppler helps distinguish a transleaflet jet from a commissural jet, while three-dimensional reconstruction identifies the crossing point. In the presence of endocarditis, infectious perforation and vegetation must be considered separately from sterile mechanical injury.

With entanglement, the lead or its appendages wrap around chordae and papillary muscles, restricting multiple segments or distorting the apparatus. Tined electrodes and direct advancement through the ventricle may favor snagging; a redundant curve, the so-called tricuspid kick, may also press on the valve plane. Fluoroscopy defines slack but does not directly show chordae and leaflets: an apparently regular trajectory does not exclude anatomical entrapment.

Thrombus, vegetations, fibrous sheaths, and multiple leads occupying the same orifice add to the four cardinal mechanisms. An abandoned lead may interact with the functioning lead, reduce the coaptation space, or complicate future transcatheter therapy. Removal itself is a potential iatrogenic mechanism: a sheath or traction may cause leaflet avulsion, chordal rupture, and acute regurgitation. For this reason, “lead-related” also includes damage produced by management of the system, not only by the original implantation.

The device can worsen regurgitation even without visibly obstructing a leaflet because right ventricular pacing changes the activation sequence, alters free-wall contraction and papillary muscle timing, and can promote annular dilation and tethering. A high pacing burden, loss of atrioventricular synchrony, and pacing-induced cardiomyopathy amplify this process, to which left ventricular dysfunction and increased pulmonary pressure may be added.

The distinction between direct and indirect mechanisms is not always binary. A mildly eccentric lead may produce a small initial restriction; years of pacing and atrial fibrillation dilate the annulus, transforming that contact into a large gap. Conversely, pre-existing secondary TR may make it more likely for the lead to rest against a leaflet. Assessment must assign the relative contribution of each component because extraction corrects the obstruction but does not reverse established fibrosis, tethering, or ventricular dysfunction.

A leadless pacemaker avoids a permanent body crossing the tricuspid valve but does not guarantee the absence of regurgitation. Delivery requires passage of a large-bore catheter through the valve, and implantation too close to the annulus can alter function; ventricular pacing can also still induce dyssynchrony. The benefit is therefore primarily anatomical. Likewise, physiologic pacing reduces some electrical effects but must also be judged according to the physical trajectory of the lead.

Causal diagnosis and multimodality imaging

A complete transthoracic echocardiogram before implantation provides the most useful reference by documenting regurgitation severity, leaflet anatomy, annular diameter, right ventricular size and function, pulmonary pressure, and left-sided disease. If at least moderate TR, an abnormal valve, or right-sided dilation is already present, device selection should be discussed before the procedure; an early follow-up examination in the following weeks can then detect any changes while the lead is still relatively recent and less incorporated by tissue.

Two-dimensional imaging quantifies severity using a multiparametric approach and looks for a new eccentric jet, focal restriction, or leaflet discontinuity. Images and hemodynamic conditions should be compared with baseline because rhythm, volume status, and pulmonary pressure modify regurgitation. Failure to see the lead in a single section does not prove that it is distant from the leaflet: a three-dimensional structure is sampled by thin planes, and acoustic dropout may conceal the point of contact.

Three-dimensional transthoracic or transesophageal echocardiography is central to establishing causality. En face views from the atrial and ventricular sides locate the lead relative to leaflets and commissures, follow its mobility, and superimpose the jet origin. Impingement shows diastolic separation and systolic restriction; with adherence, the lead and leaflet remain coupled; perforation crosses the tissue; entanglement distorts chordae and motion. Multiplanar reconstruction avoids reliance on a single surface image.

Transesophageal echocardiography is indicated when significant TR appears or worsens, when transthoracic imaging does not define the mechanism, and before extraction or intervention. The anterior position of the tricuspid valve, lead shadowing, and insonation angle may limit it, so the absence of visible interference is not always conclusive. An experienced laboratory combines mid-esophageal, transgastric, 3D, and color Doppler views, explicitly describing the involved leaflet, commissure, gap, tethering, and dynamic relationship.

Multiphase cardiac CT with optimized opacification of the right-sided chambers reconstructs the relationship among the lead, annulus, leaflets, and subvalvular apparatus when echocardiography is uncertain. It defines the number and course of leads, slack, calcifications, venous stenoses, and signs of fibrosis relevant to extraction; in TTVR planning it measures the landing zone and the potential jailing site. Metal artifacts and blooming may simulate contact or conceal a thin layer of tissue, so CT complements rather than replaces dynamic imaging.

Cardiac magnetic resonance quantifies right ventricular volumes and ejection fraction when echocardiographic findings are discordant, using device-compatible protocols and controlling for artifacts. It is less suitable for demonstrating subtle lead-leaflet interaction, but it clarifies ventricular reserve and remodeling, which are decisive for assessing reversibility and the risk of eliminating regurgitation. Right-heart catheterization and measurement of pulmonary vascular resistance complete the evaluation when estimated pressure is uncertain or a precapillary component is suspected.

CIED interrogation is part of the cardiologic assessment, not an ancillary check. The original indication, intrinsic rhythm, pacing dependence, percentage of atrial and ventricular pacing, mode, any CRT, thresholds, sensing, impedance, battery status, arrhythmic episodes, and previous appropriate ICD therapies should be documented. Abandoned leads, venous access, infections, and previous procedures are recorded. These data determine whether a lead can be removed, replaced, or jailed without depriving the patient of an essential function.

The final diagnosis should state a graded causal conclusion rather than merely “severe TR with a lead.” A useful description specifies severity, direct or indirect mechanism, involved leaflet and segment, lead mobility or fixation, gap and tethering, implant duration, right ventricular function, and competing causes. If the lead is an innocent bystander, treatment follows valve anatomy; if it is causal, every procedure must include a lead-management plan before the valve is treated.

Prevention and lead management

Prevention begins before the first venous access. A patient with an abnormal valve, significant TR, a dilated annulus, or a likely future tricuspid procedure requires discussion among the electrophysiologist, imager, and valve specialist. The indication, expected duration of pacing, need for defibrillation, and possibility of a solution without a transvalvular lead must be balanced. Avoiding an unnecessary lead is safer than extracting it after years of fibrosis.

When an endocardial lead is necessary, passage under fluoroscopic and echocardiographic guidance aims for a central or commissural trajectory away from the leaflet bodies, with sufficient but not redundant slack. A technique that prolapses the lead through the valve may reduce chordal snagging compared with direct advancement, although it does not eliminate the risk. The number, caliber, and stiffness of leads should be minimized. There is no evidence that an apical or septal tip position alone guarantees protection.

If important new interference is recognized early, repositioning can move the lead toward a commissure, often posteroseptal or anteroposterior depending on individual anatomy, before adherence develops. The maneuver requires imaging confirmation that the leaflet has been released and verification of stability, thresholds, and slack. Waiting until dilation and heart failure develop reduces the likelihood that a simple revision will normalize valve function.

Valve-sparing strategies include leadless pacemakers, epicardial pacing, stimulation through coronary sinus branches, and, in selected cases, His bundle pacing from the atrial side of the tricuspid valve. For prevention of sudden death, a subcutaneous or extravascular defibrillator can be considered when complex antitachycardia or bradycardia pacing is not required. Each option has limitations related to access, thresholds, longevity, synchronization, and extractability; selection is not a technological reflex.

Left bundle branch area pacing improves ventricular activation compared with apical pacing, but its lead usually crosses the tricuspid valve and is not mechanically valve-sparing. The distance between the septal entry site and the annulus matters: observational studies have associated distances greater than approximately 16-19 mm with less deterioration of TR. This finding can guide technique but does not establish a universal threshold and does not replace visualization of the lead course through leaflets and commissures.

Transvenous extraction is not indicated solely because a patient with TR has a lead. Potential benefit is weighed against lead age and type, number of leads, calcification and adherence, pacing dependence, venous access, right ventricular function, annular dilation, tethering, and infection. The subsequent pacing and defibrillation strategy must be defined in advance, because removing the system and reimplanting a lead along the same trajectory recreates the problem.

Improvement after extraction is more plausible when imaging demonstrates mobile impingement, the lead is relatively recent, and the annulus and ventricle are not yet severely remodeled. In a cohort specifically studying lead-dependent dysfunction, 35.3% improved after removal; the result cannot be generalized because selection, definitions, and chronicity differ. TR dominated by late tethering or a healed perforation may persist and require repair.

Extraction can also worsen regurgitation. In contemporary series, an acute increase of at least one grade was observed in 11.5% of 208 patients undergoing TLE, while severe injury to the valve apparatus was reported in approximately 2.5% of a series exceeding 2,600 procedures; longer implant duration increases risk. These data require an experienced center, intraprocedural echocardiography, appropriate surgical backup, and consent that includes avulsion, chordal rupture, and the potential need for urgent correction.

When infection is present, the indication for complete extraction follows CIED recommendations and cannot be avoided to protect the valve. A transcatheter prosthesis that jailed an infected lead would make adequate source control impossible. In the absence of infection, by contrast, preventive extraction before a structural procedure is an individualized decision: it should provide an anatomical benefit or avoid a future risk greater than the immediate extraction risk.

Heart Team, tricuspid interventions, and prognosis

The decision belongs to a CIED-valve Heart Team that includes an electrophysiologist experienced in extraction, structural interventionalist, imager, cardiac surgeon, heart-failure specialist, and anesthesiologist; infectious-disease and hepatorenal expertise are added when necessary. The team reconstructs causality, extraction risk, repair feasibility, replacement options, and the definitive pacing strategy. Device dependence and previous appropriate ICD shocks carry the same weight as valve anatomy.

Diuretics reduce congestion and procedural risk, while heart-failure therapy, rhythm control, and appropriate resynchronization may attenuate the indirect component. They do not, however, release an entrapped leaflet or close a perforation. Symptomatic improvement should not postpone referral until refractory ascites, severe ventricular dysfunction, precapillary pulmonary hypertension, or hepatorenal failure develops, because even technically perfect correction may then be futile.

Surgery allows direct lead removal, debridement, leaflet reconstruction, and annuloplasty or replacement, together with an epicardial system when indicated. It is preferable in endocarditis with destruction, lesions not amenable to percutaneous treatment, a need for other cardiac surgery, or low operative risk. In late isolated disease, comorbidities and previous sternotomy often increase risk; this has favored transcatheter solutions without making surgery merely a residual option.

TEER is feasible when the lead is an innocent bystander, remains outside the device trajectory, and does not occupy the grasping zone. If it is mobile and contributes to the defect, the catheter or a steerable sheath may sometimes move it and immobilize it in a commissure or between clips, provided it is not stretched or damaged. A lead adherent to a leaflet, perforating it, or interposed in the main gap may prevent effective grasping and require extraction, surgery, or replacement.

In the TRILUMINATE Pivotal substudy, 98 of 469 patients treated with TEER had a transvalvular lead selected as compatible with the procedure. Regurgitation was reduced to moderate or less in 88% at 30 days and 81% at one year, values similar to those in patients without a lead, with no device-related revisions. These results demonstrate feasibility in selected anatomies, not indiscriminate safety in every lead-induced mechanism excluded by the trial criteria.

TTVR eliminates regurgitation even with large gaps, but an orthotopic prosthesis may trap the lead between the frame and native tissue: lead jailing exposes the system to dislodgement, insulation abrasion, conductor fracture, changes in sensing, threshold, and impedance, loss of pacing or defibrillation, and inability to perform future extraction. Infection of a jailed system may require complex surgery and may involve the prosthesis.

The 2026 HRS consensus recommends involvement of a lead-management expert and advises removal of the right ventricular lead before planned TTVR when this avoids entrapment and facilitates the procedure, always after individualized risk assessment. Pacing dependence, an ICD with previous appropriate therapies, multiple transvalvular leads, a history of infection, high lead tension, and pre-existing interference are arguments against unplanned jailing. An alternative system should be active or immediately available.

Clinical data confirm that jailed leads require specific surveillance. In 32 patients with an EVOQUE prosthesis and an entrapped lead, lead abnormalities occurred in 31%, with suspected insulation breach in 13% and revision in 3%, more than 80% within 90 days. In another series of 52 jailed leads, residual TR was mild or less at 30 days, but lead dislodgement, two ICD lead fractures, and endocarditis with death occurred, as well as late noise managed by reprogramming.

Before and after TEER or TTVR, sensing, thresholds, impedances, dependence, ICD therapies, and fluoroscopic images of the lead are documented. Remote monitoring with alerts is preferable; when unavailable, close follow-up is reasonable, at intervals no longer than approximately three months during the first year after jailing, because many abnormalities occur early. Any sudden change, noise, inappropriate shock, or loss of capture requires comparison with baseline values and joint electrophysiologic and structural assessment.

Success is not synonymous with jet reduction alone. Survival, hospitalizations, functional class, quality of life, diuretic dose, remodeling and right ventricular function, renal and hepatic status, and system integrity are measured. Abrupt elimination of the regurgitant pathway increases effective right ventricular afterload; severely reduced reserve may therefore become manifest after TTVR. Pulmonary pressure, ventriculoarterial coupling, and organ damage enter the assessment of benefit and futility.

A coherent strategy follows the mechanism: observation and medical therapy if the lead is innocent and TR is not significant; early revision if impingement is correctable; selective extraction with valve-sparing reimplantation if benefit exceeds risk; a valve procedure when remodeling has made the disease autonomous; and combined treatment when obstruction and structural damage coexist. Prognosis is improved mainly by preserving the window in which the valve, ventricle, and organs can still recover, not by applying the same technology to everyone.