Transcatheter tricuspid valve-in-valve implantation for very early bioprosthetic tricuspid stenosis secondary to pacemaker lead entrapment: a case report.

Background: Tricuspid stenosis (native and prosthetic) is rare. Redo-sternotomy for isolated tricuspid replacement is associated with a higher risk. The efficacy and durability of transcatheter valve implantation for severe tricuspid stenosis are unclear. Case summary: Successful tricuspid valve-in-valve implantation (Edwards 26 mm Ultra) was performed to exteriorize a retained, unextractable pacemaker lead causing very early surgical bioprosthetic valve dysfunction in a 66-year-old Caucasian woman. The original indication for surgical replacement was pacemaker lead-related severe tricuspid regurgitation. History of CABG and subsequent surgical replacement rendered the risk of a third sternotomy and open-heart surgery prohibitive.
Conclusion: Successful reduction in the severity of bioprosthetic tricuspid stenosis and improvement of right heart failure with transcatheter valve-in-valve implantation was observed. Percutaneous tricuspid valve implantation could be considered an alternative to redo-sternotomy for severe bioprosthetic tricuspid stenosis.

Atrial pacing lead impingement restricting tricuspid leaflet motion is a rare cause of bioprosthetic tricuspid valve stenosis.

Redo-sternotomy for isolated tricuspid valve replacement is associated with increased perioperative risk.

Transcatheter tricuspid valve-in-valve implantation may be explored as an alternative in high-surgical risk patients—especially when, as in the described case, the cause of bioprosthetic valve stenosis could be treated with transcatheter valve implantation (exteriorizing and immobilizing the surgically unresectable atrial lead out of the bioprosthetic tricuspid annulus).

Introduction

Pacemaker lead-related tricuspid regurgitation is being increasingly recognized.[1] Perioperative risk of surgical tricuspid valve replacement increases with redo-sternotomy.[2] There is limited data on transcatheter tricuspid valve implantation; we describe a case where it was utilized for severe bioprosthetic tricuspid stenosis to circumvent the need for a redo-sternotomy and surgical tricuspid valve replacement.

Case summary

History of presentation

A 66-year-old Caucasian woman presented with recurrence of NYHA-4 dyspnoea and bilateral lower extremity oedema on high-dose diuretics (torsemide 40 mg twice daily and metolazone 2.5 mg weekly) 3 months after tricuspid valve surgery. She underwent isolated surgical bioprosthetic tricuspid valve replacement (27 mm Hancock II), extraction of endocardial right atrium (RA)/right ventricle (RV) pacing leads, and pacemaker explanation for long-standing, severe, symptomatic tricuspid regurgitation related to pacemaker leads. Complete surgical endocardial lead extraction was not possible due to fibrosis around the atrial lead and left brachiocephalic vein stenosis. Mid and distal portions of the RA lead were retained proximal to the tricuspid valve. A dual-chamber (RA/left ventricle) epicardial pacemaker was implanted. Post-operative echocardiography showed trivial prosthetic tricuspid regurgitation with a mean diastolic gradient of 5 mmHg.

Past medical history

In 1986, the patient underwent cryoprobe freezing of right and left free lateral accessory bypass pathways (Wolff-Parksinson-White syndrome). In 1991, following pacemaker implantation, AV node alcohol ablation for recurrent supraventricular tachycardia was complicated by iatrogenic right coronary artery (RCA) dissection requiring an emergent saphenous vein bypass graft (SVG) to the RCA. AV node ablation was completed surgically.

In 1995, an atrial lead fracture and intra-operative defect identified in the original ventricular lead prompted extraction and replacement of both leads. Left brachiocephalic vein stenosis was identified at the time.

In 1999, the first echocardiographic evidence of moderate–severe tricuspid regurgitation was recorded.

Subsequent generator replacements were performed routinely in 2003 and 2011.

Although echocardiographic evidence of moderate–severe tricuspid regurgitation dated back to 1999, right-sided heart failure remained diuretic-responsive until late 2019, when she was referred for redo-sternotomy and bioprosthetic tricuspid replacement. The chronological sequence of events is summarized in Timeline.

Transoesophageal Echocardiography, non-standard mid-oesophageal view: retained pacemaker lead (yellow arrow) is seen within the bioprosthetic tricuspid orifice. Posterior aspect of tricuspid annulus marked for reference (pink asterisk). Colour Doppler (right panel) suggestive of tricuspid stenosis.

Additional comorbidities include gout and hypertension; there was no known history of atrial fibrillation/flutter or a hypercoagulable state.

Physical examination

The patient appeared fatigued. Lung auscultation was unremarkable. Regular rhythm with a faint (3/6) diastolic murmur on cardiac auscultation was observed and marked jugular venous distension and bilateral lower extremity oedema were noted.

Investigations

Transthoracic echocardiogram showed interval increase in bioprosthetic tricuspid valve gradient (8 mmHg, HR 67 bpm) and mild–moderate right ventricular enlargement.

Right heart catheterization confirmed an elevated RA/RV gradient (16 mmHg) consistent with severe tricuspid stenosis. Mean pulmonary arterial pressure was 30 mmHg (43/20 mmHg, Pulmonary Vascular Resistance 2.8WU) with elevated wedge pressure (20 mmHg). A coronary angiogram showed a patent SVG-RCA graft and native left coronary arteries.

Transoesophageal echocardiography was utilized to assess the aetiology and anatomy of the very early bioprosthetic tricuspid valve failure. The retained right atrial lead was trapped in the tricuspid orifice, causing restricted leaflet motion (, see Supplementary material online, ).

Retained pacemaker lead across bioprosthetic tricuspid annulus on fluoroscopy.

Management

In view of NYHA-4 symptoms despite adherence to outpatient high-dose diuretics, the local cardiothoracic surgery and interventional cardiology teams determined a transcatheter approach to be beneficial in improving this relatively young patient’s quality of life. Fluoroscopy confirmed the retained RA lead extending through the bioprosthetic tricuspid orifice (). Due to known fibrosis around the atrial lead and the risk of underlying tissue damage from manipulation, no percutaneous attempt was made to displace the lead out of the tricuspid orifice. Edwards 26 mm Ultra valve-in-valve implantation via right femoral vein successfully exteriorized the retained pacemaker lead from the tricuspid valve orifice (, see Supplementary material online, ) with no residual tricuspid regurgitation. The mean tricuspid diastolic gradient improved from 8 to 5 mmHg ().

Transoesophageal echocardiography, non-standard, mid-oesophageal view after valve-in-valve implantation: retained pacemaker lead (yellow arrow) is exteriorized out of the tricuspid orifice and is seen between the implanted bioprosthetic tricuspid valve (blue asterisk) and native tricuspid annulus (pink asterisk).

CW Doppler: improvement of tricuspid mean diastolic gradient after transcatheter valve-in-valve implantation. The mean diastolic gradient of 8 mmHg (upper panel) decreased to 5 mmHg (lower panel).

Discussion

Bioprosthetic tricuspid stenosis is rare because tricuspid valve replacement is infrequently performed compared with left-sided valves. Clear guidelines for management are not available.[3]

Isolated surgical tricuspid valve replacement is uncommon partly due to high inpatient mortality (10.9%) and morbidity (20% of patients were discharged due to skilled nursing facilities) despite being performed in a largely non-elderly population with a mean age of 62 years.[4] Non-structural causes of bioprosthetic tricuspid valve dysfunction are similar to those for left-sided valves (pannus formation, thrombus, infection, and native valve attachment). Prosthetic tricuspid valve dysfunction, when present, becomes clinically evident after or toward the end of the first decade after replacement.[5-7] Additionally, re-operation rates for bioprosthetic tricuspid valve replacement have been reported to be as high as 37.3%.[5]

The described case is a series of unusual events spanning three decades, leading to severe tricuspid stenosis due to very early failure of the surgical bioprosthetic tricuspid valve. The already high perioperative risk of a redo-surgical replacement was rendered unequivocally prohibitive by the single-vessel CABG done 30 years ago for iatrogenic RCA dissection.

Evidence of transcatheter valve-in-valve implantation for bioprosthetic tricuspid stenosis is limited to case reports. Edwards SAPIEN valve-in-valve implantation has been utilized for degenerative bioprosthetic tricuspid stenosis in patients for whom the original indication for tricuspid valve replacement was rheumatic heart disease,[8,9] or infective endocarditis.[10,11] Similar to percutaneous balloon valvuloplasty for bioprosthetic tricuspid stenosis,[12] transcatheter valve-in-valve implantation was an inferior therapeutic alternative acceptable only because it avoided the high-surgical risk associated with redo-surgical tricuspid valve replacement.

During surgical tricuspid valve replacement in the described case, RA lead extraction was unsuccessful due to brachiocephalic vein stenosis and fibrosis around the leads. The retained lead was above and not within the tricuspid annulus at that time. Even if the risk of a redo-sternotomy was not prohibitive, the likelihood of successfully extracting the retained lead on redo-surgical replacement was low. This observation raises the question of whether, in this specific situation, a percutaneous valve-in-valve implantation that treats bioprosthetic tricuspid stenosis by ‘exteriorizing’ the retained pacemaker lead out of the tricuspid orifice is non-inferior to surgery. It must be noted that surgery remains the gold standard for native and bioprosthetic tricuspid stenosis. Treatment options for transcatheter valve-in-valve dysfunction, in this case, would include balloon valvuloplasty or high-risk surgery.

Follow-up

On a 6-week follow-up, the patient reported improvement in exertional tolerance (NYHA-2) and lower extremity oedema. However, she continues to require torsemide 40 mg daily and metolazone 2.5 mg weekly.

Lead author biography

Cardiology Fellow at University of South Dakota Sanford School of Medicine.

Supplementary material

Supplementary material is available at European Heart Journal – Case Reports online.

Slide sets: A fully edited slide set detailing these cases and suitable for local presentation is available online as Supplementary data.

Consent: Written consent was obtained from the patient in line with COPE guidelines for the submission and possible publication of this manuscript.

Conflict of interest: No industry relationships or competing interests to disclose.

Funding: None declared.

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