Lead Extraction

Tricuspid Valve Dysfunction in Patients with a CIED and Transvenous Leads: A Case Review

Raymond G. Cutro, Jr., MD, CCDS, FHRS1, Nicholas Kotch, DO2, and Robert Hooker, MD, FACS
1
James A. Haley Veterans Hospital, Tampa, Florida; 2University of South Florida College of Medicine, Tampa General Hospital, Tampa, Florida

Raymond G. Cutro, Jr., MD, CCDS, FHRS1, Nicholas Kotch, DO2, and Robert Hooker, MD, FACS
1
James A. Haley Veterans Hospital, Tampa, Florida; 2University of South Florida College of Medicine, Tampa General Hospital, Tampa, Florida

Case Description

A 76-year-old male with a known history of structural heart disease and left ventricular systolic dysfunction presented to the emergency department with several weeks of progressive dyspnea and weight gain. The constellation of symptoms was consistent with that of heart failure (HF). On arrival to the hospital, physical exam was notable for jugular venous distention, bibasilar crackles, and lower extremity edema. Further, ascites was suggested by abdominal exam with presence of a fluid wave. Despite known prior admissions for HF, these findings were new. The patient confirmed this, having been unable to fit into his regular size of pants for several weeks. Serologic and radiographic evidence supported the above diagnosis of heart failure, and the patient was admitted to the coronary care intensive unit for aggressive diuresis with continuous parenteral diuretic infusion. 

A review of his history revealed a combined four-vessel surgical revascularization and bioprosthetic aortic valve replacement 4 years prior. Despite this and goal-directed medical therapy, his left ventricular ejection fraction (LVEF) remained at 25%, so a dual-chamber ICD system was implanted in 2015. Permanent atrial fibrillation was noted, as prior attempts at rhythm control, including left atrial ablation and antiarrhythmic drug therapies, had failed. The patient further developed increasing ventricular pacing burden, and cardiac resynchronization device upgrade was offered and performed in late 2016. Symptomatic improvement was noted, and the patient did well for the ensuing 18 months. We assumed care of this patient after the above procedures were completed. 

After admission and diuresis, significant symptomatic improvement occurred, and the patient was nearing his perceived dry weight based on initial clinic visits and recorded weights from home. Standard two- and three-dimensional transthoracic echocardiography were performed, and significant tricuspid valve regurgitation was seen. The course of the right ventricular lead can be seen in several views, along with its interaction with the TV leaflet and interventricular septum (Figures 1, 2, and 4). Corresponding tricuspid valve dysfunction is appreciated with severe tricuspid valve regurgitation on Doppler echo images (Figures 3 and 5). The RV was felt to be moderately dilated with a mid-RV diameter of 3.5 cm. Significant RV systolic dysfunction was seen and felt to be moderate with a tricuspid annular plane systolic excursion (TAPSE) of 1.25 cm. The tricuspid valve regurgitation was severe with a vena contracta width of 0.9 cm and PISA radius of 1.0 cm. LV systolic function was essentially unchanged, with an EF of 25%. The bioprosthetic aortic valve was well seen and without significant dysfunction.

Since the clinical presentation was consistent with right-sided heart failure, a combined heart catheterization procedure was performed. All coronary artery bypass grafts were seen to be patent. Right-sided heart catherization pressures revealed a pulmonary capillary wedge pressure of 12 mmHg and pulmonary artery systolic pressure of 62 mmHg. Right ventricular pressure was 62/22, and right atrial pressure was 22. There was a giant V wave seen on the right atrial pressure tracing. 

Based on all available clinical data, hemodynamics, and echocardiographic findings, we felt that the most likely etiology of the RV systolic dysfunction and right-sided heart failure was tricuspid valve regurgitation related to the transvenous RV ICD lead. Thus, corrective valve surgery was considered and discussed with our cardiothoracic surgical colleagues. Given the patient’s low EF, significant RV dysfunction, and need for redo sternotomy, this patient was considered high risk from a surgical standpoint. Additionally, given his advanced age, he was not considered to be a candidate for orthotopic heart transplantation. Finally, the need for ongoing CRT and a current transvenous system posed a significant challenge. 

Ultimately, after careful consideration and discussion with the patient, we elected to proceed with a combined lead extraction of the transvenous ICD system, tricuspid valve replacement, and placement of an epicardial pacing system. We also elected to place a subcutaneous ICD system as a means of mitigating risk of sudden cardiac death. Immediate postoperative chest x-ray can be seen in Figure 6. The procedure was uncomplicated; however, it required several days of inotropic therapy to augment RV function. This was ultimately weaned, and the patient was discharged 11 days after surgery. In outpatient clinic follow-up, he remains euvolemic and has experienced a dramatic improvement in his HF symptoms. 

Discussion

Tricuspid valve dysfunction/regurgitation (TR) related to pacemaker and defibrillators leads is becoming increasingly recognized, with the incidence of worsened TR severity varying depending on study; up to an increase in 1 grade in 24.2%, to an increase in at least 2 grades in 18.3%.1 The mechanism is likely multifactorial, and includes abnormal valve coaptation due to lead impingement or adhesions to the leaflets or subvalvular structures, redundant lead loops (whether ventricular, atrial, or coronary sinus), as well as possibly even functional TR due to RV asynchrony. While most lead-related tricuspid valve (TV) dysfunction cases involve regurgitation, significant TV stenosis with regurgitation has also been reported in 4% of lead-related TV dysfunction cases in one series.2 Various risk factors associated with lead-related TV dysfunction have been identified and include presence of defibrillator leads, older age, location of leads in relation to the posterior and septal leaflets, and leads passing between chordae.1

It is already recognized that TR of at least moderate grade (2+) is associated with increased morbidity and mortality. Furthermore, moderate to severe TR is seen more frequently in patients with implantable devices, and is also associated with increased mortality and HF events.3,4 However, much of this data has been derived from retrospective observational studies or case reports. Data from the MADIT-II and EVADEF study populations have shown an increase in HF events in those that have received single- or dual-chamber ICDs.5,6 While some of this increase has been attributed to RV pacing and defibrillator shocks, the increase even in those receiving single-chamber devices with low pacing burden suggest other device-related factors may be important.6 A 2014 single-center review reported significant lead-induced TR in 38% of patients who had undergone pacemaker or ICD implantation, which was associated with worse long-term survival (HR=1.687), more HF events (HR=1.641), and an independent association with all-cause mortality (HR=1.749), over a median follow-up of 58 months.7 Additionally, a 2016 retrospective review of significant pacemaker lead-associated TR found the presence of moderate to severe TR to also be associated with increased mortality (HR of 1.4).8 A multicenter, prospective study of 300 consecutive patients is underway to evaluate whether cardiac device-associated TR is real, its potential mechanisms, and the clinical impact.9

Diagnosis of lead-related TV dysfunction relies primarily on the use of 2D, 3D Doppler transthoracic and transesophageal echocardiography, with the assessment of the severity similar to those without device leads. Some caveats apply, including that leads can cause imaging artifacts which may lead to underestimation of TR severity. One study reported only 63% of patients were diagnosed with severe TR during preoperative imaging.10 In these instances, it is important to also evaluate the hepatic vein flow pattern, which would not be subject to lead-related image artifacts. It can be difficult to determine the exact mechanism of TV dysfunction on 2D imaging; the use of 3D echocardiography to evaluate the interaction of leads with valvular structures has shown promise and is likely the current imaging modality of choice.3

Management varies, and in the latest guidelines on CIED lead management and extraction, there are no formal recommendations or support for lead-related TR alone as an indication for extraction in the absence of lead malfunction or infection.1 A combined evaluation and approach with cardiothoracic surgery is recommended to determine the best individualized approach regarding percutaneous or open extraction, possible tricuspid valve repair vs replacement followed by possible re-implantation, or surgical valvular intervention with lead retention. A comprehensive evaluation is needed, as the presence of severe RV enlargement/dysfunction, significant TV annular dilation, or severely elevated pulmonary artery pressures or pulmonary vascular resistance may predict the lack of clinical improvement after lead extraction. In a 2017 review, Chang et al presented a decision tree algorithm for lead removal and valve intervention for TR in the absence of device or endovascular infection. In the absence of severe annular dilation, significantly elevated pulmonary artery pressures, and when there is imaging evidence of a lead interfering with TV function, lead extraction along with possible TV repair or replacement was a reasonable strategy.3

Finally, future studies are needed to determine whether alternatives to transvalvular leads, such as a leadless pacer or His bundle pacing lead to avoid crossing the TV, or even alternative lead coatings to reduce lead-valvular adhesions, will result in reduction of lead-related TR, and ultimately, improved morbidity and mortality.

Disclosures: The authors have no conflicts of interest to report regarding the content herein.   

References

  1. Kusumoto FM, Schoenfeld MH, Wilkoff BL, et al. 2017 HRS expert consensus statement on cardiovascular implantable electronic device lead management and extraction. Heart Rhythm. 2017;14:e503-e551. 
  2. Polewczyk A, Kutarski A, Tomaszewski A, et al. Lead dependent tricuspid dysfunction: analysis of the mechanism and management in patients referred for transvenous lead extraction. Cardiol J. 2013;20(4):402-410. 
  3. Chang JD, Manning WJ, Ebrille E, Zimetbaum PJ. Tricuspid Valve Dysfunction Following Pacemaker or Cardioverter-Defibrillator Implantation. J Am Coll Cardiol. 2017;69:2331-2341. 
  4. Nath J, Foster E, Heidenreich PA. Impact of tricuspid regurgitation on long-term survival. J Am Coll Cardiol. 2004;43:405-409. 
  5. Marijon E, Trinquart L, Otmani A, et al. Predictors for short-term progressive heart failure death in New York Heart Association II patients implanted with a cardioverter defibrillator—the EVADEF study. Am Heart J. 2010;159:659-664.e1. 
  6. Goldenberg I, Moss AJ, Hall JW, et al. Causes and Consequences of Heart Failure After Prophylactic Implantation of a Defibrillator in the Multicenter Automatic Defibrillator Implantation Trial II. Circulation. 2006;113:2810-2817. 
  7. Höke U, Auger D, Thijssen J, et al. Significant lead-induced tricuspid regurgitation is associated with poor prognosis at long-term follow-up. Heart. 2014;100:960-968. 
  8. Delling FN, Hassan ZK, Piatkowski G, et al. Tricuspid Regurgitation and Mortality in Patients With Transvenous Permanent Pacemaker Leads. Am J Cardiol. 2016;117:988-992. 
  9. Dokainish H, Elbarasi E, Practice MS. Prospective study of tricuspid valve regurgitation associated with permanent leads in patients undergoing cardiac rhythm device implantation: background, rationale, and design. Glob Cardiol Sci Pract. 2015;2015(3):41. 
  10. Lin G, Nishimura RA, Connolly HM, Dearani JA, Sundt TM 3rd, Hayes DL. Severe Symptomatic Tricuspid Valve Regurgitation Due to Permanent Pacemaker or Implantable Cardioverter-Defibrillator Leads. J Am Coll Cardiol. 2005;45(10):1672-1675.
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