SRoGJR

Ppcpcrranwri

M

Wgov

SMr

2

Journal of the American College of Cardiology Vol. 45, No. 10, 2005© 2005 by the American College of Cardiology Foundation ISSN 0735-1097/05/$30.00P

Heart Rhythm Disorders

evere Symptomatic Tricuspid Valveegurgitation Due to Permanent Pacemakerr Implantable Cardioverter-Defibrillator Leadsrace Lin, MD,* Rick A. Nishimura, MD, FACC,* Heidi M. Connolly, MD, FACC,*

oseph A. Dearani, MD,† Thoralf M. Sundt III, MD,† David L. Hayes, MD, FACC*ochester, Minnesota

OBJECTIVES We report a series of patients with severe tricuspid valve regurgitation due to a permanentpacemaker (PPM) or implantable cardioverter-defibrillator (ICD) lead.

BACKGROUND Severe tricuspid regurgitation caused by a PPM or ICD lead is an under-recognized buttreatable etiology of severe right heart failure.

METHODS We reviewed the records of 41 patients who underwent tricuspid valve operation for severetricuspid regurgitation caused by previously placed PPM or ICD leads.

RESULTS During surgery, severe tricuspid regurgitation was found to be caused by the PPM or ICDleads in all 41 patients. There was a perforation of the tricuspid valve leaflet by the PPM orICD lead in 7 patients, lead entanglement in the tricuspid valve occurred in 4 patients, leadimpingement of the tricuspid valve leaflets occurred in 16 patients, and lead adherence to thetricuspid valve occurred in 14 patients. The septal leaflet was most often perforated (6 of 7).In the preoperative evaluation, valve malfunction due to the PPM or ICD lead was diagnosedpreoperatively in only 5 of 41 (12%) patients by transthoracic echocardiography. All patientsunderwent successful tricuspid valve operation (22 tricuspid valve replacement), with oneperioperative death occurring. During follow-up (range, 1 to 99 months), there was onepatient who died from left-sided heart failure and three patients died of other causes. Theremaining patients showed improvement in signs and symptoms of heart failure.

CONCLUSIONS Damage to the tricuspid valve by PPM or ICD leads may result in severe symptomatictricuspid regurgitation and may not be overtly visualized by echocardiography. This etiologyshould be considered when evaluating patients with severe right heart failure after PPM orICD implantation. (J Am Coll Cardiol 2005;45:1672–5) © 2005 by the American College

ublished by Elsevier Inc. doi:10.1016/j.jacc.2005.02.037

of Cardiology Foundation

ppp3pbwiippbs

ppoatnwfa

atients who present with severe right heart failure out ofroportion to left-sided heart disease present a diagnostichallenge because the etiology may be due to constrictiveericarditis, restrictive cardiomyopathy, or pulmonary vas-ular disease (1–5). We recently have observed the occur-ence of right heart failure due to tricuspid regurgitationesulting from a permanent pacemaker (PPM) and implant-ble cardioverter-defibrillator (ICD) leads, entities that haveot been well recognized. We report on a series of patientsho underwent surgical intervention for severe tricuspid

egurgitation proven to be due to PPM or ICD leads, as thiss a correctable cause of right heart failure.

ETHODS

e identified 41 patients who had severe tricuspid regur-itation caused by a PPM or ICD lead and underwentperation to repair or replace the malfunctioning tricuspidalve. Using a Mayo Institutional Review Board-approved

From the *Division of Cardiovascular Disease and the †Division of Cardiovascularurgery, Mayo Clinic, Rochester, Minnesota. Dr. Hayes’ industry disclosures includeedtronic (sponsored research, speaker, public stockholder), Guidant (sponsored

esearch, speaker, public stockholder, advisory board), and St. Jude (speaker).

pManuscript received July 28, 2004; revised manuscript received December 24,

004, accepted February 1, 2005.

rotocol, we reviewed the records of 1,465 consecutiveatients with severe tricuspid regurgitation who had tricus-id valve operation between January 1, 1993, and December1, 2003. One hundred fifty-six of these patients hadreviously placed endocardial PPM or ICD leads. On theasis of operative findings, we identified 64 patients inhom the tricuspid regurgitation was due to the previously

mplanted PPM or ICD lead. To rule out other confound-ng causes for the tricuspid regurgitation, we excludedatients who had a morphologic abnormality of the tricus-id valve (previous history of cardiac trauma, [n � 2],acterial endocarditis [n � 5], previous tricuspid valveurgery [n � 2], or congenital heart disease [n � 14]).

Thus, 41 patients comprised the study population. Theseatients all had severe tricuspid regurgitation and a mor-hologically normal tricuspid valve apparatus with evidencef tricuspid valve leaflet damage by the PPM or ICD leadst the time of operation. Forty patients underwent surgery athe Mayo Clinic; one patient had an evaluation and diag-osis made at the Mayo Clinic but tricuspid valve surgeryas performed at another institution. Survival and

ollow-up information was obtained from the clinical recordt the Mayo Clinic or from a questionnaire mailed to all

atients.

reetviHrmho

R

C4wTrpotahssPpla7yPl

CkFhtErmmDmwtreohtgottctOhto

T

AMERCP

TP

*

T

L

L

F

AV

*

T

O

O

1673JACC Vol. 45, No. 10, 2005 Lin et al.May 17, 2005:1672–5 Pacemaker Lead-Related Tricuspid Regurgitation

All 41 patients had preoperative transthoracic echocardiog-aphy performed at the Mayo Clinic, 13 patients had preop-rative transesophageal echocardiography, and 38 had intraop-rative transesophageal echocardiography. The reports fromhe preoperative and intraoperative echocardiograms were re-iewed in all cases; all available echocardiographic images werendependently reviewed by two of the authors (G.L. and

.M.C.). All available preoperative chest X-rays (n � 38) wereeviewed by two of the authors (G.L. and D.L.H.) to deter-ine PPM or ICD lead position before surgery. Eight patients

ad their PPM or ICD placed at the Mayo Clinic, and allther patients had their devices placed at other institutions.

ESULTS

linical presentation. Baseline clinical characteristics of the1 patients are shown in Table 1. The mean age of the patientsas 70 � 10 years, and there were 20 men and 21 women.here were 21 patients who presented primarily with severe

ight heart failure, including a referral diagnosis of constrictiveericarditis or restrictive cardiomyopathy in three patients. Thether 20 patients subsequently were found to have severericuspid regurgitation in addition to other abnormalities, suchs prosthetic valve malfunction, mitral or aortic valve disease, orypertrophic obstructive cardiomyopathy. All patients hadevere New York Heart Association functional class III or IVymptoms upon presentation.reviously placed pacemaker or ICD. There were 35atients who had PPM leads and 6 patients who had ICD

eads that caused the severe tricuspid regurgitation. Theverage time from PPM or ICD placement to surgery was2 months (i.e., 6 years) with a range of 2 months to 19ears. Six patients had had subsequent revisions of theirPM systems, including placement of additional ventricular

eads or upgrades to an ICD or biventricular pacemaker.

Abbreviations and AcronymsICD � implantable cardioverter-defibrillatorPPM � permanent pacemaker

able 1. Baseline Characteristics

MeanTotal

(Patient Number)

ge (yrs) 70 � 10 41en 20

jection fraction (%) 54 � 14 41heumatic heart disease 14oronary artery disease* 16revious valve surgery 16Aortic 7Mitral 9Both 3

ricuspid annular dilation 15PM placement, time from

placement to operation (months)72 (2–228)

Previous coronary artery bypass grafting or percutaneous intervention.PPM � permanent pacemaker.

haracteristics of the PPM and ICD lead systems werenown in 30 patients (37 leads) and are listed in Table 2.our patients had multiple leads. Of the seven patients whoad tricuspid valve leaflet perforation, two had multiple (i.e.,wo or three) leads.chocardiographic findings. Transthoracic echocardiog-

aphy was performed preoperatively in all 41 patients. Theean ejection fraction of the left ventricle was 54%. Theean pulmonary artery systolic pressure derived fromoppler echocardiography was 48 mm Hg (range, 28 to 84m Hg). There were only 5 of 41 (12%) of patients inhom tricuspid valve leaflet perforation or impingement by

he PPM or ICD lead was detected on the initial transtho-acic echocardiography interpretation. Although all patientsventually were found to have severe tricuspid regurgitation,nly 26 of 41 (63%) of these patients were diagnosed asaving severe tricuspid regurgitation on the initial interpre-ation of the transthoracic echocardiography. Transesopha-eal echocardiography was performed either preoperativelyr postoperatively in 38 patients. Valve malfunction due tohe PPM lead was observed in 17 of 38 (45%) patients byransesophageal echocardiography. Transesophageal echo-ardiography was able to diagnose severe tricuspid regurgi-ation in all 38 patients studied.

perative methods and results. All patients were found toave morphologically normal tricuspid valve with malfunc-ion of the valve caused by the PPM or ICD lead at the timef operation (Table 3). Tricuspid valve perforation by the

able 2. Device Lead Characteristics

ead typePPM 40ICD 6

ead insulation*Silicone 34Polyurethane 12

rench size*11 39 308 27 56 5

ctive fixation 23entricular lead (multiple) 6

Data from 46 leads in 36 patients.ICD � implantable cardiovertor-defibrillator; PPM � permanent pacemaker.

able 3. Operative Findings

perative findings: mechanism of tricuspid regurgitationLead adherence 14Lead entanglement 4Lead perforation 7Lead impingement 16perative procedureTricuspid valve replacement

Mechanical 5Bioprosthesis 17

AnnuloplastyPursestring 7

Ringed 12

Pgpovmrpp

tostoedfaticattpdrrctpF(tdcrs

D

Ts

lhtsoaEpodr

tAfil

rliOoo

fwiresamvcpacrtePrt

T

GBVPCCR

C

1674 Lin et al. JACC Vol. 45, No. 10, 2005Pacemaker Lead-Related Tricuspid Regurgitation May 17, 2005:1672–5

PM or ICD lead occurred in seven patients, lead entan-lement of the tricuspid valve apparatus occurred in fouratients, lead impingement of the tricuspid valve leafletsccurred in 16 patients, and lead adherence to the tricuspidalve occurred in 14 patients. Fourteen patients had involve-ent of the posterior leaflet. When the leaflet was perfo-

ated, the septal leaflet was most often involved (6 of 7atients). Secondary annular dilatation was noted in 15atients.Nineteen patients had an isolated tricuspid valve opera-

ion. Twenty-two patients required surgical intervention onther valves at the time of surgery, and 15 patients had otherurgical interventions, including pericardiectomy and myec-omy. The surgical approach to the tricuspid valve atperation varied according to individual surgeon prefer-nces. In the absence of extensive tricuspid valve leafletamage, valve repair was preferred. When valve repair waseasible, it consisted of: 1) removing or displacing the leadway from the affected leaflet; 2) suture repair of a defect inhe leaflet; or 3) positioning the PPM lead by suture fixationn recess of either the posteroseptal or anteroposteriorommissure. Intraoperative echocardiography was used tossure that the tricuspid regurgitation was reduced afterricuspid valve repair. Tricuspid annular dilatation wasreated by either a DeVega purse string or ringed annulo-lasty. When tricuspid repair was not possible because ofamage to the leaflet by the PM or ICD lead, valveeplacement was performed (22 patients). Tricuspid valveeplacement was performed by maintaining the native tri-uspid valve intact and positioning the pacing lead externalo the sewing ring of the prosthesis. There was oneerioperative death (operative mortality 2.4%).ollow-up. Patient follow-up ranged from 1 to 99 months

mean, 8.2 years). Seven patients were lost to follow-up, andwo declined to answer the questionnaire. There were foureaths, one due to left heart failure and three of unknownauses. No patient required additional surgery or leadevisions. The remaining patients all noted improvement inymptoms of their right heart failure.

ISCUSSION

his series is the first reporting on patients with severeymptomatic tricuspid regurgitation due to PPM or ICD

able 4. Reported Cases of Tricuspid Valve Leaflet Perforation b

No. ofCases

Found at Autopsyor Surgery

TricuspiValve

Leaflet

ould et al. (12) 1 Autopsy Anterioecker et al. (16) 1 Autopsy Posterioecht et al. (15) 1 Autopsy Posterioetterson et al. (14) 1 Autopsy Anteriohristie and Keelan (13) 1 Autopsy Septalhampagne et al. (17) 1 Surgery Posterioubio and Al-Basram (18) 1 Surgery Posterio

HF � congestive heart failure; PPM � permanent pacemaker.

eads requiring tricuspid valve surgery. Isolated case reportsave been noted of entrapment of a PPM lead in thericuspid apparatus during implantation, resulting in avul-ion or laceration of the tricuspid valve leaflets upon removalf the PPM lead (6–11) and case reports of perforation of

tricuspid valve leaflet by a PPM (Table 4) (12–18).chocardiographic detection of tricuspid regurgitation inatients with a PPM has been reported (19). However, theccurrence of severe symptomatic tricuspid regurgitationue to damage from PPM or ICD leads is not a well-ecognized entity.

The mechanism by which a PPM or ICD lead causesricuspid regurgitation has not been previously evaluated.utopsy reports have indicated that PPM leads can causebrosis and subsequent adherence to the tricuspid valve

eaflets as early as 17 days after implantation (16,20–22).As shown in this study, the mechanism of tricuspid

egurgitation due to PPM or ICD leads is variable. Theargest subset of patients in our study (n � 16) had only leadmpingement on the tricuspid valve leaflets at surgery.

ther mechanisms include leaflet perforation, entanglementf the tricuspid valve apparatus, and adhesion of the PPMr ICD to the tricuspid valve leaflet.It is necessary to have a high clinical index of suspicion

or this particular disease entity. Elevated venous pressureith large “V” waves upon physical examination is an

mportant clue to the diagnosis, and one cannot rely on aoutine echocardiogram to provide the diagnosis. Even inxperienced echocardiographic laboratories, the detection ofevere tricuspid regurgitation may be missed because ofcoustic shadowing from the pacemaker wires and subopti-al visualization of the regurgitant jet. In addition, direct

isualization of the mechanism of the PPM or ICD leadausing severe regurgitation was identified in only 12% ofatients with routine transthoracic echocardiography. Withhigh index of suspicion, further diagnostic information

ould be obtained from goal-directed imaging by transtho-acic or transesophageal echocardiography. On a retrospec-ive independent review of the images of the transthoracicchocardiogram, there were 22% of patients in whom thePM or ICD lead was identified as a cause of the tricuspid

egurgitation. Transesophageal echocardiography was ableo visualize the PPM or ICD lead as a cause of tricuspid

PM Lead (12–18)

ClinicalPresentation

Time from PPM Implantationto Presentation Insulation

CHF 4 months UnknownPPM failure 6 months UnknownPPM failure 9 months UnknownBradycardia 1 year SiliconeCHF 2 years Polyurethane tinedCHF 9 years Polyurethane tinedCHF 10 years Unknown

y a P

d

rrrr

rr

rdmanP

cdoifilpPrt

mecno

totrttnopaaSptaehsfctceit

isftta

wP

RMM

R

1

1

1

1

1

1

1

1

1

1

2

2

2

2

2

2

1675JACC Vol. 45, No. 10, 2005 Lin et al.May 17, 2005:1672–5 Pacemaker Lead-Related Tricuspid Regurgitation

egurgitation in 45% of patients. In the future, three-imensional echocardiographic imaging may be helpful toore clearly delineate the location of the PPM or ICD leads

nd the impact on the tricuspid valve. Also, patients mayot develop symptoms of right heart failure for years afterPM implantation, as shown in this study herein.We were unable to determine a relationship between lead

haracteristics and the likelihood of PPM or ICD leadamage to the tricuspid valve as a result of the small numberf patients in this study. The increased number of silicone-nsulated leads, larger French sizes, and number of passivexation leads may simply reflect the characteristics of older

eads identified in this retrospective study. There are limitedublished data regarding the physical characteristics of thePM leads identified in the cases of perforations we

eviewed or in autopsy series describing PPM lead adhesiono the tricuspid valve leaflets (12,14–18,20–23).

Although previous series have suggested that havingultiple PPM leads across the tricuspid valve may increase

chocardiographic findings of tricuspid regurgitation whenompared with patients with single leads (24,25), we couldot determine whether this relationship was present becausef the small number of patients in this series.The number of cases of severe tricuspid regurgitation due

o PPM or ICD leads is probably larger than identified inur series. There has been an increase in the number ofricuspid valve operations to correct tricuspid regurgitationelated to PPM lead-related injury performed at our insti-ution in the last few years. From 1993 to 2001, only one tohree cases occurred each year, but in 2002 and 2003 weoted 11 and 16 cases, respectively. Thirteen of 27 of theperations performed in 2002 and 2003 were referredrimarily for tricuspid valve surgery. We believe this reflectsn increasing awareness of this clinical problem rather thantrue higher incidence.tudy limitations. This was a retrospective analysis ofatients undergoing operation for severe tricuspid regurgi-ation due to PPM or ICD leads, and we were unable toddress the incidence of this complication. We did notxclude patients with left-sided valvular disease, ischemiceart disease, or known rheumatic heart disease. Thus,econdary pulmonary hypertension may have contributed tourther increase the severity of tricuspid regurgitation. Weannot rule out the possibility that dyssynchronous contrac-ion caused by right ventricular apical pacing could haveontributed to the severity of tricuspid regurgitation. How-ver, in all patients at the time of operation, the surgeondentified the PPM or ICD lead as the primary cause ofricuspid regurgitation.

Our findings suggest that PPM or ICD lead-relatednjury to the tricuspid valve can result in clinically importantevere tricuspid regurgitation and secondary right heartailure. These patients have symptomatic improvement afterricuspid valve repair or replacement. The diagnosis ofricuspid valve injury can be difficult by echocardiography

nd, thus, a high index of clinical suspicion must be present

hen patients present with severe right heart failure afterPM or ICD implantation.

eprint requests and correspondence: Dr. Rick A. Nishimura,ayo Clinic, Gonda 5-468 East, 200 First Street SW, Rochester,innesota 55905. E-mail: nishimura.rick@mayo.edu.

EFERENCES

1. Kabbani S, LeWinter M. Diastolic heart failure. Constrictive, restric-tive, and pericardial. Cardiol Clin 2000;18:501–9.

2. Hancock E. Differential diagnosis of restrictive cardiomyopathy andconstrictive pericarditis. Heart 2001;86:343–9.

3. Asher C, Klein A. Diastolic heart failure: restrictive cardiomyopathy,constrictive pericarditis, and cardiac tamponade: clinical and echocar-diographic evaluation. Cardiol Rev 2002;10:218–29.

4. Weitenblum E. Chronic cor pulmonale. Heart 2003;89:225–30.5. Runo J, Loyd J. Primary pulmonary hypertension. Lancet 2003;361:

1533–44.6. Assayg P, Thuaire C, Benamer H, et al. Partial rupture of the tricuspid

valve after extraction of permanent pacemaker leads: detection bytransesophageal echocardiography. Pacing Clin Electrophysiol 1999;22:971–4.

7. Fishenfeld J, Lamy Y. Laceration of the tricuspid valve by a pacemakerwire. Chest 1972;61:697–8.

8. Ong L, Barold S, Craver W, et al. Partial avulsion of the tricuspidvalve by tined pacing electrode. Am Heart J 1981;102:798–9.

9. Res JC, Decock CC, VanRossum AC, Schreuder J. Entrapment oftined leads. Pacing Clin Electrophysiol 1989;12:1583–5.

0. Frandsen F, Oxhoj H, Nielsen B. Entrapment of a tined pacemakerelectrode in the tricuspid valve. A case report. Pacing Clin Electro-physiol 1990;13:1082–3.

1. Furstenberg S, Bluhm G, Olin C. Entrapment of an atrial tinedpacemaker electrode in the tricuspid valve—a case report. Pacing ClinElectrophysiol 1984;7:760–2.

2. Gould L, Reddy C, Yacob U, et al. Perforation of the tricuspid valveby a transvenous pacemaker. JAMA 1974;230:86–7.

3. Christie J, Keelan M. Tricuspid valve perforation by a permanentpacing lead in a patient with cardiac amyloidosis: case report and briefliterature review. Pacing Clin Electrophysiol 1985;9:124–6.

4. Petterson S, Singh J, Reeves G, et al. Tricuspid valve perforation byendocardial pacing electrode. Chest 1973;63:125–6.

5. Vecht R, Fontaine C, Bradfield J. Fatal outcome arising from use of asutureless ’corkscrew’ epicardial pacing electrode inserted into the apexof left ventricle. Br Heart J 1976;38:1359–62.

6. Becker A, Becker M, Claudon D, et al. Surface thrombosis and fibrousencapsulation of intravenous pacemaker catheter electrode. Circulation1972;46:409–12.

7. Champagne J, Poirer P, Dumensil J, et al. Permanent pacemaker leadentrapment: role of transesophageal echocardiography. Pacing ClinElectrophysiol 2002;25:1131–4.

8. Rubio P, Al-Bassam M. Pacemaker-lead puncture of the tricuspidvalve successful diagnosis and treatment. Chest 1991;99:1519–20.

9. Paniagua D, Aldrich H, Lieberman E, et al. Increased prevalence ofsignificant tricuspid regurgitation in patients with transvenous pace-maker leads. Am J Cardiol 1998;82:1130–1.

0. Friedberg H, D’Cunha G. Adhesions of pacing catheter to tricuspidvalve: adhesive endocarditis. Thorax 1969;24:498–9.

1. Huang T, Baba N. Cardiac pathology of transvenous pacemakers. AmHeart J 1972;83:469–74.

2. Robboy S, Harthorne J, Leinbach R, et al. Autopsy findings withpermanent pervenous pacemakers. Circulation 1969;39:495–501.

3. Christie J, Keelan M. Tricuspid valve perforation by a permanentpacing lead in a patient with cardiac amyloidosis: case report and briefliterature review. Pacing Clin Electrophysiol 1986;9:124–6.

4. DeCock C, Vinkers M, Campe LV, et al. Long-term outcome ofpatients with multiple noninfected transvenous leads: a clinical andechocardiographic study pacing. Clin Electrophysiol, 2000;23:423–6.

5. Postaci N, Eksi K, Bayata S, et al. Effect of the number of ventricular

leads on right ventricular leads on right ventricular hemodynamics inpatients with permanent pacemaker. Angiology 1995;46:421–4.