Address for correspondence:

Reviews Samir R. Kapadia, MD

Cardiac Catheterization Laboratory
Cleveland Clinic

Tricuspid Regurgitation in Patients With 9500 Euclid Avenue, J2-211

Cleveland, OH 44195

Pacemakers and Implantable Cardiac kapadis@ccf.org

Defibrillators: A Comprehensive Review

Rasha Al-Bawardy, MD; Amar Krishnaswamy, MD; Mandeep Bhargava, MD;
Justin Dunn, MD; Oussama Wazni, MD; E. Murat Tuzcu, MD; William Stewart, MD;
Samir R. Kapadia, MD
Department Internal Medicine (Al-Bawardy) and the Department of Cardiovascular Medicine
(Krishnaswamy, Bhargava, Dunn, Wazni, Tuzcu, Stewart, Kapadia), Cleveland Clinic Foundation,
Cleveland, Ohio

Implantable cardiac devices, including defibrillators and pacemakers, may be the cause of tricuspid
regurgitation (TR) or may worsen existing TR. This review of the literature suggests that TR usually occurs
over time after lead implantation. Diagnosis by clinical exam and 2-dimensional echocardiography may
be augmented by 3-dimensional echocardiography and/or computed tomography. The mechanism may be
mechanical perforation or laceration of leaflets, scarring and restriction of leaflets, or asynchronized activation
of the right ventricle. Pacemaker-related TR might cause severe right-sided heart failure, but data regarding
associated mortality are lacking. This comprehensive review summarizes the data regarding incidence,
mechanism, and treatment of lead-related TR.

Introduction (P < 0.05).4,5 Numerous authors have found worsening of

Tricuspid regurgitation (TR) is a common valvular lesion,
with 1.6 million people in the United States affected by
moderate or severe TR.1 The pathophysiology is divided
into 2 major categories: functional (associated with left or
right heart pathology) and structural (from primary leaflet
abnormalities). Functional tricuspid regurgitation often
results from left-sided heart valve disease.1 The incidence of
TR may be increasing in frequency coincident with the use of
implanted cardiac devices, such as implantable cardioverter-
defibrillators (ICDs) and permanent pacemakers (PPMs).
This association was first described by Gibson and
colleagues in 1980.2 The current literature regarding
symptomatic, lead-related TR following ICD or PPM is
based mainly on case reports and observational studies.3
In this article, we provide a comprehensive review of the
incidence, diagnosis, mechanism, and outcomes of TR in
patients with cardiac devices.
Incidence
The prevalence of TR is between 25% to 29% of patients
with PPM, compared to 12% to 13% in the control group
The authors have no funding, financial relationships, or conflicts
of interest to disclose.
preexisting TR by 1 or 2 grades in 11% to 25% of patients, over
a period of 1 to 827 days after PPM or ICD placement 6 – 10
(Table 1). Tricuspid regurgitation may worsen, or new TR
may develop after up to 7 years of device implantation.4 – 10
Evidence Supporting an Increase in TR After Cardiac Device
Implantation: Paniagua and colleagues retrospectively eval-
uated 374 patients who were studied with echocardiography
after pacemaker implantation, and reported an increase in
the prevalence of moderate–severe TR (25% vs 12%, odds
ratio [OR]: 4.75).4 De Cock and colleagues prospectively
compared 48 patients with PPM, followed them over a
mean of 7.4 years, with age-matched controls without PPM.
The prevalence of TR was 29% compared to 13.5% in the
control group (P < 0.05).5 However, they did not look at
preimplantation tricuspid valve function.
Kim and colleagues studied 248 patients with either
an ICD or PPM, with pre- and postimplantation
echocardiograms.10 Tricuspid regurgitation, based on jet
area by color Doppler, worsened by at least 1 grade in 24.2%
of patients (P = 0.048). The average TR grade increased by
0.15 ± 0.8 (P = 0.004) in the entire population. Clinically
significant TR of grades 1.5 to 3 were found in 21.2% of
patients who had no clinically significant TR prior to lead
insertion, 5% of which was moderate–severe to severe. Inter-
estingly, regurgitation was more common in patients with
ICDs compared to PPM (32.4% vs 20.7%, P = 0.048), which

Received: November 10, 2012 Clin. Cardiol. 36, 5, 249–254 (2013) 249
Accepted with revision: February 6, 2013 Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22104 © 2013 Wiley Periodicals, Inc.
Table 1. Studies Assessing Prevalence of Lead-Related TR in Patients With PPM or ICD

Increase in Prevalence Statistical Significance of

No. of Median Preprocedure Echo Postprocedure Echo of TR by at Least Difference in Prevalence
Author of Study Patients Age, y ICD, % (Average Timing) (Average Timing) 1 Grade, % (P Value)
5
De Cock et al 48 62 0 No Yes (7.4 years) 16a <0.05

Paniagua et al4 745b 77.5 0 No Yes (unknown) 13 <0.001

Leibowitz et al9 35 67 57 Yes (4.5 days) Yes (1.2 days) 11 Unknown

8
Kucukarslan et al 61 53 10 Yes (3 days) Yes (1 day) 13 Unknown
7 c
Webster et al 123 16 55 Yes (unknown) Yes (242 days and 827 days) 25 <0.05

Kim et al10 248 75.4 30 Yes (7 days) Yes (93 days) 24 <0.05

Klutstein et al6 410 72-77 0 Yes (75 days) Yes (113 days) 18 <0.001

Abbreviations: ICD, implantable cardiac defibrillator; PPM, permanent pacemaker; TR, tricuspid regurgitation.
a
Unknown grade. b Paniagua et al. studied 374 patients but the prevalence of TR in the PPM group was reported out of the 745 patients. c At second
postimplantation echocardiogram.

may result from thicker or more rigid leads or from the
additional exposed metal shocking coil that could cause
more fibrosis.
Klutstein and colleagues studied 410 patients with PPM,
with less than moderate TR at baseline, finding that TR
worsened by >2 grades in 18.3% of the patients (P <
0.001) after a median of 113 days (range, 1–3549 days).
Interestingly, TR improved by ≥ 2 grades in 4.4% of patients.6
Webster and colleagues studied 123 pediatric patients
(median age, 16 years), each with preimplantation and
2 follow-up echocardiograms postimplantation (first after
a mean of 242 days, second after a mean of 827 days).7
They did not find evidence of worsening of TR based on
echocardiograms performed <1 year after implantation.
However, TR did progress from a mean of grade 1.54 to 1.69
(P < 0.02) over 2 years. Tricuspid regurgitation developed
or worsened by at least 1 grade in 22% of patients and by 2
grades in 3% of patients, whereas 63% who had no change in
their tricuspid valve function and 12% had improvement in
existing TR.
Evidence Against Worsening of TR: On the other hand,
evidence against worsening of TR is limited. Other
investigators have illustrated that TR does not worsen
acutely after cardiac device implantation, but may develop
or worsen later in the chronic phase.7 – 9,11 Kucukarslan and
colleagues evaluated 61 patients with either ICD or PPM, of
whom 49% had TR prior to cardiac device implantation.8
The study reported an increase from normal/trivial to
mild in 5 patients (16%) and an increase from mild to
moderate in 3 patients (10%), with no patients showing an
increase from moderate to severe TR. In their subjective
assessment, new or worsening TR was considered rare,
and therefore argued against deterioration acutely or after
6 months. Leibowitz and colleagues found no significant
change in TR grade acutely in 35 patients with ICD or
pacemakers. Unexpectedly, 6 patients had improvement in
their TR after lead implantation, possibly related to the
improved hemodynamics and decreased right ventricular
pressure.9
Morgan and colleagues assessed the incidence of TR
6 months after PPM implantation in 20 patients who had
undergone saline-contrast echocardiography. By assessing
inferior vena cava contrast reflux during systole as a
marker for TR, they found no significant occurrence of TR
after device implantation.12 Two major limitations of their
study were the lack of comparison with preimplantation
echocardiograms, and the use of a nonstandardized method
to detect the presence of TR.13
Unfortunately, many studies assessing the incidence of
TR after device placement are fraught with limitations based
on retrospective and uncontrolled evidence, and variability
in the diagnostic criteria used. Nevertheless, many of the
larger studies have demonstrated worsening in TR later
after several years of implantation, with some suggestion of
acute worsening of TR in a small number of patients.
Predictors of TR After Device Implantation: The predictors
of developing TR after cardiac device implantation are not
well understood. Investigations of adult population have
found that advanced age is a risk factor for developing
TR (age range, 72–75 years),6 whereas the pediatric study
mentioned previously (age range, 2–52 years) did not find
age to be a factor.7
Placement of more than 1 lead also may or may not worsen
TR, with conflicting data in the literature (Table 2). Celiker
and colleagues assessed TR after each of 2 pacemaker leads
was implanted in 40 patients, and after a single ventricular
lead was implanted in 22 patients, finding no difference in
mild to moderate TR among the 2 groups (83% vs. 77%).
However, 1 of the main limitations of the study is the
absence of echocardiographic assessment of the tricuspid
valve prior to lead implantation.14
On the other hand, Postaci and colleagues found that
patients with 2 device leads have more grade 3 TR, present
in 55.6% of patients with 2 ventricular leads, compared to
9.4% in those with 1 lead (P < 0.05).15 In the pediatric
population, it was found that a risk factor for lead-related TR
was congenital heart disease that is not right sided.7
Clinical Presentation
Patients may present with clinical symptoms of right-sided
congestive heart failure; however, many are asymptomatic

250 Clin. Cardiol. 36, 5, 249–254 (2013)

R. Al-Bawardy et al: TR in patients with pacemakers and ICDs
Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22104 © 2013 Wiley Periodicals, Inc.
Table 2. Studies Assessing the Prevalence of Pacemaker Lead-Related TR in Patients With 1 Ventricular Lead vs 2 Leads
No. of Median Preprocedure
Author of Study Patients Age, y ICD, % Echo
14
Celiker et al
1-lead group 22 69 0 No
2-lead group 18 67 0 No
15
Postaci et al
1-lead group 32 61 0 No
2-lead group 18 61 0 No
Abbreviations: ICD, implantable cardiac defibrillator; NS, not significant; TR, tricuspid regurgitation.
even when TR is present. Physical examination may
reveal the typical respirophasic systolic murmur at the
left sternal border that increases with inspiration, but
in many the murmur is unimpressive. Rahko describes
only a 28% prevalence of a regurgitant murmur in
echocardiographically detected TR.16 The classic physical
exam would be right-sided findings (jugular venous
distention, pulsatile liver, peripheral edema) without left-
sided findings.17,18
The TR murmurs that increase with inspiration are
different than TR murmurs related to congestive heart
failure, which usually diminish with inspiration. This
murmur that gets louder with inspiration is Carvallo’s
maneuver, which has a specificity of 100% and a sensitivity
of 80%.19 Other physical exam findings typical of TR include
hepatojugular reflux (specificity and sensitivity of 100% and
66%, respectively, in detecting TR).19 The right atrial V wave
is highly sensitive but not specific in detecting the presence
and the severity of TR.20
Imaging Diagnosis
Both 2-dimensional (2D) echocardiography and color
Doppler flow mapping are essential in diagnosing TR.
The severity is based on the direction and the size of the
regurgitant jet, the presence of proximal flow convergence,
and vena contracta width.21 The sensitivity and specificity of
classifying TR as severe using vena contracta width ≥6.5 mm
is 88.5% and 93.3%, respectively.22
The diagnosis of TR may be underestimated by 2D
echocardiography. It is difficult to appreciate the full
anatomical relationship between the tricuspid valve and
the ICD or PPM lead(s), as only 2 leaflets are visible
simultaneously when using any 2D imaging plane.3,23
Furthermore, the posterior leaflet, which is implicated in
many PPM lead-related TR cases, is only visualized in some
views, and is less commonly imaged during the routine
echocardiographic examination.23
The PPM lead may become entrapped in the thickened,
fibrotic, and fused posterior and septal leaflets.23 Three-
dimensional (3D) transthoracic echocardiography (TTE)
maybe useful in diagnosing lead-related TR, particularly
in visualizing the short axis of the tricuspid valve,
not obtainable with 2D echocardiography, which allows
Statistically Significant Difference
Postprocedure Echo Prevalence of Between the Groups With 1 and 2
(Average Timing) TR (Grade), % Leads (P Value)
Yes (2433 days) 18.2 (moderate), 59.1 (mild) NS
Yes (1186 days) 22.2 (moderate), 61.1 (mild)
Yes (2 years) 9.4 (grade 2) <0.05
Yes (2 years) 55.6 (grade 2)
assessment of the route and the position of the lead within
the tricuspid valve apparatus.3,18,23 Unfortunately, due to the
need for dedicated probes and image analysis software, as
well as greater cost, 3D echocardiography is not as widely
used currently.
In their review of more than 1000 patients undergoing
tricuspid valve replacement, Lin and colleagues found 41
patients whose significant TR was due to PPM or ICD leads,
based on operative findings of leaflet damage. Interestingly,
the TR was severe in only 63% of those 41 patients. One
significant limitation to visualizing TR on TTE is that
the shadow created by the pacemaker wires may lead to
suboptimal visualization of the regurgitant jet. Therefore,
the clinical examination and the large V waves in the jugular
venous pulse contour are important.17
Other evolving methods include contrast-enhanced
multidetector computed tomography, which may be used
indirectly to detect and grade TR based on early opacification
of hepatic veins or inferior vena cava during first-pass
intravenous contrast enhancement. This method has a
sensitivity of 90.4% and a specificity of 100% in detecting
echocardiographic TR.1,24
Another modality is cardiac magnetic resonance (CMR),
which can be used to both detect and quantify TR based
on regurgitant jet area and volume, with a sensitivity and
specificity of 88% and 94%, respectively, compared to right
ventricular angiography. However, most pacemaker devices
and leads are not compatible with CMR.25
Mechanism
Tricuspid regurgitation after lead placement can occur via
multiple mechanisms (Figure 1). It may be the result of
mechanical causes such as scar formation or thrombus on
the leads impairing closure. Perforation or laceration of
valve leaflets is another cause of TR. Another mechanism
is asynchrony, resulting from abnormal right ventricle
(RV) activation from a pacemaker. This may resolve if
the patient returns to his/her intrinsic rhythm.23,26,27 Kim
and colleagues demonstrated that TR after ICD or PPM
implantation is not related to an increase in pulmonary
artery pressure.10
Early postmortem investigations in the 1970s demon-
strated that pacemaker leads can adhere to the tricuspid
Clin. Cardiol. 36, 5, 249–254 (2013) 251
R. Al-Bawardy et al: TR in patients with pacemakers and ICDs
Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22104 © 2013 Wiley Periodicals, Inc.

Figure 1. Mechanisms of mechanical tricuspid regurgitation in the setting
of permanent pacemaker or implantable cardioverter-defibrillator leads.
(a) Valve obstruction caused by lead placed in between leaflets. (b) Lead
adherence due to fibrosis and scar formation to valve causing incomplete
closure. (c) Lead entrapment in the tricuspid valve apparatus. (d) Valve
perforation or laceration. (e) Annular dilatation.
valve leaflets, and even more commonly to the papillary
muscles.2 Leaflet perforation or lacerations are most com-
monly noted at the posterior leaflet. In TR that develops
years after PPM implantation, Iskandar and colleagues posit
that adhesion of the tricuspid valve (TV) leaflet to the pacer
lead results in restricted movement and therefore abnor-
mal coaptation of the posterior leaflet with the septal and
anterior leaflets.26
As early as 12 hours postprocedure, there is neoendo-
cardium formation, with development of fibrous sheaths
around the electrode, resulting in multiple endocardial
attachments, fibrosis, and adhesion that may affect the
TV function. A thin fibrin layer starts developing around the
wire soon after lead implantation. Thrombosis and edema of
the valve tissue may also occur 4 to 5 days after implantation.
A study by Huang and colleagues found that thrombosis on
the lead often occurs within 4 to 5 days after implantation.28
This may or may not result in acute TR. As described
previously, the frequency of acute TR varies in the many
published studies.7 – 9,11
Leads that are positioned directly on the annulus, or in
the commissure between leaflets, may lead to obstruction of
valve closure and a progression of TR. Seo and colleagues
demonstrated that the majority of lead-related TR occurs
when the leads are placed between the posterior and septal
leaflets.3 Moreover, 7 out of 12 patients with severe TR
had their leads obstructing the closure of the valve either
on the posterior or the septal leaflet. In contrast, a study
of 86 patients by Krupa and colleagues did not show any
dominant lead topography in patients who develop TR after
either ICD or PPM.29
Lin and colleagues found that the mechanism of TR
after pacemaker implantation in 41 patients was lead
impingement in 39%, lead adherence in 34%, lead perforation
in 17%, and lead entanglement in 39%.17
Other less-common causes of lead-related TR are tricuspid
annular dilatation, perforation, and laceration of leaflets
252 Clin. Cardiol. 36, 5, 249–254 (2013)
R. Al-Bawardy et al: TR in patients with pacemakers and ICDs
Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22104 © 2013 Wiley Periodicals, Inc.
by the leads.3,17,27 Novak and colleagues, based on their
postmortem study, showed that out of the 78 single
ventricular leads, 11 leads (14%) were fixed by fibrous
tissues to the tricuspid orifice, and 25 leads (32%)
penetrated through the chordae tendineae of the tricuspid
valve.30
Another uncommon mechanism is the occurrence of TR
after other valvular interventions. Loupy and colleagues
reported the case of a severe TR 17 years after original
PPM implantation, 9 years after placement of a second
ventricular lead, and 1 month after aortic valve replacement
(AVR).31 The authors suggest that the AVR may have led
to conformational changes between the tricuspid valve and
the pacemaker leads.
Management and Prognosis
Medical Management
Medical treatment has been studied mostly in patients
with functional TR, and includes treating the underlying
cause and congestive heart failure management.1 There is
a paucity of data about the outcomes of lead-related TR
managed medically. Aggressive volume management using
diuretics may be beneficial.
Lead(s) Extraction
Chronically implanted leads may cause fibrosis and scar
tissue formation, resulting in adherence to the tricuspid
valve. Device-related infection is the main cause for lead
extraction.32 Lead extraction has become both increasingly
sophisticated and specialized. Sometimes leads can be
removed by simple traction. Some patients require advanced
techniques using stylets and laser-equipped sheaths.
Percutaneous removal of PPM and ICD leads is often
performed in large specialty centers with significant
experience, but carries with it significant and sometimes
fatal risk.18 Rickard and Wilkoff32 reported an incidence of
major complications after lead extraction (death, cardiac
or vascular avulsion requiring intervention, pulmonary
embolism requiring surgical intervention, respiratory
distress, stroke, or pacing system-related infection) of 1.6%
among patients seen between 1994 and 1999. However, in
the last decade, the success rate has been 95% to 97%, and
the complication rate is down to 0.4% to 1%.
Consequently, the extraction procedure may itself lead to
worsening TR.18,23,33 The major risk factors for developing
TR after extraction are the use of a laser sheath (OR: 10.17,
95% confidence interval [CI]: 2.16-94.74, P = 0.001) or any
additional tools for extraction beyond simple traction (OR:
8.96, 95% CI: 2.02-81.45, P = 0.001), extraction of more than
2 leads (OR: 4.67, 95% CI: 1.38-14.48, P = 0.003), female
patients (OR: 3.36, 95% CI: 1.14-9.90, P = 0.01), and patients
with longer duration of implantation.34 Franceschi and
colleagues reported no statistically significant increase in
mortality in those who develop TR postextraction (31.6%)
vs those who do not develop TR postextraction (13.7%)
(P = 0.26).34 TR is more likely to occur after PPM extraction
than ICD lead extraction, but this may be from a longer
duration of implantation or more fibrous tissues deposition
and adherence to the tricuspid valve.33
Surgical Treatment
TR is usually treated by either surgical repair (usually
consisting of ring annuloplasty) or by tricuspid replacement
in some patients with advanced valvular disease. Currently,
percutaneous tricuspid repair remains experimental and
is under study using animal models. It is estimated that
8000 surgical tricuspid repairs occur annually. The majority
of these cases involve patients without device-related TV
pathology. The success rate of tricuspid valve repair is
generally reported to be 85%, although recurrence of TR
is common.1 Tricuspid valve replacement is associated
with a 6%, 30-day operative mortality, and 8% in-hospital
mortality.11,23,26 The 10-year survival for patients undergoing
tricuspid valve replacement in conjunction with left-sided
heart valve surgery is 78% and drops to 41% in patients with
triple valve surgery, as compared to the 10-year survival rate
after AVR (65%), mitral valve replacement (MVR) (55%), and
combined AVR and MVR (55%).1,35
There are limited data about surgical treatment in patients
with lead-related TR. In the study above by Lin and
colleagues, the average time to surgery was 72 months after
device implantation, arguing that severe lead-related TR is
likely to occur over a longer time frame, and the majority of
patients showed significant improvement postoperatively.17
There are not enough data assessing mortality in patients
with lead-related TR to make any firm conclusion about their
benefits from surgery. In particular, long-term durability
of surgery remains unknown. Baman and colleagues
studied patients with cardiac-device infection and reported
18% all-cause mortality after 6 months of infection. The
majority of their patients had their devices extracted either
percutaneously (81%) or surgically (8%), whereas 11% had
medical management only. Moderate to severe TR was
identified as an independent variable associated with higher
mortality (hazard ratio: 4.24, 95% CI: 1.84-9.75, P ≤ 0.01).36
Prevention
Data are limited when it comes to preventing TR while
placing ICDs or PPM leads. Few data exist on the type
of leads, the technique used and the locations of the
leads that may be associated with less TR. Lin and
colleagues, in their study of patients who had lead-related
TR, found that the majority of the leads were silicone
(74%) compared to polyurethane (26%).17 However, the
authors could not conclude the relationship between lead
characteristics and the development of TR due to the small
number of patients.17 Lead characteristics data otherwise
are lacking in other human studies. However, Wilkoff and
colleagues, in their animal-based study, found that expanded
polytetrafluoroethylene-coated coils are easily extracted
compared to backfilled with medical adhesive coils and
uncoated coils, as they are usually associated with less
fibrosis and possibly less TR.37
As far as techniques, some experts suggest that the
prolapsing technique is sometimes the preferred technique,
as the leads are not directly placed, and therefore the risk
of damaging the tricuspid apparatus is reduced. Rajappan
explained the 3 techniques of RV lead placement, of which
the prolapsing technique may be less traumatic compared
to the direct-crossing and drop-down techniques.38 One of
the disadvantages of the prolapsing technique is possible
injury to the structures surrounding the tricuspid valve prior
to getting into the RV. However, there is a lack of evidence
on which of these techniques is associated with a higher
risk of TR after lead implantation.
Based on experts’ opinion, apically placed leads have the
potential of tethering to the posterior leaflet of the tricuspid
valve more than septally placed leads, which may suggest
that sometimes ICD leads have higher TR associated with
the leads because they have to be placed apically.
Although there are no data regarding surveillance,
patients who may benefit from close echocardiography
monitoring are those who develop new-onset right-sided
heart failure symptoms, have preexisting TR, or those who
have more than 1 apical lead.
Summary
Device-related TR is usually due to either mechanical
(perforation/laceration of leaflets, entrapment of leads
resulting in scar tissue, or interference with valve
coaptation) or physiological (asynchronized activation of
the RV from apex to base) mechanisms. When clinically
significant, management typically involves percutaneous
extraction of the offending leads. Larger, prospective, and
well-controlled studies are needed to truly assess the
incidence and timing of TR after lead implantation along
with associated prognosis and mortality.
Acknowledgments
The authors thank Marion Tomasko for her contribution of
the medical illustration.
References
1. Agarwal S, Tuzcu E, Rodriguez E, et al. Interventional cardiology
perspective of functional tricuspid regurgitation. Circ Cardiovasc
Interv. 2009;2:565–573.
2. Gibson TC, Davidson RC, DeSilvey DL. Presumptive tricuspid
valve malfunction induced by a pacemaker lead: a case report and
review of the literature. Pacing Clin Electrophysiol. 1980;3:88–95.
3. Seo Y, Ishizu T, Nakajima H, et al. Clinical utility of 3-dimensional
echocardiography in the evaluation of tricuspid regurgitation
caused by pacemaker leads. Circ J. 2008;72:1465–1470.
4. Paniagua D, Aldrich HR, Lieberman EH, et al. Increased
prevalence of significant tricuspid regurgitation in patients with
transvenous pacemakers leads. Am J Cardiol. 1998;82:1130–1132,
A9.
5. De Cock CC, Vinkers M, Van Campe LC, et al. Long-term outcome
of patients with multiple (≥3) noninfected transvenous leads: a
clinical and echocardiographic study. Pacing Clin Electrophysiol.
2000;23:423–426.
6. Klutstein M, Balkin J, Butnaru A, et al. Tricuspid incompetence
following permanent pacemaker implantation. Pacing Clin
Electrophysiol. 2009;32(suppl 1):S135–S137.
7. Webster G, Margossian R, Alexander ME, et al. Impact of
transvenous ventricular pacing leads on tricuspid regurgitation
in pediatric and congenital heart disease patients. J Interv Card
Electrophysiol. 2008;21:65–68.
8. Kucukarslan N, Kirilmaz A, Ulusoy E, et al. Tricuspid insufficiency
does not increase early after permanent implantation of pacemaker
leads. J Card Surg. 2006;21:391–394.
9. Leibowitz DW, Rosenheck S, Pollak A, et al. Transvenous
pacemaker leads do not worsen tricuspid regurgitation: a
prospective echocardiographic study. Cardiology. 2000;93:74–77.
10. Kim JB, Spevack DM, Tunick PA, et al. The effect of
transvenous pacemaker and implantable cardioverter defibrillator
Clin. Cardiol. 36, 5, 249–254 (2013) 253
R. Al-Bawardy et al: TR in patients with pacemakers and ICDs
Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22104 © 2013 Wiley Periodicals, Inc.
 lead placement on tricuspid valve function: an observational study.
J Am Soc Echocardiogr. 2008;21:284–287.
11. McCarthy PM, Bhudia SK, Rajeswaran J, et al. Tricuspid valve
repair: durability and risk factors for failure. J Thorac Cardiovasc
Surg. 2004;127:674–685.
12. Morgan DE, Norman R, West RO, et al. Echocardiographic
assessment of tricuspid regurgitation during ventricular demand
pacing. Am J Cardiol. 1986;58:1025–1029.
13. Skjaerpe T, Hattle L. Diagnosis of tricuspid regurgitation. Sensitiv-
ity of Doppler ultrasound compared with contrast echocardiography.
Eur Heart J. 1985;6:429–436.
14. Celiker C, Kucukoglu MS, Arat-Ozkan A, et al. Right ventricular
and tricuspid valve function in patients with two ventricular
pacemaker leads. Jpn Heart J. 2004;45:103–108.
15. Postaci N, Eksi K, Bayata S, et al. Effect of the number of
ventricular leads on right ventricular hemodynamics in patients
with permanent pacemaker. Angiology. 1995;46:421–424.
16. Rahko PS. Prevalence of regurgitant murmurs in patients with
valvular regurgitation detected by Doppler echocardiography.
Ann Intern Med. 1989;111:466–472.
17. Lin G, Nishimura RA, Connolly HM, et al. Severe symptomatic
tricuspid valve regurgitation due to permanent pacemaker or
implantable cardioverter-defibrillator leads. J Am Coll Cardiol.
2005;45:1672–1675.
18. Nucifora G, Badano LP, Allocca G, et al. Severe tricuspid
regurgitation due to entrapment of the anterior leaflet of
the valve by a permanent pacemaker lead: role of real time
three-dimensional echocardiography. Echocardiography. 2007;24:
649–652.
19. Maisel AS, Atwood JE, Goldberger AL. Hepatojugular reflux:
useful in the bedside diagnosis of tricuspid regurgitation. Ann
Intern Med. 1984;101:781–782.
20. Pitts WR, Lange RA, Cigarroa JE, et al. Predictive value of
prominent right atrial V waves in assessing the presence and
severity of tricuspid regurgitation. Am J Cardiol. 1999;83:617–618.
21. Rogers J, Bolling S. Current perspective and evolving management
of tricuspid regurgitation. Circulation. 2009;119:2718–2725.
22. Tribouilloy CM, Enriquez-Sarano M, Bailey KR, et al. Quantifica-
tion of tricuspid regurgitation by measuring the width of the vena
contracta with Doppler color flow imaging: a clinical study. J Am
Coll Cardiol. 2000;36:472–478.
23. Chen TE, Wang CC, Chern MS, et al. Entrapment of permanent
pacemaker lead as the cause of tricuspid regurgitation. Circ J.
2007;71:1169–1171.
254 Clin. Cardiol. 36, 5, 249–254 (2013)
R. Al-Bawardy et al: TR in patients with pacemakers and ICDs
Published online in Wiley Online Library (wileyonlinelibrary.com)
DOI:10.1002/clc.22104 © 2013 Wiley Periodicals, Inc.
24. Groves AM, Win T, Charman SC, et al. Semi-quantitative
assessment of tricuspid regurgitation on contrast-enhanced
multidetector CT. Clin Radiol. 2004;59:715–719.
25. Nagel E, Jungehulsing M, Smolarz K, et al. Diagnosis and clas-
sification of tricuspid valve insufficiency with dynamic magnetic
resonance tomography: comparison with right ventricular angiog-
raphy [in German]. Z Kardiol. 1991;80:561–568.
26. Iskandar SB, Ann Jackson S, Fahrig S, et al. Tricuspid valve
malfunction and ventricular pacemaker lead: case report and
review of the literature. Echocardiography. 2006;23:692–697.
27. Champagne J, Poirier P, Dumesnil JG, et al. Permanent pacemaker
lead entrapment: role of the transesophageal echocardiography.
Pacing Clin Electrophysiol. 2002;25:1131–1134.
28. Huang TY, Baba N. Cardiac pathology of transvenous pacemakers.
Am Heart J 1972;83:469–474.
29. Krupa W, Kozlowski D, Derejko P, et al. Permanent cardiac pacing
and its influence on tricuspid valve function. Folia Morphologica
(Warszawa). 2001;60:249–257.
30. Novak M, Dvorak P, Kamaryt P, et al. Autopsy and clinical context
in deceased patients with implanted pacemakers and defibrillators:
intracardiac findings near their leads and electrodes. Europace.
2009;11:1510–1516.
31. Loupy A, Messika-Zeitoun D, Cachier A, et al. An unusual
cause of pacemaker-induced severe tricuspid regurgitation. Eur J
Echocardiogr. 2008;9:201–203.
32. Rickard J, Wilkoff BL. Extraction of implantable cardiac electronic
devices. Curr Cardiol Rep. 2011;13:407–414.
33. Glover BM, Watkins S, Mariani JA, et al. Prevalence of tricuspid
regurgitation and pericardial effusions following pacemaker and
defibrillator lead extraction. Int J Cardiol. 2010;145:593–594.
34. Franceschi F, Thuny F, Giorgi R, et al. Incidence, risk factors, and
outcome of traumatic tricuspid regurgitation after percutaneous
ventricular lead removal. J Am Coll Cardiol. 2009;53:2168–2174.
35. Groves P. Surgery of valve disease: late results and late
complications. Heart. 2001;86:715–721.
36. Baman TS, Gupta SK, Valle JA, et al. Risk factors for mortality
in patients with cardiac device-related infection. Circ Arrhythm
Electrophysiol. 2009;2:129–134.
37. Wilkoff BL, Belott PH, Love CJ, et al. Improved extraction of
ePTFE and medical adhesive modified defibrillation leads from the
coronary sinus and great cardiac vein. Pacing Clin Electrophysiol.
2005;28:205–211.
38. Rajappan K. Permanent pacemaker implantation technique: part
II. Heart. 2009;95:334–342.