Pacemaker-induced tricuspid regurgitation is uncommon
Daniel P. Rothschild
James A Goldstein
Amr E. Abbas
Wai Shun Wong
Received: 12 May 2017 /Accepted: 18 June 2017 /Published online: 6 July 2017
Springer Science+Business Media, LLC 2017
Background Prior studies report permanent pacemaker
(PPM)-induced tricuspid regurgitation (TR) in up to one third
of cases late post-implantation. We sought to assess the extent
of immediate PPM-induced TR.
Methods Forty patients undergoing PPM implant were pro-
spectively enrolled. Patients with pre-existing moderate or
severe TR or an RVSP >50 mmHg were excluded. Pre- and
immediate post-implantation transthoracic echocardiography
(TTE) analyzed TR grade according to established methods.
3D TTE was utilized to determine lead position in relation to
tricuspid leaflets as well as lead mobility across the TV.
Results Of 40 patients, four were excluded due to baseline
moderate TR (n = 3) or RVSP >50 mmHg (n = 1). In the
remaining cohort (n = 36), immediate post-implantation TTE
showed no increase in TR grade in 30 patients (83%), whereas
a one-grade increase from no/trace to mild occurred in six
(17%) others. In no patient did immediate moderate or severe
TR develop. Exclusive RV pacing was present in 47% of the
patients; however, only two of the six patients with increased
TR were paced. 3D TTE identified lead position in 92% of the
cases—more than 50% of the cases showed RV lead distribu-
tion in the middle or post eroseptal commissure of the TV.
Lead immobility was seen in only three of the six patients
with increased TR.
Conclusions These findings show that significant PPM-
induced TR is uncommon immediately post-implantation
and, when it occurs, causes no greater than mild TR. RV
pacing and lead mobility do not correlate with worsening of
TR. 3D TTE is highly reliable at identifying lead position.
Cardiac implantable electronic device (CIED) lead-induced
tricuspid regurgitation (TR) occurs in 7–39% ofcases,a
complication which is associated with poor prognosis over
time [2, 3]. Two lead-related TR mechanisms have been pro-
posed: (1) mechanical valve impingement and (2) lead-related
fibrosis [4, 5]. These two different pathophysiologic mecha-
nisms would be expected to occur at different time frames,
with direct mechanical impingement occurring earlier and
lead-induced fibrosis occurring later.
Prior reports of lead-related TR have been predominantly
retrospective observational studies or case reports and meth-
odologically limited by lack of baseline TR assessment .
Further, previous studies analyzed lead-induced TR late (3–
36 months) post-implantation [2, 7–10]. Two prior studies in
small numbers of patients have assessed development of lead-
induced TR immediately post-implantation, documenting 11
and 13% of cases with one-grade worsening TR by 2D
Doppler alone [11, 12]. Unfortunately, these studies lacked
3D ECHO imaging to examine the mechanisms of TR.
Accordingly, the present study was designed to assess pro-
spectively the incidence of lead-induced TR immediately after
permanent pacemaker (PPM) implantation employing 2D
Doppler ECHO and to determine lead position and its inter-
actions with the tricuspid apparatus using 3D transthoracic
* Wai Shun Wong
Department of Cardiovascular Medicine, Beaumont Health, 3601
West 13 Mile Road, Royal Oak, MI 48073, USA
Oakland University William Beaumont School of Medicine, 586
Pioneer Drive, Rochester 48309, MI, USA
J Interv Card Electrophysiol (2017) 49:281–287