Case Reports
Acta Cardiol Sin 2008;24:39-42
Successful Treatment of Superior Vena Cava
Syndrome Induced by Transvenous
Permanent Pacemaker Implantation with
Balloon Angioplasty
Wen-Po Chuang,1 Jyh-Ming Juang,1 Kwan-Lih Hsu,1 Fu-Tien Chiang1,2 and Chuen-Den Tseng1
Superior vena cava (SVC) syndrome is a rare but potentially lethal complication of transvenous permanent
pacemaker implantation. The pathogenesis is unclear, but thrombosis and fibrotic constriction of the vessels are
believed to be responsible for this situation. Multiple, severed, and previously infected leads may increase the risk of
SVC syndrome, but are not prerequisite for it. Anticoagulation, thrombolytics, percutaneous balloon angioplasty
with or without stent, and surgery have been used to solve the problem. We report a case who developed SVC
syndrome three years after the implantation of a DDD pacemaker for sick sinus syndrome. Anticoagulation alone
failed to relieve his symptoms. After successful balloon angioplasty, the patient remained asymptomatic one year
after the procedure.
Key Words:
Pacemaker · Superior vena cava syndrome · Balloon angioplasty
INTRODUCTION
taneous balloon angioplasty successfully solved the problem after it didn’t respond to conservative treatment.
The patient remained asymptomatic one year after the
procedure. Pacemaker function also remained intact one
year after the procedure.
Symptomatic SVC syndrome is a rare but potentially
lethal complication after implantation of transvenous
pacemaker. Available strategies of treatment include
anticoagulation, thrombolysis, balloon angioplasty with
or without stent, and surgery. As percutaneous angioplasty has advanced, it has become the most popular
method for treating this situation. Here, we report a case
who presented with superior vena cava syndrome three
years after permanent pacemaker implantation. Percu-
CASE REPORT
A 61-year-old hypertensive man was diagnosed as
sick sinus syndrome due to syncope with long pause up
to 3.2 seconds in 2002. A DDDR permanent pacemaker
(Generator: Medtronic SigmaTM SDR203; Leads: Medtronic CAPSURE Ò SP 4024 and 4524) was implanted
via left subclavian vein approach in a hospital in Kaohsiung, Taiwan. Three years later, he began to suffer
from progressive swelling of his head, neck and both
arms. The swelling was exacerbated by leaning over
and lying down. Purplish discoloration of the patient’s
anterior chest due to ectasia of superficial veins was
also noted. Under the impression of superior vena cava
Received: June 7, 2006
Accepted: September 10, 2007
1
Cardiovascular Center, Far Eastern Memorial Hospital; 2Division of
Cardiology, Department of Internal Medicine, National Taiwan
University Hospital; 3Department of Laboratory Medicine, National
Taiwan University Hospital, Taipei, Taiwan.
Address correspondence and reprint requests to: Dr. Chuen-Den
Tseng, Division of Cardiology, Department of Internal Medicine,
National Taiwan University Hospital, No. 7, Chung Shan South
Road, Taipei 100, Taiwan. Tel: 886-2-2312-3456 ext. 2152; E-mail:
cdtseng@ha.mc.ntu.edu.tw
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Acta Cardiol Sin 2008;24:39-42
Wen-Po Chuang et al.
12 ´ 40 mm was then used to dilate the lesion with pressure up to 10 atm. Due to recoil of the stenotic site, a
Tyshak balloon 15 ´ 40 mm was then used to dilate it
with 4 atm. After that, no more residual stenosis was
noted. Also, the pressure of the right brachiocephalic
vein dropped from 24 mmHg to 12 mmHg, which was
equal to that of the right atrium.
The patient’s symptoms were then relieved. He was
discharged on wafarin and remained free of symptoms
one year after the procedure.
syndrome, enoxaparin (1 mg/kg q12h) was administered subcutaneously.
Contrasted computed tomography of the thorax
showed stricture of the superior vena cava with prominent collaterals in the perivascular, paratracheal and left
upper chest walls (Figure 1). No definite hypodense filling defect was found in the SVC or brachiocephalic
veins. Due to persistent symptoms after one week of
anticoagulation, the patient was brought to our catheterization lab.
Using the right femoral vein as vascular access, we
retrogradely passed terumo wire through the stenotic site
and brought a 6 Fr. multipurpose A2 catheter to the right
brachiocephalic vein. Venography then showed stenosis
at the SVC (Figure 2) just below the junction of the
azygous vein and superior vena cava. A Smash balloon
DISCUSSION
Although around 30% of patient receiving transvenous permanent pacemaker implantation may have peripheral or central venous stenosis and occlusion, only 4
in 1000 to 3 in 10000 implants will develop superior
vena cava syndrome.1,2 Multiple lead placement and previous infected or severed leads may increase the risk of
SVC syndrome but aren’t prerequisite. This complication may occur as early as two days following pacemaker implantation or as late as 15 years after implantation. The pathogenesis is unclear. In those with early
Figure 2. Venography (lateral view) obtained by injection of contrast
from multipurpose catheter placed below the stricture site (arrows) of
superior vena cava (A), in the azygous vein (arrow heads, B), and in the
brachiocephalic trunk (C). Early snapshot during the inflation of
balloon showed the tight stricture (D) which was fully dilated later.
Figure 1. Computed tomography of thorax showed stricture of
superior vena cava (arrowheads in A) and prominent collaterals in the
perivascular, paratracheal (arrows in A) and left upper chest walls
(arrows in B).
Acta Cardiol Sin 2008;24:39-42
40
Angioplasty for Pacemaker Induced SVC Syndrome
presentation, acute thrombosis was believed to be the
cause. Fibrotic stenosis has been shown during surgery
and autopsy and likely plays a role in chronic cases. Using intravenous ultrasound, intimal thickening was also
demonstrated in one case report.3
The modalities of treatment for this situation include
anticoagulation, thrombolysis, 4,5 endovascular treatment6-9 and surgery.10,11 Anticoagulation is reasonable
for all patients as pulmonary embolism can occur in
SVC syndrome caused by pacemaker and may be lethal.
Anticoagulation alone is often not sufficient and is usually used in combination with other treatment modalities.
However, some mild symptomatic cases may be managed only with anticoagulation therapy alone, even without opening the occluded vein. Successful long-term follow-up experience of conservative treatment has been
reported.12
Thrombolysis is also used systemically or locally
alone or in combination with percutaneous treatment.4
The early treatment appears to be the key to successful
thrombolysis.5 If thrombolysis is given before the fifth
day of occlusion, it can be effective in 88% of cases; but
if the delay is longer than five days, only 25% of cases
can be successfully treated.
Surgical treatment consists of bypassing the stenosis with a polytetrafluoroethylene tube, autologous spiral vein or azygous vein. Long-term patency of spiral
vein graft up to 15 years was reported. 11 Epicardial
leads can also be placed during the operation if necessary. But the procedure’s relatively invasive nature led
to its loss of popularity after the introduction of endovascular treatment.13
Angioplasty for SVC syndrome has been well documented in the literature.6,8,9,13 Restenosis due to elastic
recoil may occur but is manageable by repeating angioplasty.14 Stents are usually placed if the lesions recoil
despite repeated balloon angioplasty. Self-expandable
stents are often preferred rather than balloon-mounted
ones because they have larger diameter and are more
flexible. They can adapt to the greater diameter of the
vessel after the flow re-establishes, thus have lower risk
for stent migration. Smayra et al. demonstrated that the
1-year patency rates after stenting of SVC syndrome for
malignant, benign and hemodialysis patients were, respectively, 74%, 50% and 22%.6 Retraction of the pacemaker wire before the deployment of stents should be
tried. Although the leads may be incorporated into the
venous wall and not directly contact with stents, risk of
damage of the lead is still a concern. Besides, once the
pacemaker wire is dysfunctional, insertion of additional
lead may further increase the risk of recurrent venous
obstruction. Bolad et al. showed that it was feasible to
perform lead extraction, angioplasty with or without
stenting and re-implantation of new systems during one
procedure. 7 Rupture of superior vena cava15 and stent
migration to pulmonary artery 10 are possible serious
complications of angioplasty for stenosis of superior
vena cava.
In our case, fibrotic stricture is believed to be the
cause of SVC syndrome as the computed tomography
showed no definite hypodense material in the SVC and
the symptoms persisted after anticoagulation. Our case
demonstrates that angioplasty can treat SVC syndrome
with mid-term success. The pacemaker function remained normal after angioplasty. We suggest that balloon angioplasty alone should be attempted first in patients with SVC syndrome if the stenotic lesion is dilatable, because restenosis may occur even after stenting
and can be treated by repeating angioplasty. Stenting for
all cases may be not necessary, but should be considered
for refractory cases. Retraction of the old lead first
should be done before stenting, as it may ameliorate the
concern of possible lead damage and jailing. Bypass surgery should be reserved for those in whom angioplasty
was failed, or whose leads are dysfunctional and have no
feasible vascular access to place the new system.
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