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From the University of Alabama at Birmingham and Vanderbilt University,
Nashville, Tenn.
Correspondence to G. Neal Kay, MD, Division of Cardiovascular Disease, 321J Tinsley Harrison Tower, University of Alabama at Birmingham, Birmingham, AL 35294.
Methods and Results—Three months after successful catheter
ablation of atrial fibrillation, both patients developed progressive
dyspnea and pulmonary hypertension. Both were found to have
severe stenosis of all 4 pulmonary veins near the
junction with the left atrium. Balloon dilation of the stenotic
pulmonary veins was performed in these patients, with
improvement in dyspnea and pulmonary hypertension.
Conclusions—The complication of pulmonary vein
stenosis is potentially life-threatening, and the application
of radiofrequency current within the pulmonary veins with
standard catheter technology should be avoided. This complication can
be treated with balloon dilation, although the long-term course is
unknown.
Case 1
After having given written, informed consent, the patient was enrolled
in a multicenter protocol for catheter ablation of AF that had been
approved by the Institutional Review Board for Research Involving Human
Subjects at the University of Alabama at Birmingham.
Echocardiography demonstrated normal left
ventricular function, with an LA dimension of 38 mm
and mild mitral and tricuspid regurgitation and an
estimated PA systolic pressure by Doppler
echocardiography of 39 mm Hg. On April 23,
1997, the patient underwent catheter ablation under general
anesthesia. Standard transseptal puncture was performed
with a Brockenbrough needle and a 13F outer sheath and 11F inner sheath
(Daig Corp). The activated clotting time was maintained at
>300 seconds with heparin. Catheter ablation involved application of
radiofrequency current within both atria to create 5 lines of
conduction block. The radiofrequency current was applied with a target
temperature of 55°C as the ablation catheter was gradually withdrawn
in increments of 2 to 3 mm every 30 seconds. The ablation lines
were (1) from the right upper PV to the left upper PV, which was
extended to the mitral annulus; (2) from just to the left of the
posterior interatrial septum 1 cm above the mitral annulus to the
ostium of the right superior PV; (3) diagonally across the roof of the
LA, starting anteriorly along the interatrial septum and continued to
the left superior PV; (4) from the superior vena cava to the
inferior vena cava along the posterior wall of the right
atrium; and (5) from the tricuspid annulus to the Eustachian ridge, as
used for ablation of typical atrial flutter. The total procedural
duration was 8.0 hours. During the ablation session, the intracardiac
electrograms in AF became progressively more organized, with
lengthening of the average atrial cycle length and widening of the
isoelectric segments in the right atrial and LA electrograms and
conversion to normal sinus rhythm. The patient developed typical atrial
flutter in June 1997 that was successfully ablated with radiofrequency
applications in the isthmus between the tricuspid valve and the
Eustachian ridge. AF has not recurred in follow-up of >12 months
(Figure 2
In July 1997, the patient noted the onset of progressive dyspnea on
exertion and nonproductive cough. The ECG demonstrated normal sinus
rhythm throughout the postoperative course (Figure 2
On December 18, 1997, the patient underwent right and left heart
catheterization by the transseptal technique. The PA
pressure was 98/36 mm Hg (mean, 58 mm Hg), with an LA
pressure of 23 mm Hg, cardiac output of 4.78 L/min, and PVR of
586 dynes · cm2/s. Selective cannulation
of each of the 4 PV ostia and venography were performed. All 4 of the
PVs demonstrated localized stenosis within 10 mm from the
ostium draining into the LA. The left superior PV was severely
stenotic
The patient noted an immediate improvement in his dyspnea and was
discharged 5 days after catheterization. He was
reevaluated at a clinic visit on January 2, 1998, and reported marked
improvement in his dyspnea on exertion. Right heart
catheterization was performed on January 2, 1998, and
demonstrated a PA pressure of 54/24 mm Hg, with PCWP of 16
mm Hg, cardiac output of 5.9 L/min, and PVR of 293 dynes ·
cm2/s.
Case 2
After informed, written consent to the investigational protocol, she
underwent radiofrequency catheter ablation by the same technique as
described above. The total procedural duration was 12.5 hours. The
patient developed atypical atrial flutter and returned for repeat
ablation on December 31, 1996. An echocardiogram before the procedure
demonstrated an estimated PA systolic pressure of 38
mm Hg. Catheter ablation was performed in the usual isthmus of tissue
between the tricuspid annulus and the Eustachian ridge, with reversion
to sinus rhythm. AF was induced with programmed electrical stimulation,
and a linear application of radiofrequency current was delivered from
the superior vena cava to the inferior vena cava along the
posterior wall of the right atrium. AF reverted to normal sinus rhythm
during this application and was no longer inducible with up to 4
extrastimuli. An LA flutter was then induced with programmed electrical
stimulation, which was mapped and ablated in the region between the
left inferior PV and the mitral annulus. She has maintained
sinus rhythm for >1 year after this procedure.
Immediately after ablation, the patient complained of a persistent,
nonproductive cough. Over the next several months, she gradually
developed progressive dyspnea on exertion that did not respond to
inhaled corticosteroids or bronchodilators. An
echocardiogram on June 20, 1997, demonstrated an estimated PA
systolic pressure of 85 mm Hg, with a dilated right
ventricle. A radionuclide ventilation-perfusion lung scan demonstrated
nearly complete absence of perfusion to the right lung and left lower
lobe, with a normal pattern of ventilation. Right heart
catheterization was performed on June 21, 1997, with a
PA pressure of 81/25 mm Hg (mean, 54 mm Hg), PCWP of
16 mm Hg, PVR of 512 dynes · cm2/s,
and cardiac index of 3.1 L · min-1
· m-2. Bilateral pulmonary
arteriograms demonstrated no thromboemboli but pruning of the distal
pulmonary vascular bed, with delayed transit of contrast
through the lungs.
On September 12, 1997, the patient was reevaluated with right heart
catheterization, which demonstrated a PA pressure of
99/46 mm Hg (mean, 64 mm Hg), PVR of 1152 dynes ·
cm2/s, and cardiac output of 3.5 L/min. Inhaled
nitric oxide decreased the PA pressure to 75/36 mm Hg (mean,
52 mm Hg) and the PVR to 600 dynes ·
cm2/s. Intravenous prostacyclin
(epoprostenol) afforded minimal improvement in her dyspnea. A
transesophageal echocardiogram was performed in
November 1997 and demonstrated high-velocity turbulence within the LA
at the junction of both superior PVs. Repeat right heart
catheterization was performed on December 15, 1997, and
demonstrated a PA pressure of 90/50 mm Hg (mean, 62 mm Hg),
LA pressure of 3 mm Hg, and cardiac index of 1.9 L ·
min-1 · m-2.
Selective wedge pulmonary arteriograms demonstrated severe
stenosis of the left superior and inferior PVs and
the right superior PV near their junction with the LA. The right lower
PV was occluded.
Transseptal catheterization and balloon dilation of the
PVs was performed on January 15, 1998. Direct cannulation of the right
superior, left superior, and left inferior PVs demonstrated
gradients to the LA of 21, 16, and 33 mm Hg, respectively.
Balloon dilation of the 2 superior PVs was performed with
12-mm-diameter balloons, and an 8-mm balloon was used to dilate the
left inferior PV (Figures 8 through 10
The mechanism of PV stenosis after radiofrequency ablation in
our patients probably involves scarring and contraction of the venous
wall as a result of thermal injury. In an analogous situation,
thrombosis or stenosis of the coronary sinus has been
observed after radiofrequency catheter ablation of accessory
pathways.6 7 Whereas stenosis or
occlusion of the coronary sinus is usually not associated with
clinical sequelae, stenosis of a PV may produce dyspnea on
exertion, orthopnea, cough, hemoptysis, and recurrent pulmonary
infections. If untreated, congenital PV stenosis is usually
fatal, with most patients succumbing to right heart failure.
The treatment of PV stenosis has included surgical excision of
the localized stenosis,8 reimplantation
of the PVs with direct anastomosis to the LA appendage or
LA,9 balloon angioplasty,10
or endovascular stenting.11 12 The use of balloon
angioplasty in congenital PV stenosis has been generally
unsatisfactory, with a high incidence of restenosis and
recurrent pulmonary hypertension.10
Although experience with stenting of the PVs in congenital
stenosis is limited, the results have also been generally
disappointing.11 12 Whether acquired PV
stenosis demonstrates a similar course after balloon dilatation
has not been determined, although PVs that are not congenitally
malformed may respond better to angioplasty and
stenting.13
The present report raises several concerns regarding catheter
ablation of chronic AF. First, the exact incidence of PV
stenosis after catheter ablation is unknown. However, it is
unlikely that pulmonary hypertension would develop unless a
substantial portion of the pulmonary venous drainage is
affected. If only a single PV becomes obstructed, the clinical
manifestations may be mild or unrecognized. Second, on the basis of the
location of the PV stenoses observed in these patients,
radiofrequency current probably should not be applied within a PV.
Rather, the ablation lesion should probably be confined to the LA or
end at the PV ostium. The consequences of not extending the ablation
line into the PV on the maintenance of AF are unknown, although
it is possible that reentrant LA arrhythmias may be promoted by
such an approach. Third, the development of dyspnea or cough after
catheter ablation in the region of the PVs should raise suspicion of PV
stenosis. Finally, this complication can be treated acutely
with balloon dilation of the PVs, although the long-term outcome is
uncertain.
Conclusions
Received February 5, 1998;
revision received July 1, 1998;
accepted July 1, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Pulmonary Vein Stenosis After Catheter Ablation of Atrial Fibrillation
Abstract
Top
Abstract
Introduction
Case Summaries
Discussion
References
Background—This report describes
the complication of pulmonary vein stenosis with
resultant severe pulmonary hypertension that developed in 2
patients after successful catheter ablation of chronic atrial
fibrillation.
Key Words: stenosis • catheter ablation • fibrillation
Introduction
Top
Abstract
Introduction
Case Summaries
Discussion
References
Although catheter ablation of atrial fibrillation (AF)
has been demonstrated to be feasible, the long-term complications and
efficacy of this technique are unknown.1 2 3 4 5
Successful interruption of chronic AF usually involves application of
radiofrequency current within the left atrium (LA), linking the
ostia of the pulmonary veins (PVs) to the mitral
annulus.1 This report describes the complication
of PV stenosis resulting in severe pulmonary
hypertension that developed in 2 patients after successful catheter
ablation of chronic AF. The clinical course and treatment of this
complication are reported.
Case Summaries
Top
Abstract
Introduction
Case Summaries
Discussion
References
Both patients in this report were included in a multicenter
feasibility trial of catheter ablation for the treatment of chronic AF.
Among 18 patients enrolled in the trial, 2 patients developed a similar
clinical course, characterized by progressive dyspnea and
pulmonary hypertension. None of the other patients have
experienced similar symptoms or developed increased pulmonary
artery (PA) pressures by repeated Doppler
echocardiography at 1 month, 3 months, and 6 months
after catheter ablation. The clinical courses of the 2 patients who
have developed pulmonary hypertension are detailed below.
A 53-year-old man with chronic AF refractory to antiarrhythmic
medications and repeated cardioversion was referred for enrollment in
an investigational protocol for catheter ablation of AF. The patient
had experienced intermittent AF for 12 years, which had become chronic
for the preceding 3 years (Figure 1
).
View larger version (89K):
[in a new window]
Figure 1. 12-lead ECG before ablation, demonstrating chronic
AF. ).
View larger version (113K):
[in a new window]
Figure 2. 12-lead ECG 8 months after catheter
ablation. 
). An
echocardiogram performed on July 21, 1997, demonstrated an estimated PA
systolic pressure of 65 mm Hg, and physical examination
demonstrated an accentuated pulmonic valve closure sound.
Pulmonary function tests were normal. The patient underwent
right heart catheterization on September 18, 1997, with
a PA pressure of 60/24 mm Hg (mean, 41 mm Hg), a
pulmonary capillary wedge pressure (PCWP) of 16 mm Hg,
cardiac output of 7.0 L/min, and a pulmonary vascular
resistance (PVR) of 287 dynes · cm2/s.
Bilateral pulmonary arteriograms showed no evidence of thrombus
but diffuse pruning of the small pulmonary arteries and a
delayed transit time through the lungs to the LA. The patient
experienced no improvement with intravenous prostacyclin
(epoprostenol) or oral amlodipine. Because of worsening dyspnea on
exertion and radiographic evidence of pulmonary
edema, the patient was reevaluated with transesophageal
echocardiography on December 12, 1997, which
demonstrated an estimated PA systolic pressure of 88
mm Hg and high-velocity turbulence (2.5 m/s) within the LA near the
ostia of both superior PVs, suggesting PV stenosis. 
10 mm from the ostium, with a mean pressure of
42 mm Hg and a simultaneously recorded LA
pressure of 17 mm Hg (Figure 3A).
Venous dilatation was performed with a 6-mm-diameter balloon at an
inflation pressure of 16 atm, which resulted in a decrease in the
gradient between the left superior PV and the LA to 5 mm Hg
(Figure 3B and Figure 4). The ostium of
the left superior PV was sequentially dilated with balloons having
diameters of 8 and 10 mm. Balloon dilation was performed to
relieve stenoses within all 4 PVs (Figures 5 through 7). At the
conclusion of the procedure, the PA pressure had decreased to
60/24 mm Hg, with an LA pressure of 15 mm Hg and a PVR of
557 dynes · cm2/s.
View larger version (141K):
[in a new window]
Figure 3. Top, Simultaneously recorded
pressure tracings from left upper PV (LUPV) and LA. Note that mean LA
pressure is 17 mm Hg, with mean LUPV pressure of 42 mm Hg.
Bottom, After balloon dilation, mean pressure in LA is 21 mm Hg,
with mean pressure in LUPV of 25 mm Hg.
View larger version (70K):
[in a new window]
Figure 4. Top, Contrast injection into left superior PV.
Note localized stenosis of vein with absence of flow into LA.
Middle, A 6-mm-diameter balloon is inflated within left upper PV.
Bottom, Contrast injection into left superior PV after balloon
inflation, demonstrating resolution of stenosis.
View larger version (70K):
[in a new window]
Figure 5. Top, Contrast injection into left
inferior PV. Note localized stenosis of PV. Middle,
A 10-mm-diameter balloon is inflated within ostium of vein. Bottom,
Contrast injection into left inferior PV after balloon
inflation, demonstrating mild focal stenosis.
View larger version (102K):
[in a new window]
Figure 6. Top, Contrast injection into right superior PV
with localized stenosis. Bottom, An 8-mm-diameter balloon is
inflated within ostium of PV.
View larger version (101K):
[in a new window]
Figure 7. Top, Contrast injection into right
inferior PV with localized stenosis. Bottom,
Contrast injection into right inferior PV after balloon
inflation, demonstrating resolution of stenosis.
The second patient is a 36-year-old woman with paroxysmal AF since
age 17 years that had been refractory to flecainide, propafenone,
disopyramide, sotalol, dofetilide, ß-blockers, calcium
blockers, and digoxin. Despite multiple electrical cardioversions, AF
became chronic and associated with marked fatigue, dyspnea, and
palpitations. Transthoracic and
transesophageal echocardiograms showed an estimated PA
systolic pressure of 28 mm Hg and a mildly dilated right
ventricle, with no evidence of intracardiac shunting. ). The
gradients between the PVs and the LA decreased to 3, 4, and 0
mm Hg, and the PA systolic pressure decreased to 55
mm Hg, with marked improvement in her symptoms.
View larger version (77K):
[in a new window]
Figure 8. Top, Contrast injection into right superior
PV in patient 2, with stenosis at junction of PV with LA.
Bottom, After balloon dilation with a 12-mm balloon, there is
resolution of stenosis.
View larger version (66K):
[in a new window]
Figure 9. Top, Balloon inflation in ostium of left superior
PV in patient 2. Note severe stenosis at junction of PV with
LA, as demonstrated by waist on 12-mm-diameter balloon. Bottom,
Contrast injection into left superior PV after balloon dilation, with
resolution of stenosis.
View larger version (79K):
[in a new window]
Figure 10. Top, Contrast injection into left
inferior PV in patient 2. Note severe stenosis of
PV 1 cm from its junction with LA. Bottom, Contrast injection into
left inferior PV after balloon dilation with an 8-mm
balloon, with resolution of stenosis.
Discussion
Top
Abstract
Introduction
Case Summaries
Discussion
References
Catheter ablation of AF is in its infancy. However, the early
experience with this procedure has shown that chronic AF can be
interrupted by the application of radiofrequency current within the LA
in most patients, although some patients require additional
applications in the right atrium.1 2 3 4 5 The
complications of this procedure as performed with standard catheters
have been substantial, including pericardial effusion, systemic emboli,
pulmonary dysfunction, and bleeding from the intense
anticoagulation that is required.1 2 3 4 5 This report
demonstrates that PV stenosis is an additional, potentially
severe complication of this procedure. During the present
multicenter trial of catheter ablation for chronic AF, PV
stenosis has been identified in 2 of 18 patients undergoing
this procedure.
This report demonstrates that PV stenosis may occur
after catheter ablation of AF, leading to severe pulmonary
hypertension. Future ablation strategies must prevent damage to the
PVs.
Acknowledgments
This study was supported in part by InControl Europe SA/NV,
Brussels, Belgium.
References
Top
Abstract
Introduction
Case Summaries
Discussion
References
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