Download Coronary compression caused by stenting a right pulmonary artery

Catheterization and Cardiovascular Interventions 74:144–147 (2009)
Coronary Compression Caused by Stenting
a Right Pulmonary Artery Conduit
Marc Gewillig,1* PhD and Stephen Brown,2
MD
Extrinsic compression of the left main coronary artery is a rare and life-threatening
complication of endovascular stenting of pulmonary artery conduits. This case report
describes fatal myocardial infarction caused by compression of the left main coronary
artery due to stent placement in a stenosed right pulmonary artery conduit. ' 2009
Wiley-Liss, Inc.
Key words: external coronary compression; complication; pulmonary artery stent
INTRODUCTION
Large numbers of pulmonary homografts are being
implanted for congenital cardiac malformations. These
conduits may become restrictive due to peal formation,
shrinkage, external compression, or somatic growth.
Endovascular stenting of pulmonary artery conduits
has been shown to be effective and safe [1,2]. Percutaneous pulmonary valve implantation will further
increase the number of conduits being stented [3].
Compression of a coronary artery has been reported as
a rare and potential life-threatening complication of
stents in the main pulmonary artery [4,5]. This case
report describes fatal myocardial infarction due to extrinsic compression of the left main coronary artery
because of stent implantation in a stenosed right pulmonary artery conduit. Insights gained into mechanisms of conduit dilation and stent expansion are discussed.
expanded; the stent opened predominantly in an inferior-anterior direction (Fig. 1B). There was no residual
gradient left and postimplantation angiography showed
a good result.
However, immediately after stent expansion, the
baseline right bundle branch block became wider with
some regression after a couple of minutes. The left
ventricle was clearly hypocontractile and dysfunctional.
Selective coronary angiography was attempted: the
right coronary artery was normal but the left coronary
artery could not be identified. Aortic root angiography
was also performed which showed no sign of a left
coronary artery. It was believed that acute occlusion of
the left coronary artery would have caused immediate
hemodynamic disaster and therefore, due to the fact
that she was hemodynamically stable, it was believed
that it was probably a chronic long-standing problem.
The electrocadiogram still had a wider right bundle
branch pattern and mild ST-segment elevation, but the
patient remained remarkably stable.
CASE REPORT
A 11-year old, 50 kg, female with tetralogy of Fallot-pulmonary atresia, presented with increasing exercise intolerance. She had multiple previous procedures
involving two thoracotomies for shunts, two sternotomies for repair and later extensive reconstruction of
the right ventricular outflow tract with sequential
homografts extending into the lung hilae (necessitating
transsection of the ascending aorta), as well as a total
of five percutaneous interventions with balloon angioplasty of the pulmonary arteries. Upon reassessment,
angiography showed a marked stenosis of the distal
right pulmonary artery (Fig. 1A). A Genesis PG 2910
stent (Johnson & Johnson Interventional Systems, Warren, NJ) on an 18-mm BIB balloon (NuMED, Hopkinton, NY) was passed through a long 11 French Mullins
sheath over the stenotic area and successfully
' 2009 Wiley-Liss, Inc.
1
Department of Pediatric Cardiology, University Hospital Gasthuisberg, Leuven, Belgium
2
Department of Pediatric Cardiology, University of the Free
State, Bloemfontein, South Africa
Grant sponsor: Rotary Tienen, Belgium
Conflict of interest: Nothing to report.
*Correspondence to: Marc Gewillig, MD, PhD, University Hospital
Gasthuisberg, Herestraat 49, B 3000 Leuven, Belgium.
E-mail: [email protected]
Received 6 November 2008; Revision accepted 22 November 2008
DOI 10.1002/ccd.21928
Published online 29 April 2009 in Wiley InterScience (www.
interscience.wiley.com).
Coronary Compression by Stent
145
Fig. 1. A–C. Pulmonary angiogram before (A) and after (B) stent implantation; asymmetrical
inferior expansion of the stent is observed. C: selective coronary angiogram after 3 hr shows
a critical stenosis of the left main coronary artery caused by the pulmonary stent.
She was subsequently uneventfully extubated. On
specific questioning, she did not complain of chest
pain and remained clinically well. Old echocardiograms and angiograms were urgently reviewed and by
way of exclusion, we concluded that the pulmonary artery stent was most likely responsible for obstruction
of the left coronary artery. She was immediately taken
back to the catheterization laboratory; now minimal
anterograde flow in the main left coronay artery was
present. A selective angiogram showed proximal critical obstruction with marginal flow in the left main coronary artery due to external compression by the stent
in the right pulmonary artery (Fig. 1C). The coronary
artery was stented with a 3 3 10 mm Tsunami Gold
stent (Terumo, Tokyo, Japan) which resulted in immediate relief of the obstruction. The patient was again
extubated and remained in a clinically stable condition.
However, 36 hr later she developed an atrioventricular
block and cardiogenic shock in the ward. After successful resuscitation, she was admitted to the intensive
care unit where she was intubated and ventilated, a
temporary pacemaker and intra-aortic counterpulsation
balloon pump inserted. Transesophageal echo confirmed patency of the coronary stent. Heart enzymes
and lactate were markedly elevated (creatine kinase >
600,000 U/l, lactate 12 mmol/l) and the diagnosis of a
hemorrhagic myocardial infarction was made. Because
of severe cardiac failure, a MEDOS ventricular assist
device (Medos Medizintechnik AG, Stolberg, Germany) was implanted. The patient’s condition gradually worsened and she was presented for urgent cardiac
transplant. However, she developed overwhelming septicemia with multiorgan failure and succumbed 38
days after the initial procedure.
Postmortem showed the stent in situ as well as a
healed endothelialized longitudinal tear in the lower
inner curvature of the right pulmonary artery homo-
Fig. 2. Lateral view of heart. Open arrow in right pulmonary
artery pointing at the longitudinal tear; closed arrow pointing
at probe in left main coronary artery. Ao, Aorta; LA, left
atrium.
graft (Fig. 2). The stem of the main left coronary artery passed directly underneath this tear and was adherent to the fibrotic tissue surrounding the homograft.
The left main also originated from a pure posterior
position from a dilated aortic sinus. The left ventricle
had massive infarction with necrosis.
DISCUSSION
Cases with disastrous outcomes are hardly ever
seen in published literature. As a matter of fact, we
experienced a certain degree of reluctance from colleagues to share similar experiences when we wanted
to write it up as a series, most likely due to emotional
and/or medico-legal reasons. However, the lessons
learned and insights offered by this dreadful case must
outweigh the negative connotations.
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
146
Gewillig and Brown
Fig. 3. Schematic representation of normal (A) relationship of ascending aorta and right pulmonary artery; (B) represents a shrunken homograft in right pulmonary artery. The stent
deployed in (C) expands eccentrically towards the left main coronary artery. Ao, aorta; LCA,
left coronary artery; RPA, right pulmonary artery; S, stent.
Increasing numbers of homografts are being
implanted and from experience we know they are
prone to calcification, shrinkage, external compression,
and intimal proliferation resulting in stenosis as time
progresses. Homograft conduits can be balloon-dilated
or stented, but insight into mechanisms of conduit dilation and stent expansion are required to avoid complications.
During balloon angioplasty, native vessels dilate
more or less uniformly in a radial direction and the
expansion forces are distributed equally all around the
circumference. The surrounding tissues simply ‘‘shift’’
out of the way or are compressed over a wide surface
area with an attenuated effect over short distances. In
contrast, a conduit frequently is a rigid tube and the
only way it can expand is by fracturing. This is usually well tolerated without extravasation due to the surrounding fibrotic scar tissue. The cylindrical tube most
likely first ruptures along one tear and all further
expansion may occur in this area, explaining the
eccentric opening of the stenosis. The surrounding stiff
fibrotic tissues results in full transmission of the compression force over a significant distance. In this case,
the homograft had a lower-inner longitudinal tear as
demonstrated by autopsy. When the stent was inflated,
the only direction of expansion was infero-anteriorly
through this ‘‘area of weakness’’ (Fig. 3). The combination of the eccentric expansion of the stent and the
unusual position of the left main coronary artery due
to a dilated aortic sinus together with the pure posterior origin of the left coronary artery, made the left
main coronary artery vulnerable for compression.
The implications therefore are that before stenting is
performed, careful thought should be given to the spatial relationships with the adjacent structures to prevent
extrinsic compression of any of these structures (cardiac or noncardiac). A good practice is to preballoon
the lesion. Low pressure ballooning delineates the
waist to accurately and safely position a stent [6].
High pressure ballooning in combination with coronary
or other angiography allows assessment of the possible
effects of stent expansion to threatened structures
[5,7]. This is currently routinely carried out before implantation of percutaneous pulmonary valves.
Coronary artery anomalies in tetralogy are well
documented [8,9]. One should always be aware that a
coronary artery may originate from purely posterior to
lateral, and that any stenting of the area ranging from
the main pulmonary trunk distal to where the right pulmonary artery crosses the ascending aorta, may compress a coronary artery [10,11].
The fact that the patient did not complain of chest
pain is also noteworthy. Because of its absence, we
felt more secure that the left ventricular dysfunction
was not due to acute coronary compression. The fact
that the patient had an aortic transsection is thus very
important because this led to cardiac denervation,
which explains the absence of chest pain in the presence of severe myocardial ischemia. The fact that she
did not instantaneously present with dysrrhythmias and
cardiogenic shock, also shows that even critical
obstruction of the left main coronary artery may be
temporarily tolerated. A lesson to be learned is that
one must be careful of not concluding what one wishes
to believe when confronted with an unusual complication. Although the patient was taken back to the catheterization laboratory within 3 hr for successful left coronary artery stenting, this procedure unfortunately did
not prevent the development of severe late hemorrhagic infarction. Case reports of immediate stenting of
obstructions of the left main coronary artery following
pulmonary artery stenting or compressing the stent by
external massage have shown more favorable outcomes
[12–14]. Urgent surgical revascularization is frequently
problematic because of the fact that in this patient
population multiple sternotomies with multiple adhesions impede fast coronary reperfusion.
In conclusion, dilation of stiff pulmonary conduits
may be achieved by causing tearing of the circular
tube. After extensive surgical dissections and multiple
Catheterization and Cardiovascular Interventions DOI 10.1002/ccd.
Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).
Coronary Compression by Stent
dilations, all expansion can be expected to occur in
one direction only, which may cause obstruction of
any adjacent or distant structure. The left coronary artery may originate from unusual positions, and therefore stenting of the pulmonary trunk or right pulmonary artery may cause compression of it.
6.
7.
ACKNOWLEDGMENTS
The authors acknowledge the assistance of Dr.
Derize Boshoff in the preparation of the manuscript.
This work was performed in part during sabbatical
leave of Dr. S. Brown granted by the University of the
Free State and Free State Department of Health,
Bloemfontein, South Africa.
8.
9.
10.
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