Catheterization and Cardiovascular Interventions 85:611–614 (2015)

Case Reports Coronary Artery Compression Three Months After Transcatheter Pulmonary Valve Implantation Payam Dehghani,1* MD, FRCPC, FACC, FSCAI, Greg Kraushaar,2 MD, FRCPC, and Dylan A. Taylor,3 MD, FRCPC, FACC, CHE We report a case of a 29-year-old man who developed exercised-induced myocardial infarction 3 months post Melody valve implantation. We introduce the concept of ruling out dynamic coronary artery compression by simulating transcatheter pulmonary valve implant while increasing cardiac output and thus aortic dimensions in the catheterization laboratory. VC 2014 Wiley Periodicals, Inc. Key words: adult; congenital; interventions

INTRODUCTION

Transcatheter pulmonary valve (TPV) was developed for patients with stenotic and/or regurgitant right ventricular outflow (RVOT) conduits. Due to favorable outcomes in RVOT obstruction, conduit regurgitation, and hemodynamics after TPV implantation [1,2], it received US Food and Drug administration in 2010 as a palliative measure to delay surgical intervention. Coronary artery compression (CAC) during TPV implantation is a rare but known complication [3–9] with the potential for catastrophic consequences. We review risk factors of CAC and report our case of exercisetriggered delayed presentation of CAC three months post TPV implantation.

CASE

A 29-year-old man with double outlet right ventricle, transposition of the great arteries, ventricular septal defect, and pulmonary stenosis was treated with a Rastelli procedure as an infant. He underwent right ventricle (RV) to pulmonary artery (PA) conduit replacement in his teenage years and successfully underwent Melody (Medtronic, Minneapolis, MN) TPV implantation 3 months prior to presentation due to conduit stenosis with a gradient of 70 mm Hg in the presence of NYHA III symptoms. His cardiac MRI (CMR) prior to TPV showed the aorta was dilated to 4.7 cm at the sinuses of Valsalva (Fig. 1A). It did not suggest any C 2014 Wiley Periodicals, Inc. V

coronary anomalies and did not raise any concerns for CAC. Therefore, our patient did not undergo simulation testing with balloon inflation in the RVOT and simultaneous coronary artery angiography. A 20-mm covered stent was deployed in the RV to PA conduit followed by a 22-mm Melody valve. There were multiple post-dilations using a 22-mm high-pressure balloon due to presence of a gradient that eventually decreased to 15 mm Hg. Patient was discharged one-day post implant with an unchanged ECG, and was Additional Supporting Information may be found in the online version of this article. 1 Unit 3A, Interventional Cardiology Research Office, Prairie Vascular Research Network (PVRN), Regina General Hospital, Regina, Saskatchewan, S4P 0W5, Canada 2 Department of Radiology, Prairie Vascular Reseasrch Network, Regina General Hospital, Regina, Saskatchewan, S4P 0W5, Canada 3 University of Alberta, Edmonton, Alberta, Canada. Conflict of interest: Nothing to report. *Correspondence to: Payam Dehghani, Clinical Co-Director, Prairie Vascular Research Network (PVRN), Unit 3A, Interventional Cardiology Research Office, Regina General Hospital 1440 – 14th Ave., Regina, Saskatchewan, S4P 0W5 Canada. E-mail: [email protected] Received 4 March 2014; Revision accepted 10 August 2014 DOI: 10.1002/ccd.25628 Published online 12 August 2014 in Wiley Online Library (wileyonlinelibrary.com)

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Fig. 1. A: Cardiac MRI image showing dilated sinuses of Valsalva. B: Left anterior oblique aortogram showing proximity of dilated sinuses of aorta and RCA ostium (multiple arrow heads) to the melody valve (designated by *). C: Non-selective shot of the RCA with the arrowheads pointing to a linearity at the ostium suggestive of a dissection. D: Multi-planar reconstruction cardiac computed tomography image showing relationship of the right coronary artery and Melody valve (multiple arrow heads).

asymptomatic while on disability from work looking after his 11 month old infant. Three months after discharge, while running on a treadmill—first episode of exercise since the TPV implant—he developed palpitations, diaphoresis, and chest pain. He presented 24 hr later to the emergency department with hypotension, decreased perfusion, and wide complex tachycardia and was cardioverted to sinus rhythm. He had biomarker evidence of an acute coronary syndrome with CK rise of 542 U/L and Troponin I of 7.2 ug/L. His post cardioversion ECG showed right ventricular hypertrophy and Q waves inferiorly. Echocardiogram suggested mild left ventricular dysfunction. CMR confirmed hypokinetic inferior wall segments without evidence of scar on delayed enhancement (Fig. 1B). Aortography during

cardiac catheterization showed close proximity of the RCA to the recent Melody valve implant (Fig. 1B, Supporting Information Video 1) and non-selective RCA injection suggested ostial RCA dissection (Fig. 1C, Supporting Information Video 2). Angiography revealed retrograde flow from the left coronary artery collateralizing the RCA (Supporting Information Video 3). Although there was metal streak artifact from the stent and the melody valve on computed tomography angiography, the figures were highly suggestive of close proximity of the RCA to the Melody valve (Fig. 1D). Patient was discussed at our cardiothoracic rounds and a decision was made to explant the Melody valve, replace the RVOT conduit, and reimplant the RCA to the native aorta given the presence of viability on CMR.

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

LMCA 9 days Cardiac arrest 10

14

Divekar et al. [9]

Mauri et al. [8]

Biermann et al. [7]

CAC, coronary artery compression; CCTGA, congenitally corrected transposition of the great arteries; DORV, double outlet right ventricle; Hr, hours; LAD, left anterior descending; LM, left main; yrs, years; N/A, not available; PCI, percutaneous coronary intervention; TGA, Transposition of the Great Arteries; TPV, trans-pulmonary valve.

Alive and well

Alive and well

Emergency surgery, tear of homograft with thrombus causing CAC Bail-out PCI LAD 1 hr Acute coronary syndrome

Alive and well Emergency surgery, direct CAC LAD 4 days Acute coronary syndrome

performed, felt to be safe Performed, felt to be safe Not performed 26

Alive and well LMCA Immediate Cardiac arrest NA 9

Dextrocardia, CCTGA, DORV, pulmonary stenosis, VSD; mustard procedure TGA; arterial switch procedure, RV to PA conduit Bicuspid aortic valve/Ross procedure Tetralogy of Fallot/ Kostolny et al. [6]

Outcome Intervention/findings

Emergency surgery, direct CAC Emergency surgery, direct CAC LMCA 4 hr Cardiac arrest N/A N/A TGA; Rastelli procedure

Reference

Eicken et al. [3]

Affected coronary artery Time from TPV to presentation Patient presentation Balloon simulation testing Age (years) Congenital lesion and repair

TABLE I. Reported Cases of Coronary Arterial Compression After Transcatheter Pulmonary Valve Deployment

Death

Delayed Coronary Compression and Melody Valve

613

DISCUSSION

CAC is a rare, but well documented complication in TPV implants with potentially catastrophic implications. Table I summarizes reported CAC post TPV implants. In a contemporary series of more than 400 patients intended for TPV implantation, 5% of patients did not undergo valve placement because of a documented risk of CAC [5]. Documented risk factors for CA compression include (1) congenital coronary anomaly, (2) tetralogy of Fallot and transposition of the great arteries, (3) patients with re-implanted coronary ostia such as the Ross procedure, (4) abnormal relationship of the RVOT and CA, and (5) any of the combination of above factors. In those with congenital coronary anomalies, the subset with anomalous left coronary artery arising from the RCA in tetralogy of Fallot or transposition of the great arteries pose a great risk for CAC [5]. As exemplified in our case, even in case of “normal” arteries arising in any of these two lesions, the anterior aortic root displaces the origins of the coronary arteries relative to normal allowing the RVOT conduit to pass directly over a major coronary branch (the RCA in our case). Thirdly, patients with Ross procedure in which the coronary arteries are implanted into the autograft in a relatively high and/or anterior position are at risk for CAC [2]. Finally, a surgically implanted conduit that becomes distorted with time can impose external compression to a coronary artery even without TPV implantation [10]. Calcified RVOT and predisposition to Melody valve fracture have led to routine pre-stenting before TPV implants. This added cage-in-a-cage layer, however, may increase the risk of CAC. The need to post-dilate the valve with residual gradient as exhibited in our case has been known to lead to coronary compromise due to homograft laceration, thrombus formation, and CAC [8]. Pre-implantation simulation test with balloon inflation in the RVOT and simultaneous coronary artery angiography, a procedure that was not done in our case, is the best way to understand the relationship between the conduit and coronary arteries. Although in retrospect, this step should not have been omitted, detailed review of the CMRI prior to, and after, the procedure suggests that this would have likely been a negative test. There are reports of two cases with “negative” balloon simulation tests that have not accurately predicted CAC. Bierrmann likely misinterpreted LAD stenosis as spasm [7] and Mauri’s CAC was likely related to aggressive post-dilatation causing a rupture in the homograft [8]. While the mechanisms of acute CAC are related to stent expansion and or valve implantation, mechanisms of delayed CAC remain elusive.

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

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Possible etiologies include tissue edema which may take a few days to evolve [7,9], and/or thrombus formation from lacerations due to post dilatation [8]. Our case sheds light into another potential mechanism of CAC in patients who may have a negative simulation test and dilated sinuses of Valsalva. As both enlarged aorta and altered aortic distensibility can be seen at rest and exercise in this patient population [11], a study of the interplay between the dynamic nature of the sinus of Valsalva and its proximity to the RVOT would be helpful. That CAC did not occur until exercise three months later suggests that the increased cardiac output leading to increase in aortic size must have contributed to compression of the RCA ostium. Therefore, the ideal simulation test should not just focus on full expansion of the RVOT to look at proximity to the coronary vessels, but to also assess a dynamic relationship of aorta and RVOT as can occur during exercise. The implications of this case are threefold. Firstly, CMR screening cannot replace balloon simulation testing pre-TPV implantation. Secondly, CAC can occur months after valve implantation and therefore meticulous follow-up including a supervised exercise stress test should be considered after TPV. Thirdly, in patients with a negative resting balloon simulation test but with large sinuses of Valsalva, a simulation test should be performed while the aorta is maximally dilated. This can be achieved in the catheterization laboratory with pharmacologic agents that increase cardiac output such as dobutamine or isoproterenol. CONCLUSION

CAC can occur months after TPV implantation and is not a static phenomenon. Mandated simulation testing with balloon dilatation of the RVOT with simultaneous coronary injections only looks at the relationship between a fully expanded RVOT and the coronary tree. In selected patients, the simulation test should take place with a maximally dilated aorta, which can be simulated in the cardiac catheterization laboratory using pharmacologic agents.

ACKNOWLEDGMENTS

The authors would like to thank Dr. Rodney Zimmermann, Dr. Varun Chopra and Dr. Isabelle Vonder Muhll for their care for the patient, as well as preparing, and interpreting the figures. REFERENCES 1. Zahn EM, Hellenbrand WE, Lock JE, McElhinney DB. Implantation of the melody transcatheter pulmonary valve in patients with a dysfunctional right ventricular outflow tract conduit early results from the U.S. Clinical trial. J Am Coll Cardiol 2009;54: 1722–1729. 2. McElhinney DB, Hellenbrand WE, Zahn EM, et al. Short- and medium-term outcomes after transcatheter pulmonary valve placement in the expanded multicenter US melody valve trial. Circulation 2010;122:507–516. 3. Eicken A, Ewert P, Hager A, et al. Percutaneous pulmonary valve implantation: Two-centre experience with more than 100 patients. Eur Heart J 2011;32:1260–1265. 4. Sridharan S, Coats L, Khambadkone S, Taylor AM, Bonhoeffer P. Images in cardiovascular medicine. Transcatheter right ventricular outflow tract intervention: The risk to the coronary circulation. Circulation 2006;113:e934–e935. 5. Morray BH, McElhinney DB, Cheatham JP, et al. Risk of coronary artery compression among patients referred for transcatheter pulmonary valve implantation: A multicenter experience. Circ Cardiovasc Interv 2013;6:535–542. 6. Kostolny M, Tsang V, Nordmeyer J, et al. Rescue surgery following percutaneous pulmonary valve implantation. Eur J Cardio-Thorac Surg 2008;33:607–612. 7. Biermann D, Schonebeck J, Rebel M, Weil J, Dodge-Khatami A. Left coronary artery occlusion after percutaneous pulmonary valve implantation. Ann Thorac Surg 2012;94:e7–e9. 8. Mauri L, Frigiola A, Butera G. Emergency surgery for extrinsic coronary compression after percutaneous pulmonary valve implantation. Cardiol Young 2013;23:463–465. 9. Divekar AA, Lee JJ, Tymchak WJ, Rutledge JM. Percutaneous coronary intervention for extrinsic coronary compression after pulmonary valve replacement. Catheter Cardiovasc Interv 2006; 67:482–484. 10. Jacques F, Kotani Y, Deva DP, et al. Left main coronary artery compression long term after repair of conotruncal lesions: The bow string conduit. Ann Thorac Surg 2012;94:283–285. 11. Chen RH, Wong SJ, Wong WH, Cheung YF. Arterial mechanics at rest and during exercise in adolescents and young adults after arterial switch operation for complete transposition of the great arteries. Am J Cardiol 2014;113:713–718.

Catheterization and Cardiovascular Interventions DOI 10.1002/ccd. Published on behalf of The Society for Cardiovascular Angiography and Interventions (SCAI).

Coronary artery compression three months after transcatheter pulmonary valve implantation.

We report a case of a 29-year-old man who developed exercised-induced myocardial infarction 3 months post Melody valve implantation. We introduce the ...
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