Author + information
- Received September 13, 2018
- Revision received October 8, 2018
- Accepted October 16, 2018
- Published online February 4, 2019.
- aHeart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio
- bDepartment of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio
- ↵∗Address for correspondence:
Dr. Bryan H. Goldstein, University of Cincinnati College of Medicine, The Heart Institute, Cincinnati Children's Hospital Medical Center and Department of Pediatrics, 3333 Burnet Avenue, MLC 2003, Cincinnati, Ohio 45229.
- anomalous coronary artery origin
- coronary compression
- right ventricular outflow intervention
- transcatheter intervention
- transcatheter pulmonary valve replacement
A 13-year-old girl with repaired truncus arteriosus and single right coronary artery presented with progressive exertional dyspnea for 1 year. She underwent initial cardiac repair at 6 weeks of age, followed by 2 subsequent right ventricle to pulmonary artery (RV-PA) conduit replacement surgeries, most recently at 7 years of age with a 20-mm aortic homograft. Noninvasive cardiac testing—including echocardiography and cardiac magnetic resonance imaging—demonstrated normal RV size and function with severe conduit stenosis (peak gradient ∼85 mm Hg) and moderate regurgitation. Truncal valve function was normal. The anomalous left anterior descending (LAD) coronary coursed between the aorta and RV-PA conduit (Figure 1, Online Video 1). Exercise stress testing demonstrated a maximal VO2 of 5% of predicted. She was referred for transcatheter pulmonary valve replacement.
In the catheterization laboratory, the RV-PA conduit was serially dilated, first to 12 mm and subsequently to 14 mm and 16 mm using Atlas Gold (Bard, Tempe, Arizona) balloons. Aortography was serially performed simultaneously with conduit balloon angioplasty, to evaluate for coronary artery compression, given the high-risk coronary anatomy. Coronary compression was not observed with the 12-mm or 14-mm balloons (Figures 2A and 2B, Online Video 2). However, the LAD was completely compressed during conduit angioplasty with the 16-mm balloon (Figures 3A and 3B, Online Video 3). Partial compression of the LAD persisted immediately after balloon deflation during the same cineangiogram (Figure 4A, Online Video 4), which was unusual, and prompted follow-up angiography. Selective coronary angiography confirmed persistent compression. Delivery of intracoronary nitroglycerin resulted in minimal improvement (Figure 4B). One hour after initial identification of coronary compression, long-segment LAD compression persisted (Figure 4C, Online Video 5). The patient remained stable with no hemodynamic or ischemic changes evident.
The case was discussed with a multidisciplinary team; we opted to observe the patient overnight and proceed with elective surgical conduit replacement the following day. At surgery, a longitudinal fracture of the calcified posterior conduit wall was found, along with contained local hematoma, which resulted in extrinsic compression of the interarterial LAD. The hematoma was evacuated and the conduit replaced, with post-operative computed tomography revealing an unobstructed LAD (Figure 5).
Coronary compression is a known risk during transcatheter RV-PA conduit interventions (1–3). Before conduit stent implant and transcatheter pulmonary valve replacement, balloon angioplasty is generally used to simulate a conduit stent, thereby facilitating identification of at-risk patients and avoiding permanent coronary artery compression with resultant sequelae. To our knowledge, this is the first reported case of persistent coronary compression after balloon compression testing alone. The mechanism, a contained tear of the calcified conduit with local hematoma formation, highlights the potential for irreversible anatomic changes including persistent coronary compression following angioplasty alone. Importantly, in this case, coronary angiography was performed following compression testing to evaluate for normalization of the compressed LAD. Failure to do so could lead to catastrophe, in the setting of persistent but unrecognized coronary compression after balloon deflation. This experience may suggest that in select transcatheter pulmonary valve replacement candidates with high-risk coronary anatomy, in whom the pre-test probability of coronary compression is very high, proceeding directly to surgical conduit replacement may be reasonable.
Dr. Goldstein has consulting relationships with Medtronic and Edwards Lifesciences. Dr. Batlivala has reported that he has no relationships relevant to the contents of this paper to disclose.
- Received September 13, 2018.
- Revision received October 8, 2018.
- Accepted October 16, 2018.
- 2019 American College of Cardiology Foundation
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