Author + information
- Received November 17, 2015
- Accepted November 19, 2015
- Published online March 28, 2016.
- Alessandra Giavarini, MDa,
- Giovanni Longo, MDa,∗ (, )
- Jian Chen, MDa,
- Rubén Rodríguez, MDa and
- Carlo Di Mario, MD, PhDa,b
- aNational Institute for Health Research, Cardiovascular BRU Royal Brompton & Harefield NHS Foundation Trust, London, United Kingdom
- bNational Heart & Lung Institute Imperial College, London, United Kingdom
- ↵∗Reprint requests and correspondence:
Dr. Giovanni Longo, National Institute for Health Research Cardiovascular BRU, Royal Brompton Hospital, Sydney Street, London SW3 6NP, United Kingdom.
A 59-year-old man symptomatic for effort angina, despite the maximal tolerated dose of beta-blockers and calcium-channel-blockers, presented clear evidence of inducible ischemia at the myocardial perfusion scan. Multislice computed tomography coronary angiogram showed a 60% long stenosis within a myocardial bridge (MB) in the mid-left anterior descending (LAD) coronary artery. Selective coronary angiography in February 2013 showed a tubular, 60% to 70% stenosis in the mid-LAD, with systolic worsening but persistent in diastole (Figures 1A and 1B) and confirmed by optical coherence tomography (OCT) (Figure 1b). Metallic stents often fail in muscle bridges because of fracture, and implanting a permanent foreign body in a young patient is not appealing (1,2). Therefore, we implanted a 3.0-/28-mm bioresorbable vascular scaffold (BVS) and post-dilated with a noncompliant 3.0-mm balloon at 20 atm with optimal expansion documented by angiography and OCT (Figures 1C and 1a′ to 1d′). The patient had an initial complete disappearance of his angina symptoms, followed by a progressive recurrence starting 12 to 18 months post-implant. Repeat coronary angiography 33 months after the initial treatment showed 70% to 80% mid-LAD stenosis (Figure 1D) corresponding, at OCT, to severe in-scaffold restenosis (Figures 1c′′ to 1g′′). The patient was successfully treated with a 3.0-/15-mm (proximal) and a 2.5-/34-mm (distal) zotarolimus-eluting stent (Figure 1E).
The symptomatic response to stenting MBs is unpredictable, and a “temporary” scaffold that disappears over time may allow assessment of the clinical response without committing the patient to the limits of a permanent implant prone to mechanical failure (1–3). Unfortunately, the phasic extrinsic compression of MBs appears to crush the scaffold once its mechanical integrity is lost during degradation (Figures 1b′′, 1d′′, 1f′′, and 1g′′).
Dr. Di Mario has received a research grant to his institution and speaker’s fees from Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received November 17, 2015.
- Accepted November 19, 2015.
- American College of Cardiology Foundation