Author + information
- Received December 21, 2015
- Accepted January 6, 2016
- Published online April 25, 2016.
- Andreas A. Giannopoulos, MDa,
- Antonios P. Antoniadis, MD, PhDb,
- Kevin Croce, MDa and
- Yiannis S. Chatzizisis, MD, PhDc,∗ ()
- aCardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
- bCardiovascular Department, Guy’s and St Thomas’ NHS Foundation Trust, London, United Kingdom
- cCardiovascular Division, University of Nebraska Medical Center, Omaha, Nebraska
- ↵∗Reprint requests and correspondence:
Prof. Yiannis S. Chatzizisis, Cardiovascular Division, University of Nebraska Medical Center, 982265 Nebraska Medical Center, Omaha, Nebraska 68198.
A 52-year-old man was admitted with an anterior ST-segment elevation myocardial infarction for primary percutaneous coronary intervention (Figure 1A). The diagnostic coronary angiogram showed a hazy filling defect in the midsegment of the left anterior descending artery. Optical coherence tomography (OCT) showed a significantly stenotic thin-cap fibroatheroma (TCFA) associated with erosion of the fibrous cap (no sign of rupture) and thrombus formation downstream of the plaque (asterisk in Figure 1A). Blood flow across the lesion was simulated using 3-dimensional OCT and computational fluid dynamics. Pre-erosion flow simulation revealed an area of low endothelial shear stress (ESS) at the upstream plaque shoulder (Figure 1B, section I), high ESS at the neck of the plaque (Figure 1B, section II), and low ESS and blood velocity at the downstream shoulder (Figures 1B, section III and Figure 1C), colocalizing with the site of erosion and thrombus. The lesion was treated with an everolimus-eluting stent (Promus Premier 3.0 × 16 mm, Boston Scientific, Marlborough, Massachusetts) and was further evaluated with OCT (Figure 1D). Post-stenting blood flow simulation demonstrated normal ESS and blood flow patterns across the plaque (Figure 1E, sections I, II, III and Figure 1F). The patient was discharged on double antiplatelet therapy (aspirin and ticagrelor), statin, angiotensin converting enzyme inhibitor, and beta-blocker.
Erosion commonly occurs over thick-capped fibroatheromas, yet in our case the underlying plaque was a TCFA (1). This case shows evidently a stenotic TCFA, eroded at the downstream plaque shoulder, an area exposed to low ESS, which in turn may lead to endothelial cell apoptosis, the suggested pathobiological mechanism of erosion (2–4). Although management of eroded plaques is not well elucidated, local and systemic therapies are of value. Local therapies with drug-eluting stents aim to alleviate the stenotic burden and normalize the hemodynamic milieu across the plaque, thus minimizing the proinflammatory, prothrombotic, and proapoptotic effects of low ESS. Systemic therapies, primarily with statins, stabilize the highly inflamed coronary artery microenvironment, exerting a beneficial effect in the long term.
Funding was provided by Behrakis Foundation, Boston, Massachusetts. Dr. Croce is on the Speakers’ Bureau of St. Jude Medical. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received December 21, 2015.
- Accepted January 6, 2016.
- American College of Cardiology Foundation
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