Author + information
- Received September 4, 2018
- Revision received October 12, 2018
- Accepted October 24, 2018
- Published online May 6, 2019.
- Francesco Fracassi, MDa,
- Filippo Crea, MDb,
- Tomoyo Sugiyama, MD, PhDa,
- Erika Yamamoto, MD, PhDa,
- Shiro Uemura, MD, PhDc,
- Rocco Vergallo, MD, PhDb,
- Italo Porto, MD, PhDb,
- Hang Lee, PhDd,
- James Fujimoto, PhDe,
- Valentin Fuster, MD, PhDf and
- Ik-Kyung Jang, MD, PhDa,g,∗ (, )@MGHHeartHealth
- aCardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- bDepartment of Cardiovascular and Thoracic Sciences, Catholic University of the Sacred Heart, Fondazione Policlinico Universitario Agostino Gemelli-IRCCS, Rome, Italy
- cDepartment of Cardiology, Kawasaki Medical School, Kurashiki, Okayama, Japan
- dBiostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts
- eThe Research Laboratory of Electronics, Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts
- fZena and Michael A. Wiener Cardiovascular Institute, Icahn School of Medicine at Mount Sinai, New York, New York
- gDivision of Cardiology, Kyung Hee University Hospital, Seoul, South Korea
- ↵∗Address for correspondence:
Dr. Ik-Kyung Jang, Cardiology Division, Massachusetts General Hospital, 55 Fruit Street, GRB 800, Boston, Massachusetts 02114.
Background Healed plaques, morphologically characterized by a layered phenotype, are frequently found in subjects with sudden cardiac death. However, in vivo data are lacking.
Objectives The purpose of this study was to determine the prevalence, morphological characteristics, and clinical significance of healed culprit plaques in patients with acute coronary syndromes (ACS) using optical coherence tomography (OCT).
Methods A total of 376 ACS patients (252 ST-segment elevation myocardial infarction [MI] and 124 non–ST-segment elevation acute coronary syndrome) who had undergone pre-intervention OCT imaging of the culprit lesion were enrolled. Patients were stratified according to the presence of layered phenotype, defined as layers of different optical density at OCT. Clinical and laboratory data, OCT characteristics, and 1-year outcome were compared between the 2 groups.
Results Among 376 patients, 108 (28.7%) healed plaques were identified. Hyperlipidemia, diabetes, and history of MI were more frequent in patients with healed plaques (44.4% vs. 33.2%; p = 0.041; 35.2% vs. 23.5%; p = 0.021; and 15.7% vs. 6.3%; p = 0.009, respectively). High-sensitivity C-reactive protein was significantly higher in patients with healed plaques (median 4.98 mg/l [interquartile range: 1.00 to 11.32 mg/l] vs. 3.00 mg/l [interquartile range: 0.30 to 10.15 mg/l]; p = 0.029). Plaque rupture (64.8% vs. 53.0%; p = 0.039), thin cap fibroatheroma (56.5% vs. 42.5%; p = 0.016), and macrophage accumulation (81.1% vs. 63.4%; p = 0.001) were common in the layered group. OCT also revealed greater area stenosis in plaques with layered phenotype (79.2 ± 9.5% vs. 74.3 ± 14.3%; p = 0.001). The incidence of major adverse cardiovascular events was similar between the 2 groups, except that the all-cause rehospitalization rate was higher among healed plaques (32.7% vs. 16.5%; p = 0.013).
Conclusions Healed plaques, a signature of prior plaque destabilization, were found at the culprit site in more than one-quarter of ACS patients. Such patients more frequently were diabetic, were hyperlipidemic, or had a history of MI. Healed plaques frequently showed OCT features of vulnerability with evidence of local and systemic inflammation. The combination of plaque vulnerability, local inflammation, and greater plaque burden in addition to systemic inflammation may outweigh the protective mechanism of plaque healing and predispose those plaques to develop occlusive thrombus.
- coronary vulnerability
- healed plaques
- layered plaques
- optical coherence tomography
- subclinical thrombosis
Dr. Fujimoto has received royalties from intellectual property owned by MIT. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Khaled M. Ziada, MD, served as Guest Associate Editor for this paper.
Listen to this manuscript's audio summary by Editor-in-Chief Dr. Valentin Fuster on JACC.org.
- Received September 4, 2018.
- Revision received October 12, 2018.
- Accepted October 24, 2018.
- 2019 American College of Cardiology Foundation
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