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What are the coronary atherosclerotic phenotype and prevalence of healed plaques in patients at the extremes of the coronary artery disease spectrum?
In this cohort study of 105 patients undergoing preintervention optical coherence tomography imaging, patients with recurrent acute coronary syndromes and those with single myocardial infarction followed by long-term stability showed a similar prevalence of thin-cap fibroatheroma, which was significantly lower in patients with long-standing stable angina. Healed coronary plaques were rarely observed in patients with multiple recurrent acute coronary syndromes, while their prevalence was significantly higher in patients with long-term clinical stability.
Both atherosclerotic profile and plaque healing may play a role in leading the natural history of patients with coronary artery disease toward either recurrence of acute events or long-term stability.
At one end of the coronary artery disease (CAD) spectrum, there are patients with multiple recurrent acute coronary syndromes (rACS), and at the other end there are those with long-standing clinical stability. Predicting the natural history of these patients is challenging because unstable plaques often heal without resulting in ACS.
To assess in vivo the coronary atherosclerotic phenotype as well as the prevalence and characteristics of healed coronary plaques by optical coherence tomography (OCT) imaging in patients at the extremes of the CAD spectrum.
Design, Setting, and Participants
This is an observational, single-center cohort study with prospective clinical follow-up. From a total of 823 consecutive patients enrolled in OCT Registry of the Fondazione Policlinico A. Gemelli–IRCCS, Rome, Italy, from March 2009 to February 2016, 105 patients were included in the following groups: (1) patients with rACS, defined as history of at least 3 acute myocardial infarctions (AMIs) or at least 4 ACS with at least 1 AMI; (2) patients with long-standing stable angina pectoris (ls-SAP), defined as a minimum 3-year history of stable angina; and (3) patients with a single unheralded AMI followed by a minimum 3-year period of clinical stability (sAMI). Data were analyzed from January to August 2018.
Intracoronary OCT imaging of nonculprit coronary segments.
Main Outcomes and Measures
Coronary plaque features and the prevalence of healed coronary plaques in nonculprit segments as assessed by intracoronary OCT imaging.
Of 105 patients, 85 were men (81.0%); the median (interquartile range) age was 68 (63-75) years. Median (interquartile range) time of clinical stability was 9 (5.0-15.0) years in the ls-SAP group and 8 (4.5-14.5) years in the sAMI group. Patients in the rACS and sAMI groups showed similar prevalence of lipid-rich plaque and thin-cap fibroatheroma, which was significantly higher than in those with ls-SAP (lipid-rich plaque 80.0% [n = 24 of 30] vs 76.3% [n = 29 of 38] vs 37.8% [n = 14 of 37], respectively; P < .001; thin-cap fibroatheroma 40.0% [n = 12 of 30] vs 34.2% [n = 13 of 38] vs 8.1% [n = 3 of 37], respectively; P = .006). Spotty calcifications were more frequently observed in patients with rACS than in those with ls-SAP and sAMI (70.0% [n = 21 of 30] vs 40.5% [n = 15 of 37] vs 44.7% [n = 17 of 38], respectively; P = .04). Healed coronary plaques were rarely observed in patients with rACS, whereas their prevalence was significantly higher in patients with ls-SAP and sAMI (3.3% [n = 1 of 30] vs 29.7% [n = 11 of 37] vs 28.9% [n = 11 of 38], respectively; P = .01).
Conclusions and Relevance
Patients with rACS have a distinct atherosclerotic phenotype compared with those with ls-SAP, including higher prevalence of thin-cap fibroatheroma and lower prevalence of healed coronary plaques, suggesting that atherosclerotic profile and plaque healing may play a role in leading the natural history of patients with CAD.
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Accepted for Publication: February 8, 2018.
Corresponding Author: Filippo Crea, MD, FESC, Department of Cardiovascular and Thoracic Sciences, Catholic University of the Sacred Heart, Largo Agostino Gemelli, 8 – 00168 Rome, Italy (email@example.com).
Published Online: March 13, 2019. doi:10.1001/jamacardio.2019.0275
Author Contributions: Drs Vergallo and Crea had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Drs Porto and Crea contributed equally as co–senior authors.
Study concept and design: Vergallo, Porto, D’Amario, Fracassi, Niccoli, Liuzzo, Fuster, Crea.
Acquisition, analysis, or interpretation of data: Vergallo, Porto, Annibali, Galli, Benenati, Bendandi, Migliaro, Aurigemma, Leone, Buffon, Burzotta, Trani, Niccoli, Prati, Jang, Crea.
Drafting of the manuscript: Vergallo, Annibali, Benenati, Migliaro, Niccoli.
Critical revision of the manuscript for important intellectual content: Porto, D’Amario, Annibali, Galli, Bendandi, Fracassi, Aurigemma, Leone, Buffon, Burzotta, Trani, Liuzzo, Prati, Fuster, Jang, Crea.
Statistical analysis: Vergallo, Fracassi.
Administrative, technical, or material support: Porto, Annibali, Benenati, Migliaro, Leone, Jang.
Study supervision: Porto, D’Amario, Annibali, Galli, Fracassi, Buffon, Trani, Niccoli, Liuzzo, Prati, Jang, Crea.
Conflict of Interest Disclosures: Dr Porto has received grants and speaker fees from AstraZeneca; personal fees from Daiichi Sankyo, Terumo Corporation, and Abbott/St Jude; and personal fees and nonfinancial support from Abiomed. Dr Aurigemma has received speaker fees from Abbott Laboratories and Abiomed. Dr Burzotta has received speaker fees from Abbott Laboratories, Abiomed, and Medtronic. Dr Trani has received grants and personal fees from Abbott/St Jude as well as personal fees from Abiomed, Biotronik, Boston Scientific, Medtronic, and Terumo Corporation. No other disclosures were reported.
Additional Contributions: We thank all the members of the Coronary Care Unit and the Catheterization Laboratory team at the Fondazione Policlinico A. Gemelli–IRCCS, Rome, Italy, for their invaluable help, support, and patience.
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