Author + information
- Received September 9, 2014
- Revision received January 12, 2015
- Accepted January 15, 2015
- Published online May 1, 2015.
- Francesco Saia, MD, PhD∗∗ (, )
- Kenichi Komukai, MD†,
- Davide Capodanno, MD, PhD‡,
- Vasile Sirbu, MD†,
- Giuseppe Musumeci, MD†,
- Giacomo Boccuzzi, MD§,
- Giuseppe Tarantini, MD‖,
- Massimo Fineschi, MD¶,
- Gabriele Tumminello, MD#,
- Chiara Bernelli, MD†,
- Giampaolo Niccoli, MD∗∗,
- Micol Coccato, MD†,
- Barbara Bordoni, MD∗,
- Hiram Bezerra, MD, PhD††,
- Giuseppe Biondi-Zoccai, MD‡‡,
- Renu Virmani, MD§§,
- Giulio Guagliumi, MD†,
- OCTAVIA Investigators
- ∗Institute of Cardiology, University of Bologna, Policlinico S. Orsola-Malpighi, Bologna, Italy
- †Interventional Cardiology Unit, Azienda Ospedaliera Papa Giovanni XXIII, Bergamo, Italy
- ‡Ferrarotto Hospital, University of Catania, Catania, Italy
- §Cardiology Department, Ospedale San Giovanni Bosco, Torino, Italy
- ‖Department of Cardiac Thoracic and Vascular Sciences, University of Padua, Padua, Italy
- ¶Department of Cardiology, Policlinico Le Scotte, Siena, Italy
- #Cardiology Department, Ospedale Civile, Asti, Italy
- ∗∗Institute of Cardiology, Catholic University of the Sacred Heart, Roma, Italy
- ††Case Western Reserve University, Cleveland, Ohio
- ‡‡Department of Medico-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Latina, Italy
- §§CV Path Institute, Gaithersburg, Maryland
- ↵∗Reprint requests and correspondence:
Dr. Francesco Saia, Institute of Cardiology, University of Bologna, Policlinico S. Orsola-Malpighi (Pad 21), Via Massarenti 9, 40138 Bologna, Italy.
Objectives The aim of this study was to evaluate the pathophysiological features and response to primary percutaneous coronary intervention (PCI) of nonruptured/eroded plaque versus ruptured plaque as a cause of ST-segment elevation myocardial infarction (STEMI).
Background Autopsy series identified nonruptured/eroded plaque and ruptured plaque as the principal pathological substrates underlying coronary thrombosis in STEMI. The real incidence of different plaque morphologies, associated biological factors, superimposed thrombus, and their interaction with primary PCI remain largely unknown.
Methods In a prospective study, 140 patients with STEMI underwent optical coherence tomography of the infarct-related artery (IRA) before PCI, after everolimus-eluting stent implantation and at 9-month follow-up. Histopathology and immunohistochemistry of thrombus aspirates and serum biomarkers were assessed at baseline.
Results Culprit plaque morphology was adjudicated in 97 patients: 32 plaques (33.0%) with an intact fibrous cap (IFC), 63 (64.9%) plaques with a ruptured fibrous cap (RFC), and 2 (2.1%) spontaneous dissections. Patients with an IFC and RFC had similar clinical characteristics, and serum inflammatory and platelets biomarkers. An IFC presented more frequently with a patent IRA (56.2% vs. 34.9%; p = 0.047), and had fewer lipid areas (lipid-rich areas: 75.0% vs. 100.0%; p < 0.001) and less residual thrombus before stenting (white thrombus: 0.41 mm3 vs. 1.52 mm3; p = 0.001; red thrombus: 0 mm3 vs. 0.29 mm3; p = 0.001) with a lower peak of creatine kinase-myocardial band (66.6 IU/l vs. 149.8 IU/l; p = 0.025). At the 9-month optical coherence tomography, IFC and RFC had similar high rates of stent strut coverage (92.5% vs. 91.2%; p = 0.15) and similar percentage of volume obstruction (12.6% vs. 10.2%; p = 0.27). No significant differences in clinical outcomes were observed up to 2 years.
Conclusions In the present study, an IFC was observed at the culprit lesion site of one-third of STEMIs. IFC, compared with RFC, was associated with higher rates of patent IRA at first angiography, fewer lipid areas, and residual endoluminal thrombus. However, no difference in vascular response to everolimus-eluting stent was observed. (Optical Coherence Tomography Assessment of Gender Diversity in Primary Angioplasty [OCTAVIA]; NCT01377207)
- culprit plaque
- optical coherence tomography
- percutaneous coronary intervention
- plaque erosion
- ST-segment elevation myocardial infarction
Dr. Saia has received consulting fees from Abbott Vascular, Eli Lilly, AstraZeneca, and St. Jude Medical; and speaker fees from Abbott Vascular, Eli Lilly, AstraZeneca, St. Jude Medical, Terumo, Biosensors, Edwards Lifesciences, and Boston Scientific. Dr. Capodanno has received speaker honoraria from and has been a consultant for Eli Lilly, The Medicines Company, and AstraZeneca. Dr. Vasile has received a research grant from St. Jude Medical. Dr. Sirbu has received grant support from St. Jude Medical. Dr. Musumeci has received speaker fees from St. Jude Medical, AstraZeneca, The Medicines Company, and Lilly-Daichii; and consulting fees from Lilly-Daichii, AstraZeneca, and the Medicines Company. Dr. Bezerra has received grant support and honoraria from St. Jude Medical and Abbott Vascular. Dr. Biondi Zoccai has received lecture fees from Bayer, Abbott Vascular, St. Jude Medical, Boston Scientific, Medtronic, Volcano, and Terumo; and has been a consultant for DirectFlow and Novartis. Dr. Virmani has received grant support from Abbott Vascular, Arsenal Medical, Atrium Medical Corporation, Biosensors International, GlaxoSmithKline, Lutonix, Medtronic AVE, Terumo, and W.L. Gore. Dr. Guagliumi has been a consultant for Boston Scientific and St. Jude Medical; and has received research grants from St. Jude Medical, Boston Scientific, and Abbott Vascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received September 9, 2014.
- Revision received January 12, 2015.
- Accepted January 15, 2015.
- 2015 American College of Cardiology Foundation