Author + information
- Received January 28, 2013
- Revision received March 29, 2013
- Accepted April 29, 2013
- Published online August 1, 2013.
- Tomotaka Dohi, MD, PhD∗,†,
- Gary S. Mintz, MD†,
- John A. McPherson, MD‡,
- Bernard de Bruyne, MD, PhD§,
- Naim Z. Farhat, MD⋮,
- Alexandra J. Lansky, MD¶,
- Roxana Mehran, MD†,#,
- Giora Weisz, MD∗,†,
- Ke Xu, PhD†,
- Gregg W. Stone, MD∗,† and
- Akiko Maehara, MD∗,†∗ ()
- ∗Columbia University Medical Center, New York, New York
- †Cardiovascular Research Foundation, New York, New York
- ‡Vanderbilt University Medical Center, Nashville, Tennessee
- §Cardiovascular Center Aalst, OLV Hospital, Aalst, Belgium
- ⋮North Ohio Heart Center/Elyria Memorial Hospital Regional Medical Center, Elyria, Ohio
- ¶Yale University School of Medicine, New Haven, Connecticut
- #Mount Sinai Medical Center, New York, New York
- ↵∗Reprint requests and correspondence:
Dr. Akiko Maehara, Cardiovascular Research Foundation, 111 East 59th Street, 12th Floor, New York, New York 10022.
Objectives The purpose of this study was to determine the clinical impact of non-fibroatheroma lesion phenotype in patients presenting with an acute coronary syndrome (ACS).
Background Although fibroatheromas (FAs) are known to be clinically unstable, the impact of non-FA lesion phenotype on clinical outcomes has not been studied.
Methods In the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree) study, patients presenting with an ACS underwent 3-vessel grayscale and virtual histology intravascular ultrasound (VH-IVUS) after successful percutaneous intervention for all culprit lesions and were followed for 3 years. Patients were divided into those who had only the non-FA phenotype (pathological intimal thickening or fibrotic and/or fibrocalcific lesions) versus those who had at least 1 nonculprit FA.
Results Among 2,880 nonculprit lesions identified by VH-IVUS, 39.8% were non-FAs (1,042 pathological intimal thickening, 72 fibrotic, and 33 fibrocalcific). Nonculprit major adverse cardiac events (MACE) (death, myocardial infarction, or urgent rehospitalization for progressive or unstable angina) were attributed to only 7 non-FA lesions (0.7%) versus 43 FA lesions (2.7%, p < 0.001) during 3 years follow-up. Of 609 patients, 67 (11.0%) patients had only non-FA lesion phenotypes. Patients with only non-FAs tended to be younger and more often female, have fewer nonculprit lesions and less overall plaque burden and necrotic core, and fewer nonculprit lesion MACE compared with patients with at least 1 FA. In the adjusted Cox proportional hazards model, absence of a FA was a significant predictive of a lower 3-year nonculprit MACE rate (hazard ratio: 0.23; 95% confidence interval: 0.06 to 0.95).
Conclusions Non-FA lesions were clinically stable and were rarely associated with clinical events during 3 years of follow-up. The intermediate-term prognosis in patients presenting with ACS in whom all nonculprit lesions are non-FAs is favorable. (PROSPECT: An Imaging Study in Patients With Unstable Atherosclerotic Lesions; NCT00180466)
- acute coronary syndromes
- intravascular ultrasound
- plaque lesion phenotype
- virtual histology
Dr. Dohi has received grant support from the Banyu Life Science Foundation International. Dr. Mintz has received grant support from and is a consultant to Boston Scientific and Volcano Corporation. Dr. McPherson is a consultant to CardioDx. Dr. de Bruyne has received grant support from Abbott Vascular, Medtronic, and St. Jude Medical. Dr. Mehran has received grant support from The Medicines Company, Bristol-Myers Squibb/Sanofi, and Eli Lilly and Company/Daiichi Sankyo; and is a consultant to Abbott Vascular, AstraZeneca, Boston Scientific, Covidien, Janssen Pharmaceuticals, Regado Biosciences, Maya Medical, and Merck & Co. Dr. Weisz is a consultant to InfraReDx. Dr. Stone is a consultant to Boston Scientific, InfraReDx, and Volcano Corporation. Dr. Maehara has received grant support from and is a consultant to Boston Scientific. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. Sherif Nagueh, MD, served as Guest Editor for this paper.
- Received January 28, 2013.
- Revision received March 29, 2013.
- Accepted April 29, 2013.
- American College of Cardiology Foundation