Author + information
- Received January 20, 2011
- Revision received April 15, 2011
- Accepted May 5, 2011
- Published online August 1, 2011.
- Patrick A. Calvert, MD⁎,†,
- Daniel R. Obaid, MD⁎,†,
- Michael O'Sullivan, MD, PhD†,
- Leonard M. Shapiro, MD†,
- Duncan McNab, MD†,
- Cameron G. Densem, MD†,
- Peter M. Schofield, MD†,
- Denise Braganza, MD, PhD†,
- Sarah C. Clarke, MD†,
- Kausik K. Ray, MD‡,
- Nick E.J. West, MD† and
- Martin R. Bennett, MD, PhD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Martin R. Bennett, Division of Cardiovascular Medicine, University of Cambridge, Box 110, ACCI, Addenbrooke's Hospital, Cambridge CB2 2QQ, United Kingdom
Objectives The purpose of this study was to determine whether thin-capped fibroatheromata (TCFA) identified by virtual histology intravascular ultrasound (VH-IVUS) are associated with major adverse cardiac events (MACE) on individual plaque or whole patient analysis.
Background Post-mortem studies have identified TCFA as the substrate for most myocardial infarctions. However, little is known about the natural history of individual TCFA and their link with MACE. VH-IVUS provides a method of identifying plaques in vivo that are similar (although not identical) to histologically defined TCFA, and has been validated in human atherectomy and post-mortem studies.
Methods One hundred seventy patients with stable angina or troponin-positive acute coronary syndrome referred for percutaneous coronary intervention (PCI) were prospectively enrolled and underwent 3-vessel VH-IVUS pre-PCI and also post-PCI in the culprit vessel. MACE consisted of death, myocardial infarction, or unplanned revascularization.
Results In all, 30,372 mm of VH-IVUS were analyzed. Eighteen MACE occurred in 16 patients over a median follow-up of 625 days (interquartile range: 463 to 990 days); 1,096 plaques were classified, and 19 lesions resulted in MACE (13 nonculprit lesions and 6 culprit lesions). Nonculprit lesion factors associated with nonrestenotic MACE included VHTCFA (hazard ratio [HR]: 7.53, p = 0.038) and plaque burden >70% (HR: 8.13, p = 0.011). VHTCFA (HR: 8.16, p = 0.007), plaque burden >70% (HR: 7.48, p < 0.001), and minimum luminal area <4 mm2 (HR: 2.91, p = 0.036) were associated with total MACE. On patient-based analysis, the only factor associated with nonrestenotic MACE was 3-vessel noncalcified VHTCFA (HR: 1.79, p = 0.004).
Conclusions VH-IVUS TCFA was associated with nonrestenotic and total MACE on individual plaque analysis, and noncalcified VHTCFA was associated with nonrestenotic and total MACE on whole-patient analysis, demonstrating that VH-IVUS can identify plaques at increased risk of subsequent events. The preservation of the association between VHTCFA and MACE despite various analyses emphasizes its biological importance.
- major adverse cardiac event
- necrotic core
- thin-capped fibroatheroma
- virtual histology intravascular ultrasound
This study was supported by British Heart Foundation grants PG/08/008 and FS/10/025/28196 and by the National Institute for Health Research Cambridge Biomedical Research Centre (portfolio study number 5241). All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 20, 2011.
- Revision received April 15, 2011.
- Accepted May 5, 2011.
- American College of Cardiology Foundation