Author + information
- Sadako Motoyama, MD, PhD,
- Yukio Ozaki, MD, PhD and
- Jagat Narula, MD, PhD* ()
- ↵*University of California Irvine, Division of Cardiology, 333 City Boulevard West, Suite 400, Orange, California 92868-4080
We thank Dr. Alfonso for interest in our manuscript and very insightful comments. We agree that feasibility of noninvasive identification of plaques vulnerable to rupture might have significant clinical implications, and clarify here the methodological issues raised. As described in our paper (1), acute coronary syndromes (ACS) included acute myocardial infarction with the elevation of troponin level and unstable angina without troponin elevation. Our report characterized the plaques that resulted in ACS and excluded the lesions already subjected to intervention or those selected for intervention. As noted in the report, 3 patients developed ACS involving the previously treated lesion and were excluded from the analysis. Also, target lesion could not be identified in 8 patients with ACS, because of multiple vessel disease, and were excluded. Furthermore, the lower proportion of 2-feature positive plaques in our report is because of different study populations; most of the intravascular ultrasound studies had included patients who needed percutaneous coronary intervention. The range of Framingham risk score in the patients with 1- or 2-feature positive was 3 to 56; the risk score in the patients with 1-feature positive plaques was 16 ± 8 and 19 ± 13 for patients showing 2-feature positive plaques. We agree with Dr. Alfonso that plaque rupture does not provide a complete spectrum of ACS. It would be necessary to develop strategies for identification of plaques resulting in ACS from plaque erosions and calcified nodules. However, identification of such substrates at least by computed tomography angiography would be rather difficult.
- American College of Cardiology Foundation