Author + information
- Dennis T.L. Wong, MBBS (Hons), PhD∗ ()
- ↵∗MonashHeart, Monash University, University of Adelaide & South Australian Health and Medical Research Institute (SAHMRI), 246 Clayton Road, Clayton, Victoria 3150, Australia
The study by Puchner et al. (1) revealed that the presence of high-risk plaque features on coronary computed tomography angiography (CTA) in patients presenting to the emergency department with acute chest pain, but negative initial electrocardiogram and troponin, increases the likelihood of acute coronary syndrome (ACS). This is independent of the presence of significant coronary artery disease and clinical risk assessment (age, sex, number of cardiovascular risk factors).
First, patients in this study were recruited between April 2010 and January 2012, and hence, at least 2-year medium-term clinical follow-up would be available, but the primary endpoint of this study was ACS during index hospitalization. ACS was defined as acute myocardial infarction (MI) or unstable angina pectoris that was pre-defined and adjudicated by an independent clinical events committee. This study included 472 patients, and only 37 patients had ACS. It is not clearly stated in the body of the paper how many patients had acute MI, or how many went on to have invasive coronary angiography and revascularization. It would have been clearer if the authors elaborated on this in the body of the paper. It is of further interest for the authors to report whether high-risk features on CTA predict these harder clinical endpoints. A recent study by Nasis et al. (2) reported the long-term outcome (median follow-up of 47.4 months) of 585 consecutive patients who underwent CTA assessment in the emergency department, and the event rate for coronary revascularization was 6.2% (n = 34). It is therefore of interest that Puchner and colleagues report whether high-risk or “vulnerable plaque” features in this study predicted longer-term ACS, coronary revascularization, and mortality as well.
Second, the assessment of plaque burden, which has been the strongest independent predictor of long-term ACS (3), was not reported in this study. It would have been of significant interest to compare high-risk plaque features with plaque burden for prediction of short-term and long-term ACS in this study.
Third, the authors defined low attenuation plaque as <30 HU on the basis of previously published criteria described by Motoyama et al. (4), who used a tube voltage of 135 kV. The scanner parameters were not described by Puchner et al. (1). Could Puchner and colleagues (1) speculate about the applicability of the low attenuation plaque definition used in their study if the tube voltage differed from that in the study by Motoyama et al. (4)?
- American College of Cardiology Foundation
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