Noncalcified Atherosclerotic Lesions With Vulnerable Characteristics Detected By Coronary CT angiography and Future Coronary Events

OBJECTIVES: The ability of coronary CT angiography (CTA) findings such as plaque characteristics to predict future coronary events remains controversial. We investigated whether noncalcified atherosclerotic lesions (NCALs) detected by coronary CTA were predictive of future coronary events.

METHODS: A total of 511 patients who underwent coronary CTA were followed for cardiovascular events over a period of 3.3 ± 1.2 years. The primary end point was defined as hard events, including cardiac death, nonfatal myocardial infarction, or unstable angina that required urgent hospitalization. Early elective coronary revascularizations (n = 58) were excluded. The relationship between features of NCALs and outcomes is described.

RESULTS: A total of 15 hard events (2 cardiac deaths, 7 myocardial infarctions, 6 cases of unstable angina that required urgent hospitalization) were documented in the remaining 453 patients with modest risks during a follow-up period of 3.3 ± 1.2 years. For these hard events, a univariate Cox proportional hazard model showed that the hazard ratio for the presence of >50% stenosis was 7.27 (95% CI, 2.62-21.7; P = .0002). Although the presence of NCAL by itself was not statistically significant, NCALs with low attenuation and positive remodeling (low-attenuation plaque [LAP] and positive remodeling [PR]; plaque CT number ≤34 HU and remodeling index ≥1.20) showed an adjusted hazard ratio of 11.2 (95% CI, 3.71-36.7; P 50% stenosis were added, the C-statistic was significantly improved compared with the basal model adjusted for age, sex, and log2 (Agatston score +1) (0.900 vs 0.704; P = .0018).

CONCLUSIONS: Identification of NCALs with LAP and PR characteristics by coronary CTA provides additional prognostic information to coronary stenosis for the prediction of future coronary events. 


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  1. HR of 11.2 for MACE. More support for specific plaque markers to identify vulnerable plaques (and vulnerable patients). Are we closing the gap in CAD risk assessment? What should then be our next step? Some would argue prophylactic coronary stenting (or bio-absorbable scaffolds). Will the failed concept of “plaque passivation” revive? So many un-answered questions to address, but at least this paper emphasize the prognostic importance of plaque type rather than diameter stenosis.

  2. Interesting study! Adds more weight to characteristics that have already been associated with vulnerable plaque.

    I think it will be hard to prove/justify stenting plaques on the basis of these characteristics, but it might push cardiologists to institute aggressive medical therapy. Everyone seems to get a statin now, but the risks of aspirin are greater than previously thought. I might be more compelled to add aspirin or clopidogrel in patients with vulnerable plaque characteristics and would maximize dosage of statins.

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