The patients demonstrating positively remodeled coronary segments with low-attenuation plaques on CT angiography were at a higher risk of ACS developing over time when compared with patients having lesions without these characteristics.

No abstract

CTA-verified HRP was an independent predictor of ACS. However, the cumulative number of ACS patients with HRP(-) was similar to patients with HRP(+). Additionally, plaque progression detected by serial CTA was an independent predictor of ACS.

No abstract

Sudden cardiac death and acute myocardial infarction often occur as the first manifestation of coronary artery disease. Otherwise asymptomatic individuals with subclinical atherosclerosis almost always have a classic risk-factor profile and it is essential that they are identified before the occurrence of an acute coronary event. The ability to recognize such individuals requires the development of strategies that can localize unstable atherosclerotic lesions. Plaques that are vulnerable to rupture demonstrate distinct histological characteristics, including large plaque and necrotic core volumes, extensive remodeling of the vessel at the lesion site, and attenuated fibrous caps. Precise metrics of typical vulnerable atherosclerotic plaque dimensions will need to be defined to facilitate their identification by noninvasive imaging modalities.

This preliminary study suggests that serial CTA evaluation of coronary plaques allows for the assessment of interval change in the plaque morphology. Statin treatment results in decreases in the plaque and necrotic core volume. The features known to be associated with plaque instability.

Although the incidence of dissections was comparable between RA and OA cases, OA resulted in deeper tissue modifications (lacunae) as shown by OCT imaging. The finding might provide an explanation for a better stent apposition after OA as compared to RA. Their impact on long-term outcome needs to be determined.

In contrast to the situation with RFC-ACS, distinct culprit lesion characteristics associated with non-rupture-related mechanisms are not identified by CT angiography. It will therefore not be possible to differentiate plaques likely to develop IFC-ACS from stable plaques.