CCT findings were associated with disrupted plaques confirmed by angioscopy. Ring-like enhancement had a high positive predictive value for detecting disrupted plaque.

Background: A low ratio of serum eicosapentaenoic acid to arachidonic acid (EPA/AA) has been associated with cardiovascular events. Higher-grade yellow color coronary plaques are associated with higher plaque vulnerability and higher thrombogenic potential. Therefore, the association between EPA/AA ratio and yellow color grade of coronary plaques was examined. Methods and Results:Consecutive patients (n=54) who underwent percutaneous coronary intervention were enrolled in this study. The serum EPA/AA ratio was examined on admission. All patients underwent an angioscopic examination of the culprit vessel to examine the color grade of yellow plaques (0, white; 1, slight yellow; 2, yellow; and 3, intense yellow) and the presence of thrombus. Excluding 16 patients with acute coronary syndrome (ACS), 38 patients with stable angina were divided into 2 groups according to their EPA/AA ratio: the low EPA/AA group (n=19, EPA/AA ratio <0.37 [median]) and the high EPA/AA group (n=19, EPA/AA ratio ≥0.37). The maximum color grade (2.5±0.5 vs. 1.9±0.9; P=0.01) of yellow plaques was significantly higher and the number of non-culprit yellow plaques with thrombus (1.7±0.8 vs. 1.2±1.1; P=0.06) tended to be higher in low EPA/AA than in high EPA/AA stable angina patients. Multivariate analysis revealed that the serum EPA level (odds ratio = 0.98, 95% confidence interval = 0.96-0.99, P=0.03) was associated with the presence of grade-3 yellow plaques. Conclusions:A low serum EPA level and a low EPA/AA ratio was associated with high vulnerability of coronary plaques. (Circ J 2011; 75: 2432 - 2438

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In-stent atherosclerosis evaluated by yellow plaque at 1 year after the implantation of DES and the absence of statin therapy were risks of VLSF. The underlying mechanism of VLSF appeared to be the progression of atherosclerosis as demonstrated by the yellow plaque.

Although the concept of vulnerable plaque has become common, it is still impossible to predict effectively the onset of acute coronary syndrome (ACS). Thin-cap fibroatheroma (TCFA) is regarded as vulnerable from pathological studies and various diagnostic tools have tried to detect TCFA clinically but failed to predict ACS. Because there are so many silent plaque ruptures detected, it is supposed that many vulnerable plaques might have ruptured but not caused ACS. Some factor(s) other than the rupture of vulnerable plaque is required for the onset of ACS. "Vulnerable blood" may be one of them. The thrombogenic potential of blood (ie, vulnerable blood) may play an important and determinant role in the onset of ACS, the process of which will be discussed from the angioscopic point of view. (Circ J 2010; 74: 411 - 417)