अमूर्त

Are the high-risk plaques of no-reflow phenomenon equivalent to vulnerable plaques?

Masaaki Okutsu, Satoru Mitomo, Shotaro Nakamura, Sunao Nakamura

No-reflow phenomenon during Percutaneous Coronary Intervention (PCI) in Acute Coronary Syndrome (ACS) is associated with some coronary complications such as arrhythmias, heart failure, ventricular remodeling or cardiac death. Therefore, it is very important to predict this phenomenon. The vulnerable plaque, which is almost equivalent to Thin-Cap Fibroatheroma (TCFA), is extrapolated as a predictive factor because the no-reflow phenomenon is caused by the disruption of fibroatheroma (FA). However, these two phenomena have different mechanism of occurrence. In the ACS, it is spontaneous rupture of TCFA. On the other hand, in the no-reflow phenomenon, it is the disruption of fibrous cap by mechanical stimulation such as balloon dilation, subsequent outflow of fragile necrotic core from FA and multiple microvascular obstruction. There are following three major modalities to predict this phenomenon. Intravascular ultrasound can detect whole FA other than calcification but has low resolution to detect fibrous cap. Optical coherence tomography has enough resolution to detect FA but low penetration power to detect whole FA. Cardiac computed tomography angiography can detect whole FA including calcification but has quite low resolution. Therefore, it seems to be necessary to be reconsider whether the theory, that vulnerable plaque is extrapolated as the high-risk plaques of no-reflow phenomenon, is appropriate and which modality is suitable.