Virtual histology intravascular ultrasound analysis of attenuated plaque and ulcerated plaque detected by gray scale intravascular ultrasound and the relation between the plaque composition and slow flow/no reflow phenomenon during percutaneous coronary intervention.

Objective This study aimed to assess the plaque characteristics of attenuated and ulcerated plaques in virtual-histology intravascular ultrasound (VH-IVUS) and the incidence of slow flow/no reflow during percutaneous coronary intervention (PCI). Background The attenuated and ulcerated plaques are thought as embolic prone plaque; however, the plaque characteristics are unclear. Methods Subjects were 119 patient's 121 lesions undergoing VH-IVUS before coronary stenting. These lesions were divided into the 15 lesions showing attenuated plaque, 24 lesions showing ulcerated plaque, and 82 lesions revealing neither attenuated nor ulcerated plaque (the control group). Results Fibro-fatty tissue in the attenuation group was significantly larger than the control group (27.5 ± 9.5% vs 13.9 ± 8.2%, P < 0.01, 3.5 ± 1.9 mm2 vs 1.6 ± 1.2 mm2, P < 0.01). Necrotic core in ulceration group was significantly larger than the control group (20.7 ± 9.0% vs 15.9 ± 9.0%, P < 0.05, 2.5 ± 1.3 mm2 vs 1.7 ± 1.0 mm2, P < 0.01). Dense calcium in ulceration group was significantly larger than the control group (12.3 ± 6.4% vs 8.3 ± 7.1%, P < 0.05, 1.4 ± 0.7 mm2 vs 0.9 ± 0.8 mm2, P < 0.01). In the ulceration group, the necrotic core area of acute coronary syndrome was significantly larger than the stable angina pectoris (3.0 ± 1.4 mm2 vs 1.8 ± 1.0 mm2, P < 0.05). The incidence of slow flow/no reflow was significantly higher in the attenuation and ulceration group than the control group (20.0% [3/15], 20.8% [4/24] vs 4.9% [4/82], P < 0.05, 0.05). Conclusion The attenuated plaque had significantly larger fibro-fatty tissue. The ulcerated plaque had significantly larger necrotic core and dense calcium. The lesions with the attenuated and the ulcerated plaque had more frequent slow flow/no reflow during PCI. (J Interven Cardiol 2013;26:295–301)