title: Plaque Composition and No-Reflow Phenomenon During Percutaneous Coronary Intervention of Low-Echoic Structures in Grayscale Intravascular Ultrasound.
abstract: It has been reported that coronary vasa vasorum is associated with plaque vulnerability, and low-echoic structures in grayscale intravascular ultrasound (IVUS) are consistent pathologically with vasa vasorum. However, the association of low-echoic structures with plaque composition and no-reflow phenomenon during percutaneous coronary intervention (PCI) is unclear. We investigated plaque composition in virtual histology IVUS (VH-IVUS) and no-reflow phenomenon during PCI of low-echoic structures.A total of 106 lesions being treated by VH-IVUS before PCI were included in this study. Low-echoic structure was defined as a small tubular structure exterior to media without a connection to the vessel lumen in ≥ 3 consecutive crosssectional IVUS images. Lesions with low-echoic structures were found in 42% (45/106).Lesions with low-echoic structures were more prevalent in acute coronary syndrome (ACS) patients (53% [24/45] versus 20% [12/61], P < 0.001), had more positive remodeling (49% [22/45] versus 21% [13/61], P = 0.003), a larger number of VH-IVUS derived thin-cap fibroatheromas (VH-TCFAs) (0.64 ± 0.53 versus 0.05 ± 0.22, P < 0.001), more VH-TCFAs with a baseline plaque burden of 70% or more and minimal luminal area of 4.0 mm(2) or less (29% [13/45] versus 2% [1/61], P < 0.001), and more frequent no-reflow phenomenon after stent implantation and more final TIMI flow grade 0/1/2 (38% [17/45] versus 5% [3/61], P < 0.001; 9% [4/45] versus 0% [0/61], P = 0.03) than lesions without low-echo structures.Lesions with low-echoic structures in grayscale IVUS had high plaque vulnerability and were more prevalent in ACS patients, positive remolding, and VH-TCFAs, and they had more frequent no-reflow phenomenon during PCI than lesions without low-echoic structures.
authors.affiliation: Department of Cardiovascular Medicine, Toho University Faculty of Medicine.
authors.forename: Hideo
authors.initials: H
authors.lastname: Amano
authors.forename: Takanori
authors.initials: T
authors.lastname: Ikeda
authors.forename: Mikihito
authors.initials: M
authors.lastname: Toda
authors.forename: Ryo
authors.initials: R
authors.lastname: Okubo
authors.forename: Takayuki
authors.initials: T
authors.lastname: Yabe
authors.forename: Ippei
authors.initials: I
authors.lastname: Watanabe
authors.forename: Daiga
authors.initials: D
authors.lastname: Saito
mesh_terms: D054058:Acute Coronary Syndrome / Q000175:diagnosis / Q000503:physiopathology / Q000628:therapy; D000368:Aged; D017023:Coronary Angiography / Q000379:methods; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D005260:Female; D006801:Humans; D007431:Intraoperative Complications / Q000175:diagnosis / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D054318:No-Reflow Phenomenon / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology; D062645:Percutaneous Coronary Intervention / Q000009:adverse effects / Q000379:methods; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology; D015203:Reproducibility of Results; D012189:Retrospective Studies; D018084:Ultrasonography, Interventional / Q000379:methods*; D014651:Vasa Vasorum / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology