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Outcomes After Orbital Atherectomy of Severely Calcified Left Main Lesions: Analysis of the ORBIT II Study Orbital atherectomy for the treatment of small (2.5mm) severely calcified coronary lesions: ORBIT II sub-analysis A Notch3-Marked Subpopulation of Vascular Smooth Muscle Cells Is the Cell of Origin for Occlusive Pulmonary Vascular Lesions. Comparison of 2 Different Drug-Coated Balloons in In-Stent Restenosis: The RESTORE ISR China Randomized Trial Drug-Coated Balloon for De Novo Coronary Artery Disease: JACC State-of-the-Art Review In vivo comparison of lipid-rich plaque on near-infrared spectroscopy with histopathological analysis of coronary atherectomy specimens One-Year Outcomes of Orbital Atherectomy of Long, Diffusely Calcified Coronary Artery Lesions Effect of orbital atherectomy in calcified coronary artery lesions as assessed by optical coherence tomography Right ventricular expression of NT-proBNP adds predictive value to REVEAL score in patients with pulmonary arterial hypertension Healed coronary plaque rupture as a cause of rapid lesion progression: a case demonstrated with in vivo histopathology by directional coronary atherectomy

Original Research2017 May 15;119(10):1512-1517.

JOURNAL:Am J Cardiol. Article Link

Comparison of Coronary Intimal Plaques by Optical Coherence Tomography in Arteries With Versus Without Internal Running Vasa Vasorum

Amano H, Koizumi M, Okubo R et al. Keywords: OCT; internal running vasa vasorum; plaque vulnerability; blood flow

ABSTRACT


It has been reported that the internal running vasa vasorum (VV) was associated with plaque vulnerability, and microchannels in optical coherence tomography (OCT) are consistent pathologically with VV. We investigated plaque vulnerability and incidence of slow flow during percutaneous coronary intervention of the internal longitudinal running VV. Subjects were 71 lesions that underwent OCT before percutaneous coronary intervention. Internal running VV was defined as intraplaque neovessels running from the adventitia to plaque. Lesions with internal running VV were found in 47% (33 of 71). Compared with lesions without internal running VV, lesions with internal running VV showed significantly higher incidence of intimal laceration (64% [21 of 33] vs 16% [6 of 38], p <0.001), lipid-rich plaque (79% [26 of 33] vs 26% [10 of 38], p <0.001), plaque rupture (52% [17 of 33] vs 13% [5 of 38], p <0.001), thin-cap fibroatheroma (58% [19 of 33] vs 11% [4 of 38], p <0.001), macrophage accumulation (61% [20 of 33] vs 26% [10 of 38], p = 0.004), intraluminal thrombus (36% [12 of 33] vs 3% [1 of 38], p <0.001), and slow flow after stent implantation (42% [14 of 33] vs 13% [5 of 38], p = 0.007). The multivariable analysis showed that internal running VV was an independent predictor of slow flow after stent implantation (odds ratio 4.23, 95% confidence interval 1.05 to 17.01, p = 0.042). In conclusion, compared with those without, plaques with internal running VV in OCT had high plaque vulnerability with more intimal laceration, lipid-rich plaque, plaque rupture, thin-cap fibroatheroma, macrophage accumulation, and intraluminal thrombus, and they had high incidence of slow flow after stent implantation.