Virtual Histology Intravascular Ultrasound Analysis of Non-Culprit Attenuated Plaques Detected by Grayscale Intravascular Ultrasound in Patients With Acute Coronary Syndromes

Xiaofan Wu, Akiko Maehara, Gary S. Mintz, Takashi Kubo, Kai Xu, So Yeon Choi, Yong He, Ning Guo, Jeffrey W. Moses, Martin B. Leon, Bernard De Bruyne, Patrick W. Serruys, Gregg W. Stone

Research output: Contribution to journalArticlepeer-review

73 Scopus citations

Abstract

Noncalcific attenuated plaques identified by grayscale intravascular ultrasound (IVUS) are often seen in patients with acute coronary syndromes and have been associated with no reflow and creatine kinase-MB elevation after percutaneous coronary intervention. Histopathology has shown cholesterol clefts, microcalcification, or organized thrombus. One hundred twenty-four vessels in 64 patients with acute coronary syndromes from the PROSPECT trial were identified for inclusion in the present analysis. After excluding 4 vessels with severe calcification, 9 vessels with <40% plaque burden, and 3 vessels with too few (<3) virtual histology (VH)-IVUS frames for analysis, complete grayscale IVUS and VH-IVUS was available for 108 vessels in 64 patients that contained 39 VH-IVUS thin-capped fibroatheromas (VH-TCFA), 40 thick-capped fibroatheromas (VH-ThFA), and 33 pathologic intimal thickening but no fibrotic or fibrocalcific plaques. Overall, there were 47 grayscale IVUS attenuated plaques in 43 vessels. Compared to the minimum luminal sites of the remaining 65 vessels (controls), attenuated plaques contained larger necrotic core areas (1.5 ± 0.9 vs 0.9 ± 0.8 mm2 in controls, p = 0.001). Fibroatheromas (VH-TCFA or VH-ThFA) were more common at the sites of attenuated plaques than at control sites (VH-TCFA 42.5% vs 29.2%, VH-ThFA 53.2% vs 23.1%, pathologic intimal thickening 4.3% vs 47.7%, p <0.0001). In conclusion, grayscale IVUS attenuated plaques are associated with a large amount of VH-IVUS necrotic core and are markers of the presence of fibroatheromas (VH-TCFA or VH-ThFA). This may explain the biologic instability of these lesions.

Original languageEnglish
Pages (from-to)48-53
Number of pages6
JournalAmerican Journal of Cardiology
Volume105
Issue number1
DOIs
StatePublished - 1 Jan 2010
Externally publishedYes

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