This document may be broadly used as a standard reference regarding the current state of the IVOCT imaging modality, intended for researchers and clinicians who use IVOCT and analyze IVOCT data.

for the Integrated Biomarker and Imaging Study-2 InvestigatorsBackground-Lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) is expressed abundantly in the necrotic core of coronary lesions, and products of its enzymatic activity may contribute to inflammation and cell death, rendering plaque vulnerable to rupture. Methods and Results-This study compared the effects of 12 months of treatment with darapladib (an oral Lp-PLA 2 inhibitor, 160 mg daily) or placebo on coronary atheroma deformability (intravascular ultrasound palpography) and plasma high-sensitivity C-reactive protein in 330 patients with angiographically documented coronary disease. Secondary end points included changes in necrotic core size (intravascular ultrasound radiofrequency), atheroma size (intravascular ultrasound gray scale), and blood biomarkers. Background therapy was comparable between groups, with no difference in low-density lipoprotein cholesterol at 12 months (placebo, 88Ϯ34 mg/dL; darapladib, 84Ϯ31 mg/dL; Pϭ0.37). In contrast, Lp-PLA 2 activity was inhibited by 59% with darapladib (PϽ0.001 versus placebo). After 12 months, there were no significant differences between groups in plaque deformability (Pϭ0.22) or plasma highsensitivity C-reactive protein (Pϭ0.35). In the placebo-treated group, however, necrotic core volume increased significantly (4.5Ϯ17.9 mm 3 ; Pϭ0.009), whereas darapladib halted this increase (Ϫ0.5Ϯ13.9 mm 3 ; Pϭ0.71), resulting in a significant treatment difference of Ϫ5.2 mm 3 (Pϭ0.012). These intraplaque compositional changes occurred without a significant treatment difference in total atheroma volume (Pϭ0.95). Conclusions-Despite adherence to a high level of standard-of-care treatment, the necrotic core continued to expand among patients receiving placebo. In contrast, Lp-PLA 2 inhibition with darapladib prevented necrotic core expansion, a key determinant of plaque vulnerability. These findings suggest that Lp-PLA 2 inhibition may represent a novel therapeutic approach.

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We demonstrate intravascular photoacoustic imaging of human coronary atherosclerotic plaque. The data was obtained from two fresh human coronary arteries ex vivo, showing different stages of disease. A 1.25 mm diameter intravascular imaging catheter was built, comprising an angle-polished optical fiber adjacent to a 30 MHz ultrasound transducer. Specific photoacoustic imaging of lipid content, a key factor in vulnerable plaques that may lead to myocardial infarction, is achieved by spectroscopic imaging at different wavelengths between 1180 and 1230 nm. Simultaneous imaging with intravascular ultrasound was performed.

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