Objectives We hypothesized that bright spots in intravascular optical coherence tomography (IVOCT) images may originate by co-localization of plaque materials of differing indices of refraction (IR). To quantitatively identify bright spots, we developed an algorithm that accounts for factors including tissue depth, distance from light source, and signal-to-noise ratio. We used this algorithm to perform a bright spot analysis of IVOCT images, and compared these results with histologic examination of matching tissue sections. Background Although bright spots are thought to represent macrophages in IVOCT images, studies of alternative etiologies have not been reported. Methods Fresh human coronary arteries (n=14 from 10 hearts) were imaged with IVOCT in a mock catheterization laboratory then processed for histologic analysis. The quantitative bright spot algorithm was applied to all images. Results Results are reported for 1599 IVOCT images co-registered with histology. Macrophages alone were responsible for only 23% of the bright-spot positive regions, though they were present in 57% of bright-spot positive regions. Additional etiologies for bright spots included: cellular fibrous tissue (8%), interfaces between calcium and fibrous tissue (10%), calcium and lipid (5%), and fibrous cap and lipid pool (3%). Additionally, we showed that large pools of macrophages in CD68 histology sections correspond to dark regions in comparative IVOCT images; this is due to the fact that a pool of lipid-rich macrophages will have the same index of refraction as a pool of lipid and thus will not cause bright spots. Conclusions Bright spots in IVOCT images are correlated to a variety of plaque components that cause sharp changes in the index of refraction. Algorithms that incorporate these correlations may be developed to improve the identification of some types of vulnerable plaque and allow standardization of IVOCT image interpretation.

Background Intravascular optical coherence tomography (IVOCT) images are recorded by detecting light backscattered within coronary arteries. We hypothesize that non- thin-capped fibroatheroma (TCFA) etiologies may scatter light to create the false appearance of IVOCT TCFA. Methods and Results Ten human cadaver hearts were imaged with IVOCT (N=14 coronary arteries). IVOCT and histologic TCFA images were co-registered and compared. Of 21 IVOCT TCFAs (fibrous cap <65 µm, lipid arc >1 quadrant), only 8 were true histologic TCFA. Foam cell infiltration was responsible for 70% of false IVOCT TCFA and caused both thick-capped fibroatheromas (ThCFAs) to appear as TCFA and the appearance of TCFAs when no lipid core was present. Other false IVOCT TCFA etiologies included SMC-rich fibrous tissue (12%) and loose connective tissue (9%). If the lipid arc >1 quadrant (“obtuse”) criterion was disregarded, 45 IVOCT TCFAs were identified, and sensitivity of IVOCT TCFA detection increased from 63% to 87%, and specificity remained high at 92%. Conclusions We demonstrate that IVOCT can exhibit 87% (95% CI 75% to 93%) sensitivity and 92% specificity (95% CI 86% to 96%) to detect all lipid arcs (both obtuse and “acute,” <1 quadrant) TCFA and we also propose new mechanisms involving light scattering that explain why other plaque components can masquerade as TCFA and cause low PPV of IVOCT for TCFA detection (47% for obtuse lipid arcs). Disregarding the lipid arc >1 quadrant requirement enhances the ability of IVOCT to detect TCFA.

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To investigate the clinical significance of bright spots in coronary plaque detected by optical coherence tomography (OCT) in patients with coronary artery disease. We identified 112 patients [acute coronary syndromes (ACS): n = 50, stable angina pectoris (SAP): n = 62] who underwent OCT imaging of the culprit lesion. A novel OCT algorithm was applied to detect bright spots representing the juxtaposition of a variety of plaque components including macrophages. The density of bright spots within the most superficial 250 μm of the vessel wall was measured at the site of culprit lesion. Bright spot density in the culprit lesion was significantly higher in patients presenting with ACS compared to those presenting with SAP (0.51 ± 0.43% vs. 0.37 ± 0.26%, P = 0.04), particularly in the subgroup with ruptured culprit plaque (0.59 ± 0.52%). Thin-cap fibroatheroma (TCFA) was associated with a trend towards a higher density of bright spots compared to non-TCFA plaques (0.57 ± 0.50% vs. 0.41 ± 0.31%, P = 0.08). Similar results were also obtained within 1000 μm depth. Positive linear correlation was demonstrated between bright spot density and hsCRP level (r = 0.45, P = 0.002). Using a novel algorithm, we demonstrated a significantly higher density of bright spots in the culprit lesions of patients presenting with ACS, particularly in case of plaque rupture, compared to those presenting with SAP. The density of bright spots also correlates with inflammatory status. These results suggest that the quantitative assessment of bright spot density may be useful in evaluating plaque vulnerability.

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