Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2016 Jul;9(7):10.1161/CIRCINTERVENTIONS.115.003163 e003163.
doi: 10.1161/CIRCINTERVENTIONS.115.003163.

Diagnosis of Thin-Capped Fibroatheromas in Intravascular Optical Coherence Tomography Images: Effects of Light Scattering

Jennifer E Phipps  1 , Taylor Hoyt  1 , Deborah Vela  1 , Tianyi Wang  1 , Joel E Michalek  1 , L Maximilian Buja  1 , Ik-Kyung Jang  1 , Thomas E Milner  1 , Marc D Feldman  2
Affiliations

Diagnosis of Thin-Capped Fibroatheromas in Intravascular Optical Coherence Tomography Images: Effects of Light Scattering

Jennifer E Phipps et al. Circ Cardiovasc Interv. 2016 Jul.

Abstract

Background: Intravascular optical coherence tomography (IVOCT) images are recorded by detecting light backscattered within coronary arteries. We hypothesize that non-thin-capped fibroatheroma (TCFA) causes 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 histological TCFA images were coregistered and compared. Of 21 IVOCT TCFAs (fibrous cap <65 μm, lipid arc >1 quadrant), only 8 were true histological TCFA. Foam cell infiltration was responsible for 70% of false IVOCT TCFA and caused both thick-capped fibroatheromas to appear as TCFA, and the appearance of TCFAs when no lipid core was present. Other false IVOCT TCFA causes included smooth muscle cell-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%-93%) sensitivity and 92% specificity (95% CI, 86%-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 positive predictive value 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.

Keywords: atherosclerosis; lipids; myocytes, smooth muscle; plaque, amyloid; tomography, optical coherence.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Type 1 and 2 light scattering mechanisms
Type 1: high IR gradient and size of plaque constituents within an order of the wavelength of light (1310±40 nm). Type 2: low IR gradient and plaque constituents much larger than the wavelength of light. The side scattering light demonstrated in Type 2-C could occur in any of the other light scattering mechanisms and illustrates why the back edges of these components are not visualized with IVOCT.
Figure 2
Figure 2. Flowchart of how each TCFA and ThCFA group was categorized
Expert IVOCT image readers and two cardiovascular pathologists performed the categorization.
Figure 3
Figure 3. True IVOCT TCFA (type 2 light scattering)
IVOCT image (A). H&E histology section (B). Movat pentachrome (C). CD68+ macrophages (D). A rupture can be seen in the fibrous cap at 9 o’clock. Scale bars are 1 mm.
Figure 4
Figure 4. Superficial clustered foam cells caused a false IVOCT TCFA (type 2B light scattering)
IVOCT image with false IVOCT TCFA outlined in red dashes (A). CD68 immunohistochemistry (B) shows that a long superficial cluster of foam cells inside the red dashed circle are responsible for the increased light scattering that causes the appearance of the TCFA in (A). H&E stain (C). α-SMA immunohistochemistry (D). Scale bars are 1 mm.
Figure 5
Figure 5. Loose connective tissue caused a false IVOCT TCFA (type 2 light scattering)
IVOCT image with false TCFA outlined with red dashes (A). H&E stain shows loose connective tissue and ground substance is responsible for the increased light scattering in this region (B). CD68 immunohistochemistry is negative for macrophages (C). Movat pentachrome stain shows loose collagen in the region of interest (D). Scale bars are 1 mm.
Figure 6
Figure 6. Proteoglycans caused a <1 quadrant false IVOCT TCFA (type 1 light scattering)
IVOCT image with false TCFA outlined with red dashes (A). H&E stain demonstrates that this area is hypocellular (B); α-SMA shows SMC loss (C) and CD68 immunohistochemistry is negative (D). Movat pentachrome stain shows proteoglycans superficially in the region of the false TCFA (E). Scale bars are 1 mm.
Figure 7
Figure 7. Smooth muscle cell rich fibrous tissue caused a <1 quadrant false IVOCT TCFA (type 1 light scattering)
IVOCT image with false TCFA outlined in red dashes (A). H&E stain shows cellular fibrous tissue in the bright arc of tissue before the light attenuates within the red dashed region (B). CD68 immunohistochemistry shows that this region is negative for macrophages (C). α-SMA immunohistochemistry shows dense smooth muscle cells (SMCs) in the region of bright tissue (D). Scale bars are 1 mm.
Figure 8
Figure 8. Calcified nodule caused a <1 quadrant false IVOCT TCFA (type 2 light scattering)
IVOCT image with a shadowed region with diffuse borders, indicative of lipid (A). H&E stain shows a calcified nodule that appears in (A) as a lipid pool (B). Scale bars are 1 mm.
See this image and copyright information in PMC

Comment in

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Narula J, Nakano M, Virmani R, Kolodgie FD, Petersen R, Newcomb R, Malik S, Fuster V, Finn AV. Histopathologic characteristics of atherosclerotic coronary disease and implications of the findings for the invasive and noninvasive detection of vulnerable plaques. J Am Coll Cardiol. 2013;61:1041–1051. - PMC - PubMed
    1. Virmani R, Burke AP, Farb A, Kolodgie FD. Pathology of the vulnerable plaque. J Am Coll Cardiol. 2006;47:C13–C18. - PubMed
    1. Tearney GJ, Regar E, Akasaka T, Adriaenssens T, Barlis P, Bezerra HG, Bouma B, Bruining N, Cho JM, Chowdhary S, Costa MA, de Silva R, Dijkstra J, Di Mario C, Dudek D, Falk E, Feldman MD, Fitzgerald P, Garcia-Garcia HM, Gonzalo N, Granada JF, Guagliumi G, Holm NR, Honda Y, Ikeno F, Kawasaki M, Kochman J, Koltowski L, Kubo T, Kume T, Kyono H, Lam CC, Lamouche G, Lee DP, Leon MB, Maehara A, Manfrini O, Mintz GS, Mizuno K, Morel MA, Nadkarni S, Okura H, Otake H, Pietrasik A, Prati F, Raber L, Radu MD, Rieber J, Riga M, Rollins A, Rosenberg M, Sirbu V, Serruys PW, Shimada K, Shinke T, Shite J, Siegel E, Sonoda S, Suter M, Takarada S, Tanaka A, Terashima M, Thim T, Uemura S, Ughi GJ, van Beusekom HM, van der Steen AF, van Es GA, van Soest G, Virmani R, Waxman S, Weissman NJ, Weisz G. Consensus standards for acquisition, measurement, and reporting of intravascular optical coherence tomography studies: a report from the International Working Group for Intravascular Optical Coherence Tomography Standardization and Validation. J Am Coll Cardiology. 2012;59:1058–1072. - PubMed
    1. Jang IK, Tearney GJ, MacNeill B, Takano M, Moselewski F, Iftima N, Shishkov M, Houser S, Aretz HT, Halpern EF, Bouma BE. In vivo characterization of coronary atherosclerotic plaque by use of optical coherence tomography. Circulation. 2005;111:1551–1555. - PMC - PubMed
    1. Kubo T, Imanishi T, Takarada S, Kuroi A, Ueno S, Yamano T, Tanimoto T, Matsuo Y, Masho T, Kitabata H, Tsuda K, Tomobuchi Y, Akasaka T. Assessment of culprit lesion morphology in acute myocardial infarction: ability of optical coherence tomography compared with intravascular ultrasound and coronary angioscopy. J Am Coll Cardiol. 2007;50:933–939. - PubMed

Publication types