The role of intracoronary imaging in translational research

Abstract

Atherosclerotic cardiovascular disease is a key public health concern worldwide and leading cause of morbidity, mortality and health economic costs. Understanding atherosclerotic plaque microstructure in relation to molecular mechanisms that underpin its initiation and progression is needed to provide the best chance of combating this disease. Evolving vessel wall-based, endovascular coronary imaging modalities, including intravascular ultrasound (IVUS), optical coherence tomography (OCT) and near-infrared spectroscopy (NIRS), used in isolation or as hybrid modalities, have been advanced to allow comprehensive visualization of the pathological substrate of coronary atherosclerosis and accurately measure temporal changes in both the vessel wall and plaque characteristics. This has helped further our appreciation of the natural history of coronary artery disease (CAD) and the risk for major adverse cardiovascular events (MACE), evaluate the responsiveness to conventional and experimental therapeutic interventions, and assist in guiding percutaneous coronary intervention (PCI). Here we review the use of different imaging modalities for these purposes and the lessons they have provided thus far.

Keywords: Coronary artery disease (CAD); intracoronary imaging; intravascular ultrasound (IVUS); near-infrared spectroscopy (NIRS); optical coherence tomography (OCT); plaque imaging.

Figure 1

Different intracoronary plaque imaging modalities. (A) Cross-sectional view of gray-scale IVUS imaging demonstrating coronary PB; (B) coronary atherosclerotic plaque imaging with OCT; (C) coronary artery imaging with a cross-sectional view of IVUS highlighting plaque and NIRS demonstrating lipid (yellow) content. IVUS, intravascular ultrasound; PB, plaque burden; OCT, optical coherence tomography; NIRS, near-infrared spectroscopy.

Figure 2

Comparison of standard intracoronary imaging modalities with corresponding EEL-enhanced OCT. (A) OCT image of pathological intimal thickening; (B) corresponding EEL-enhanced OCT image enabling improved visualization of the EEL; (C) corresponding IVUS image of pathological intimal thickening; (D) OCT image of fibrous plaque; (E) corresponding EEL-enhanced OCT image revealing more EEL around the arterial circumference; (F) corresponding IVUS image of fibrous plaque; (G) OCT image of fibroatheroma plaque; (H) corresponding EEL-enhanced OCT image enabling improved visualization of the EEL deep to the plaque; (I) corresponding IVUS image of fibroatheroma plaque. Key; thin-cap fibroadenoma (arrow), lipid rich pool (arrowhead), EEL (star), intimal thickening (IT), fibrous plaque (F), fibroadenoma (FA). [Images adapted with permission from Gerbaub et al. (68)]. IVUS, intravascular ultrasound; OCT, optical coherence tomography; EEL, external elastic lamina.

Figure 3

Integrated OCT and NIRAF imaging of a TCFA. (A) Coronary angiogram of the left anterior descending artery; (B) NIRAF map identifying a focal region of elevated NIRAF in the ostial left anterior descending artery, and below, the three-dimensional cutaway rendering demonstrating the highest NIRAF spot appears focally within a lipid pool; (C,D,E) OCT and NIRAF cross sections from sites in the ostial left anterior descending artery revealing subclinical fibrous cap rupture. Key: *, guide-wire shadowing artifact; OCT showing white luminal thrombus (arrow), plaque rupture (R), thrombus (T). [Images adapted with permission from Ughi et al. (19)]. OCT, optical coherence tomography; NIRAF, near-infrared autofluorescence; TCFA, thin-cap fibroatheroma.