This editorial refers to ‘Determinants of high cardiovascular risk in relation to plaque composition of a non-culprit coronary segment visualized by near-infrared spectroscopy in patients undergoing percutaneous coronary intervention’[†][1], by S.P.M. de Boer et al. , on page 282 The rupture of an unstable atherosclerotic plaque precedes the majority of acute coronary syndromes, and considerable effort has been devoted to identifying patients at increased risk of future coronary ischaemic events. Atherosclerosis imaging is a potentially attractive strategy to detect vulnerable coronary plaques, with each modality having its own advantages and limitations. Different characteristics of the atherosclerotic plaque can be targeted with imaging, such as the number and severity of luminal narrowings with angiography, atheroma burden and remodelling with intravascular ultrasonography (IVUS), elastic properties with elastography, radiofrequency-determined plaque types with virtual histology, fibrous cap thickness and necrotic core with optical coherence tomography, extent of calcifications with computed tomography, and inflammation with positron emission tomography.1 Near-infrared spectroscopy (NIRS) provides chemical assessment of tissues, and catheter-based NIRS can generate spectra that may distinguish cholesterol from collagen and may identify chemical fingerprints in coronary plaques in the cardiac catheterization laboratory ( Figure 1 ).2 Although intravascular NIRS has been compared with pathological findings, its research and clinical implications remain to be established. de Boer et al. now report their use of NIRS in a non-culprit coronary artery and the associations with clinical characteristics and biomarkers in 208 patients undergoing percutaneous coronary intervention.3 History of hypercholesterolaemia, male sex, use of beta-blockers, and a history of peripheral artery disease and/or cerebrovascular disease were modestly associated with NIRS-derived lipid core burden index (LCBI), while biomarkers such as blood lipids and high-sensitivity C-reactive protein were not. Approximately 23% of the variance in LCBI was explained by all available baseline characteristics including plasma … [1]: #fn-2