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Despite major advances in contemporary coronary care, a substantial proportion of acute coronary syndromes originate from lesions that are not angiographically severe. Intracoronary imaging has provided ‘new eyes’ on atherosclerosis by moving beyond the luminal obstruction to plaque architecture and composition—features that plausibly underpin instability. The practical challenge is no longer whether plaque vulnerability exists, but whether measuring it can be translated into decisions that improve outcomes while avoiding low-yield or unnecessary intervention (figure 1).