Background: Histopathological studies have reported the presence of cholesterol crystals in the culprit lesion in patients with sudden cardiac death. Given that cholesterol crystals themselves promote pro-inflammatory cascades, they may destabilize atherosclerotic plaques, leading to the occurrence of acute coronary events. Case summary: A 60-year-old man presented with ST-segment elevation myocardial infarction. Emergent coronary angiography revealed a severely stenotic lesion (=culprit lesion) and another non-obstructive lesion in the proximal and middle segments of the left anterior descending artery (LAD), respectively. Optical coherence tomography (OCT) imaging showed that both lesions exhibited lipid-rich plaque with cholesterol crystals, and the non-obstructive lesion in the mid-LAD did not have a thin fibrous cap (its thickness = 230 μm). A drug-eluting stent was successfully implanted at the culprit lesion in the proximal LAD. On non-contrast T1-weighted magnetic resonance imaging performed 10 days after percutaneous coronary intervention (PCI), a high-intensity signal was identified at the non-obstructive mid-LAD lesion. This lesion was medically managed with aspirin, clopidogrel, and rosuvastatin due to the absence of myocardial ischaemia. However, 12 months after PCI, the patient was hospitalized again due to unstable angina pectoris. Coronary angiography revealed substantial progression of the mid-LAD lesion. Optical coherence tomography imaging prior to the second PCI showed a severely narrowed lesion containing cholesterol crystals and covered by organized thrombus. This lesion harbored an extensive amount of lipidic materials on near-infrared spectroscopy (maximum 4-mm lipid core burden index = 809). Discussion: In our case, atherosclerotic plaques containing cholesterol crystals was associated with the occurrence of acute coronary syndrome. Our findings suggest that plaque with cholesterol crystals is a potential precursor to future acute coronary events.
ASJC Scopus subject areas