BACKGROUND: Near-infrared spectroscopy (NIRS) has been used for analysis the composition of the atherosclerotic plaque in coronary arteries. However, meaning of significant decrease in max lipid core burden index at 4 mm (max LCBI4mm) during percutaneous coronary intervention (PCI) is poorly understood. CASE SUMMARY: A 64-year-old male with unstable angina underwent coronary angiography, which demonstrated a hazy tight culprit lesion in the mid-right coronary artery. Pre-intervention NIRS-intravascular ultrasound (NIRS-IVUS) and chemogram showed plaque with high lipid burden at the culprit lesion. Then, we used a distal protection device before PCI because of high max LCBI4mm in the lesion. After pre-dilation with a scoring balloon, repeat NIRS-IVUS interrogation revealed an almost complete disappearance of the yellow signal and decrease in max LCBI4mm (from 537 to 44) significantly, suggesting decrease in the lipid content of the plaque. Finally, a drug-eluting stent deployment followed by inflation of a non-compliant balloon led to an excellent result. After PCI, we detected trapped large amounts of debris on retrieval of the filter. Pathological diagnosis confirmed that trapped material was lipid-rich plaque including cholesterol crystals. DISCUSSION: This is the first report directly demonstrated that significant decrease in max LCBI4mm at culprit lesion should be associated with the leakage of cholesterol crystals from lipid-rich plaque during PCI in the clinical patient.
BACKGROUND: Near-infrared spectroscopy (NIRS) has been used for analysis the composition of the atherosclerotic plaque in coronary arteries. However, meaning of significant decrease in max lipid core burden index at 4 mm (max LCBI4mm) during percutaneous coronary intervention (PCI) is poorly understood. CASE SUMMARY: A 64-year-old male with unstable angina underwent coronary angiography, which demonstrated a hazy tight culprit lesion in the mid-right coronary artery. Pre-intervention NIRS-intravascular ultrasound (NIRS-IVUS) and chemogram showed plaque with high lipid burden at the culprit lesion. Then, we used a distal protection device before PCI because of high max LCBI4mm in the lesion. After pre-dilation with a scoring balloon, repeat NIRS-IVUS interrogation revealed an almost complete disappearance of the yellow signal and decrease in max LCBI4mm (from 537 to 44) significantly, suggesting decrease in the lipid content of the plaque. Finally, a drug-eluting stent deployment followed by inflation of a non-compliant balloon led to an excellent result. After PCI, we detected trapped large amounts of debris on retrieval of the filter. Pathological diagnosis confirmed that trapped material was lipid-rich plaque including cholesterol crystals. DISCUSSION: This is the first report directly demonstrated that significant decrease in max LCBI4mm at culprit lesion should be associated with the leakage of cholesterol crystals from lipid-rich plaque during PCI in the clinical patient.
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