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. 2021 Mar 16;5(3):ytab095. doi: 10.1093/ehjcr/ytab095
2017 September
  • The patient was admitted to our hospital with unstable angina pectoris.

  • After primary percutaneous coronary intervention (PCI) for culprit lesion, coronary angiogram showed the presence of a non-obstructive stenotic lesion in the left main trunk artery (LMT).

  • Near-infrared spectroscopy–intravascular ultrasound (NIRS–IVUS) and optical coherence tomographic (OCT) imaging showed that the non-obstructive stenotic lesion in the LMT had lipid-rich vulnerable plaque with a thin cap and a high lipid core burden index (LCBI), which could trigger lesion-related, fatal cardiac events.

  • We treated this lesion using aggressive lipid-lowering therapy.

2017 December
  • Low density lipoprotein cholesterol significantly decreased to 14 mg/dL (91% reduction from index PCI).

  • However, the NIRS–IVUS and OCT imaging findings did not show remarkable changes in non-obstructive stenotic lesion. The maximum LCBI4mm (max LCBI4mm) value decreased from 422 to 417.

2018 May
  • The OCT imaging showed that the fibrous cap increased in size from 50 µm to 100 µm.

  • However, the decrease in the max LCBI4mm value was insufficient and was limited to 318.

2019 September
  • We continued serial observation of this lesion for up to 12 months and 24 months, respectively.

  • The grayscale IVUS imaging showed no remarkable changes were seen in the attenuation angle, which is an indicator of the lipid core.

  • We detected the stepwise decrease in the max LCBI4mm value during long-term follow-up.

  • At last follow-up, the clinical course was uneventful.