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Significance of intraplaque neovascularisation for vulnerability: optical coherence tomography study
  1. Jinwei Tian1,
  2. Jingbo Hou1,
  3. Lei Xing1,
  4. Soo-Joong Kim2,
  5. Taishi Yonetsu2,
  6. Koji Kato2,
  7. Hang Lee3,
  8. Shaosong Zhang4,
  9. Bo Yu1,
  10. Ik-Kyung Jang2
  1. 1Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin, China
  2. 2Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
  3. 3Biostatistics Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA
  4. 4Clinical Affairs, LightLab Imaging/St. Jude Medical, Westford, Massachusetts, USA
  1. Correspondence to Dr Bo Yu, Department of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Key Laboratories of Education Ministry for Myocardial Ischemia Mechanism and Treatment, Harbin 150086, P.R. China; yubodr{at}163.com

Abstract

Objectives This study aimed to investigate the role of intraplaque neovascularisation (NV) in culprit lesions and non-culprit lesions of unstable angina pectoris (UAP) and in lesions of stable angina pectoris (SAP) using optical coherence tomography (OCT).

Design This study was a retrospective study.

Setting The significance of NV for culprit and non-culprit plaques remains unclear.

Participants A total of 356 plaques from 92 UAP patients and 25 SAP patients who underwent OCT imaging were divided into three groups: culprit lesions in UAP (92), non-culprit lesions in UAP (203) and lesions of SAP (61).

Main outcome measures NV and plaque characteristics were examined by OCT and plaques with and without NV were compared.

Results Among UAP culprit lesions, plaques with NV had significantly higher incidence of thin cap fibroatheroma (81% vs 47%, p=0.002) compared with those without NV. In addition, the fibrous cap was thinner (56±20 μm vs 75±30 μm, p<0.001), lipid arc was greater (254±66° vs 222±65°, p=0.024) and lipid core length was longer (13±5 mm vs 10±6 mm, p=0.007). No significant difference was observed between non-culprit lesions of UAP with and without NV, and between lesions of SAP with and without NV.

Conclusion In patients with UAP, the culprit plaques with NV had vulnerable features such as thinner fibrous cap, greater lipid arc, longer lipid core length and more frequent thin cap fibroatheroma compared with those without NV. In both non-culprit lesions of UAP patients and in lesions of SAP patients NV was not associated with vulnerable plaque characteristics.

  • Neovascularisation
  • atherosclerosis
  • plaque vulnerability
  • optical coherence tomography
  • coronary artery disease, interventional cardiology, percutaneous coronary intervention (PCI)
  • lipids
  • lipid lowering
  • coronary physiology
  • imaging and diagnostics
  • fractional flow reserve, myocardial ischaemia and infarction
  • acute coronary syndrome
  • thrombolysis
  • thrombosis
  • platelets
  • intravascular ultrasound

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Footnotes

  • Funding This study was supported by grant 81171430/H1816 from the National Natural Science Foundation of China, and grant GC10C305-3 from the Science and Technology Key Project of Heilongjiang Province, China.

  • Competing interests SZ is an employee of LightLab Imaging/St. Jude Medical. IKJ received a research grant for the MGH Registry from LightLab Imaging/St. Jude Medical. JT, BY, JH, LX, SJK, TY, KK and HL report no conflicts.

  • Patient consent Obtained.

  • Ethics approval This study was approved by the ethics committee of the 2nd Affiliated Hospital of Harbin Medical University (Harbin, China).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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