Journal of Thrombosis and Thrombolysis

, Volume 32, Issue 2, pp 150–157 | Cite as

Comparison of ruptured coronary plaques in patients with unstable and stable clinical presentation

  • Cheol Whan Lee
  • Chan-Sik Park
  • Ilseon Hwang
  • Hyangsin Lee
  • Duk-Woo Park
  • Su-Jin Kang
  • Seung-Whan Lee
  • Young-Hak Kim
  • Seong-Wook Park
  • Seung-Jung ParkEmail author


It remains uncertain why some plaque ruptures trigger acute coronary syndrome (ACS), whereas others do not. We investigated the anatomic features and tissue factor (TF) expression at the sites of plaque rupture in 42 patients presenting with ACS (n = 23) or stable angina (n = 19). Intravascular ultrasound examination was performed before directional coronary atherectomy. Specimens were stained with antibodies against TF, CD68 positive phagocytic cells, and smooth muscle cells; and intravascular ultrasound and immunohistochemistry results were compared. Baseline demographic and clinical characteristics, as well as vessel and lumen sizes at both reference and lesion sites, were comparable in the two groups. However, the remodeling index and plaque burden at lesion sites were significantly greater in the ACS than in the stable angina group. The TF-immunopositive areas were significantly greater in the ACS than in the stable angina group (0.07%; IQR [0.02–0.16%] vs. 0.02%; IQR [0.01–0.05%], P = 0.022), whereas the proportions of CD68-positive and smooth muscle cell areas were similar. There was a significant correlation between areas positive for TF and those positive for CD68 (r = 0.83, P < 0.001). In conclusion, ruptured plaques in patients with ACS show stronger TF expression, a greater plaque burden, and a higher remodeling index than do plaques in those with stable angina, suggesting that both lesion morphology and local thrombogenicity are related to clinical symptoms after plaque rupture.


Acute coronary syndrome Intravascular ultrasound Plaque instability Tissue factor 



This study was supported by grants from the Asan Institute for Life Science (W08-408) and the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (A090264).

Conflict of interest



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Copyright information

© Springer Science+Business Media, LLC 2011

Authors and Affiliations

  • Cheol Whan Lee
    • 1
  • Chan-Sik Park
    • 2
  • Ilseon Hwang
    • 3
  • Hyangsin Lee
    • 4
  • Duk-Woo Park
    • 1
  • Su-Jin Kang
    • 1
  • Seung-Whan Lee
    • 1
  • Young-Hak Kim
    • 1
  • Seong-Wook Park
    • 1
  • Seung-Jung Park
    • 1
    • 5
    Email author
  1. 1.Department of Medicine, Asan Medical CenterUniversity of UlsanSeoulKorea
  2. 2.Department of Pathology, Asan Medical CenterUniversity of UlsanSeoulKorea
  3. 3.Department of Pathology, School of MedicineKeimyung UniversityDaeguKorea
  4. 4.Asan Institute of Life ScienceUniversity of UlsanSeoulKorea
  5. 5.Division of Cardiology, Asan Medical CenterUniversity of UlsanSeoulKorea

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