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 Park
Article

Abstract

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.

Keywords

Acute coronary syndrome Intravascular ultrasound Plaque instability Tissue factor 

References

  1. 1.
    Davies M, Thomas A (1984) Thrombosis and acute coronary artery lesions in sudden cardiac ischemic death. N Engl J Med 310:1137–1140PubMedCrossRefGoogle Scholar
  2. 2.
    Falk E, Shah PK, Fuster V (1995) Coronary plaque disruption. Circulation 92:657–671PubMedGoogle Scholar
  3. 3.
    Maehara A, Mintz GS, Bui AB, Walter OR, Castagna MT, Canos D, Pichard AD, Satler LF, Waksman R, Suddath WO, Laird JR Jr, Kent KM, Weissman NJ (2002) Morphologic and angiographic features of coronary plaque rupture detected by intravascular ultrasound. J Am Coll Cardiol 40:904–910PubMedCrossRefGoogle Scholar
  4. 4.
    Rioufol G, Gilard M, Finet G, Ginon I, Boschat J, Andre-Fouet X (2004) Evolution of spontaneous atherosclerotic plaque rupture with medical therapy: long-term follow-up with intravascular ultrasound. Circulation 110:2875–2880PubMedCrossRefGoogle Scholar
  5. 5.
    Hong MK, Mintz GS, Lee CW, Kim YH, Lee SW, Song JM, Han KH, Kang DH, Song JK, Kim JJ, Park SW, Park SJ (2004) Comparison of coronary plaque rupture between stable angina and acute myocardial infarction: a three-vessel intravascular ultrasound study in 235 patients. Circulation 110:928–933PubMedCrossRefGoogle Scholar
  6. 6.
    Thomas AC, Knapman PA, Krikler DM, Davies MJ (1988) Community study of the causes of “natural” sudden death. BMJ 297:1453–1456PubMedCrossRefGoogle Scholar
  7. 7.
    Fujii K, Kobayashi Y, Mintz GS, Takebayashi H, Dangas G, Moussa I, Mehran R, Lansky AJ, Kreps E, Collins M, Colombo A, Stone GW, Leon MB, Moses JW (2003) Intravascular ultrasound assessment of ulcerated ruptured plaques: a comparison of culprit and nonculprit lesions of patients with acute coronary syndromes and lesions in patients without acute coronary syndromes. Circulation 108:2473–2478PubMedCrossRefGoogle Scholar
  8. 8.
    Wilcox JN, Smith KM, Schwartz SM, Gordon D (1989) Localization of tissue factor in the normal vessel wall and in the atherosclerotic plaque. Proc Natl Acad Sci USA 86:2839–2843PubMedCrossRefGoogle Scholar
  9. 9.
    Tremoli E, Camera M, Toschi V, Colli S (1999) Tissue factor in atherosclerosis. Atherosclerosis 144:273–283PubMedCrossRefGoogle Scholar
  10. 10.
    Steffel J, Lüscher TF, Tanner FC (2006) Tissue factor in cardiovascular diseases molecular mechanisms and clinical implications. Circulation 113:722–731PubMedCrossRefGoogle Scholar
  11. 11.
    Murakami T, Mizuno S, Takahashi Y, Ohsato K, Moriuchi I, Arai Y, Mifune J, Shimizu M, Ohnaka M (1998) Intracoronary aspiration thrombectomy for acute myocardial infarction. Am J Cardiol 82:839–844PubMedCrossRefGoogle Scholar
  12. 12.
    Davies MJ (1990) A macro and micro view of coronary vascular insult in ischemic heart disease. Circulation 82(suppl II):II-38–II-46Google Scholar
  13. 13.
    Virmani R, Burke AP, Farb A, Kolodgie FD (2006) Pathology of the vulnerable plaque. J Am Coll Cardiol 47(8 Suppl):C13–C18PubMedCrossRefGoogle Scholar
  14. 14.
    Fujii K, Masutani M, Okumura T, Kawasaki D, Akagami T, Ezumi A, Sakoda T, Masuyama T, Ohyanagi M (2008) Frequency and predictor of coronary thin-cap fibroatheroma in patients with acute myocardial infarction and stable angina pectoris a 3-vessel optical coherence tomography study. J Am Coll Cardiol 52:787–788PubMedCrossRefGoogle Scholar
  15. 15.
    Moreno PR, Bernardi VH, Lopezcuellar J, Murcia AM, Palacios IF, Gold HK, Mehran R, Sharma SK, Nemerson Y, Fuster V, Fallon JT (1996) Macrophages, smooth muscle cells, and tissue factor in unstable angina: implications for cell-mediated thrombogenicity in acute coronary syndromes. Circulation 94:3090–3097PubMedGoogle Scholar
  16. 16.
    Annex BH, Denning SM, Channon KM, Sketch MH, Stack RS, Morrissey JH, Peters KG (1995) Differential expression of tissue factor protein in directional atherectomy specimens from patients with stable and unstable coronary syndromes. Circulation 91:619–622PubMedGoogle Scholar
  17. 17.
    Kaikita K, Ogawa H, Yasue H, Takeya M, Takahashi K, Saito T, Hayasaki K, Horiuchi K, Takizawa A, Kamikubo Y, Nakamura S (1997) Tissue factor expression on macrophages in coronary plaques in patients with unstable angina. Arterioscler Thromb Vasc Biol 17:2232–2237PubMedCrossRefGoogle Scholar
  18. 18.
    Mann J, Davies MJ (1999) Mechanisms of progression in native coronary artery disease: role of healed plaque disruption. Heart 82:265–268PubMedGoogle Scholar
  19. 19.
    Burke AP, Kolodgie FD, Farb A, Weber DK, Malcom GT, Smialek J, Virmani R (2001) Healed plaque ruptures and sudden coronary death: evidence that subclinical rupture has a role in plaque progression. Circulation 103:934–940PubMedGoogle Scholar

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
  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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