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Original article
Expression of HMG-CoA reductase in human coronary atherosclerotic plaques and relationship to plaque destabilisation
  1. Cheol Whan Lee1,
  2. Chan-Sik Park2,
  3. Ilseon Hwang3,
  4. Youngji Kim4,
  5. Duk-Woo Park1,
  6. Soo-Jin Kang1,
  7. Seung-Hwan Lee1,
  8. Young-Hak Kim1,
  9. Seong-Wook Park1,
  10. Seung-Jung Park1
  1. 1Department of Medicine, University of Ulsan, Seoul, Korea
  2. 2Department of Pathology, University of Ulsan, Seoul, Korea
  3. 3Department of Pathology, School of Medicine, Keimyung University, 194 Dongsan-Dong, Choong-Ku, Daegu, Korea
  4. 4Asan Insitute of Life Science, University of Ulsan, Seoul, Korea
  1. Correspondence to Dr Seung-Jung Park, Division of Cardiology, Asan Medical Center, University of Ulsan, 388-1 Pungnap-dong, Songpa-gu, Seoul, 138-736, Korea; sjpark{at}


Background Little is known about hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase expression in human coronary atherosclerotic plaques.

Objective To investigate the expression of HMG-CoA reductase in coronary atherectomy tissues obtained from patients with unstable and stable angina and examine the relationship of HMG-CoA with plaque instability.

Methods Atherectomy specimens were obtained from 43 patients with unstable (n=22) or stable (n=21) angina who underwent directional coronary atherectomy for de novo coronary artery lesions. The specimens were stained with haematoxylin–eosin and incubated with antibodies specific to HMG-CoA reductase, macrophages, smooth muscle cells and endothelial cells. Histology and immunohistochemistry data were morphometrically evaluated using an image-analysing system.

Results Baseline characteristics were similar between the two groups. Immunopositive areas of HMG-CoA reductase, macrophages, endothelial cells and thrombi were significantly greater in patients with unstable angina than those in patients with stable angina. However, the immunopositive area of smooth muscle cells was not different between the two groups. Macrophage-positive areas correlated well with areas of HMG-CoA reductase in patients with unstable angina (r=0.72, p<0.001), but not in patients with stable angina (r=0.02, p=0.937).

Conclusion HMG-CoA reductase was present in coronary atherosclerotic plaques and was more commonly expressed in unstable plaques than in stable plaques. Local HMG-CoA reductase in coronary artery lesions may contribute to plaque instability.

  • Coronary disease
  • HMG-CoA reductase
  • plaque instability
  • lipid lowering
  • acute coronary syndrome
  • angina - unstable
  • atherosclerosis
  • inflammation

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  • CWL and CSP contributed equally to this paper.

  • Funding The Korean Society of Interventional Cardiology (2007-1) and the Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea (A090264).

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval This study was conducted with the approval of the Asan Medical Center.

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