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Antioxidative Activity after Rosuvastatin Treatment in Patients with Stable Ischemic Heart Disease and Decreased High Density Lipoprotein Cholesterol

  • Park, Do-Sim (Department of Laboratory medicine, Wonkwang University Hospital and School of Medicine) ;
  • Yun, Kyeong Ho (Department of Cardiovascular Medicine, Regional Cardiocerebrovascular Center, Wonkwang University Hospital) ;
  • Park, Hyun Young (Institute of Wonkwang Medical Science, Wonkwang University School of Medicine) ;
  • Rhee, Sang Jae (Department of Cardiovascular Medicine, Regional Cardiocerebrovascular Center, Wonkwang University Hospital) ;
  • Kim, Nam-Ho (Department of Cardiovascular Medicine, Regional Cardiocerebrovascular Center, Wonkwang University Hospital) ;
  • Oh, Seok Kyu (Department of Cardiovascular Medicine, Regional Cardiocerebrovascular Center, Wonkwang University Hospital) ;
  • Jeong, Jin-Won (Department of Cardiovascular Medicine, Regional Cardiocerebrovascular Center, Wonkwang University Hospital)
  • Received : 2015.07.17
  • Accepted : 2015.10.06
  • Published : 2016.05.30

Abstract

Background and Objectives: The clinical significance of statin-induced high-density lipoprotein cholesterol (HDL-C) changes is not well known. We investigated whether rosuvastatin-induced HDL-C changes can influence the anti-oxidative action of high-density lipoprotein particle. Subjects and Methods: A total of 240 patients with stable ischemic heart disease were studied. Anti-oxidative property was assessed by paraoxonase 1 (PON1) activity. We compared the lipid profile and PON1 activity at baseline and at 8 weeks after rosuvastatin 10 mg treatment. Results: Rosuvastatin treatment increased the mean HDL-C concentration by $1.9{\pm}9.2mg/dL$ ($6.4{\pm}21.4%$). HDL-C increased in 138 patients (57.5%), but decreased in 102 patients (42.5%) after statin treatment. PON1 activity increased to 19.1% in all patients. In both, the patients with increased HDL-C and with decreased HDL-C, PON1 activity significantly increased after rosuvastatin treatment (+19.3% in increased HDL-C responder; p=0.018, +18.8% in decreased HDL-C responder; p=0.045 by paired t-test). Baseline PON1 activity modestly correlated with HDL-C levels (r=0.248, p=0.009); however, the PON1 activity evaluated during the course of the treatment did not correlate with HDL-C levels (r=0.153, p=0.075). Conclusion: Rosuvastatin treatment improved the anti-oxidative properties as assessed by PON1 activity, regardless of on-treatment HDL-C levels, in patients with stable ischemic heart disease.

Keywords

Acknowledgement

Supported by : The Korean Society of Cardiology, NRF of Korea

References

  1. Randomized trial of cholesterol lowering in 4444 patients with coronary heart disease: the Sacandinavian Simvastatin Survival Study (4S). Lancet 1994;344:1383-9.
  2. Shepherd J, Cobbe SM, Ford I, et al. Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland coronary prevention study group. N Engl J Med 1995;333:1301-7. https://doi.org/10.1056/NEJM199511163332001
  3. Hong YJ, Jeong MH, Lim JH, et al. The prognostic significance of statin therapy according to the level of C-reactive protein in acute myocardial infarction patients who underwent percutaneous coronary intervention. Korean Circ J 2003;33:891-900. https://doi.org/10.4070/kcj.2003.33.10.891
  4. Ridker PM, Danielson E, Fonseca FA, et al. Reduction in C-reactive protein and LDL cholesterol and cardiovascular event rates after initiation of rosuvastatin: a prospective study of the JUPITER trial. Lancet 2009;373:1175-82. https://doi.org/10.1016/S0140-6736(09)60447-5
  5. Sim DS, Jeong MH, Cho KH, et al. Effect of early statin treatment in patients with cardiogenic shock complicating acute myocardial infarction. Korean Circ J 2013;43:100-9. https://doi.org/10.4070/kcj.2013.43.2.100
  6. Yamashita S, Tsubakio-Yamamoto K, Ohama T, Nakagawa-Toyama Y, Nishida M. Molecular mechanisms of HDL-cholesterol elevation by statins and its effects on HDL functions. J Atheroscler Thromb 2010;17:436-51. https://doi.org/10.5551/jat.5405
  7. Aviram M, Rosenblat M, Bisgaier CL, Newton RS, Primo-Parmo SL, La Du BN. Paraoxonase inhibits high-density lipoprotein oxidation and preserves its functions. A possible peroxidative role for paraoxonase. J Clin Invest 1998;101:1581-90. https://doi.org/10.1172/JCI1649
  8. McElveen J, Mackness MI, Colley CM, Peard T, Warner S, Walker CH. Distribution of paraoxon hydrolytic activity in the serum of patients after myocardial infarction. Clin Chem 1986;32:671-3.
  9. Yun KH, Shin SN, Ko JS, et al. Rosuvastatin-induced high-density lipoprotein changes in patients who underwent percutaneous coronary intervention for non-ST-segment elevation acute coronary syndrome. J Cardiol 2012;60:383-8. https://doi.org/10.1016/j.jjcc.2012.07.008
  10. Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012;60:1581-98. https://doi.org/10.1016/j.jacc.2012.08.001
  11. Cebeci E, Oner FA, Usta M, Yurdakul S, Erguney M. Evaluation of oxidative stress, the activities of paraoxonase and arylesterase in patients with subclinic hypothyroidism. Acta Biomed 2011;82:214-22.
  12. Ray KK, Cannon CP, Cairns R, Morrow DA, Ridker PM, Braunwald E. Prognostic utility of apoB/AI, total cholesterol/HDL, non-HDL cholesterol, or hs-CRP as predictors of clinical risk in patients receiving statin therapy after acute coronary syndromes: results from PROVE IT-TIMI 22. Arterioscler Thromb Vasc Biol 2009;29:424-30. https://doi.org/10.1161/ATVBAHA.108.181735
  13. Ridker PM, Genest J, Boekholdt SM, et al. HDL cholesterol and residual risk of first cardiovascular events after treatment with potent statin therapy: an analysis from the JUPITER trial. Lancet 2010;376:333-9. https://doi.org/10.1016/S0140-6736(10)60713-1
  14. Barter PJ, Caufield M, Eriksson M, et al. Effects of torcetrapib in patients at high risk for coronary events. N Engl J Med 2007;357:2109-22. https://doi.org/10.1056/NEJMoa0706628
  15. AIM-HIGH Investigators, Boden WE, Probstfield JL, et al. Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. N Engl J Med 2011;365:2255-67. https://doi.org/10.1056/NEJMoa1107579
  16. Mora S, Glynn RJ, Ridker PM. High-density lipoprotein cholesterol, size, particle number, and residual vascular risk after potent statin therapy. Circulation 2013;128:1189-97. https://doi.org/10.1161/CIRCULATIONAHA.113.002671
  17. Mazer NA, Giulianini F, Paynter NP, Jordan P, Mora S. A comparison of the theoretical relationship between HDL size and the ratio of HDL cholesterol to apolipoprotein A-I with experimental results from the Women's Health Study. Clin Chem 2013;59:949-58. https://doi.org/10.1373/clinchem.2012.196949
  18. Nagila A, Permpongpaiboon T, Tantrarongroj S, et al. Effect of atorvastatin on paraoxonase1 (PON1) and oxidative status. Pharmacol Rep 2009;61:892-8. https://doi.org/10.1016/S1734-1140(09)70146-X
  19. Miyamoto-Sasaki M, Yasuda T, Monguchi T, et al. Pitavastatin increases HDL particles functionally preserved with cholesterol efflux capacity and antioxidative actions in dyslipidemic patients. J Atheroscler Thromb 2013;20:708-16. https://doi.org/10.5551/jat.17210
  20. Harangi M, Seres I, Harangi J, Paragh G. Benefits and difficulties in measuring HDL subfractions and human paraoxonase-1 activity during statin treatment. Cardiovasc Drugs Ther 2009;23:501-10. https://doi.org/10.1007/s10557-009-6205-4
  21. Blatter MC, James RW, Messmer S, Barja F, Pometta D. Identification of a distinct human high-density lipoprotein subspecies defined by a lipoprotein-associated protein, K-45. Identity of K-45 with paraoxonase. Eur J Biochem 1993;211:871-9. https://doi.org/10.1111/j.1432-1033.1993.tb17620.x
  22. Mackness MI, Arrol S, Abbott C, Durrington PN. Protection of low-density lipoprotein against oxidative modification by high-density lipoprotein associated paraoxonase. Atherosclerosis 1993;104:129-35. https://doi.org/10.1016/0021-9150(93)90183-U

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