Korean Circulation Journal

  • 제42권9호
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  • Pages.595-599
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  • 2012
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  • 1738-5520(pISSN)
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  • 1738-5555(eISSN)
대한심장학회 (The Korean Society of Cardiology)
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The Effect of Doubling the Statin Dose on Pro-Inflammatory Cytokine in Patients With Triple-Vessel Coronary Artery Disease

  • Kim, Yoo-Ri (Department of Cardiology, University of Ulsan College of Medicine, Asan Medical Center) ;
  • Park, Jae-Hong (Department of Cardiology, Han-Il General Hospital) ;
  • Lee, Hye-Jin (Department of Endocrinology, Ewah Womans University School of Medicine, Ewha University Medical Center) ;
  • Pyun, Wouk-Bum (Department of Cardiology, Ewah Womans University School of Medicine, Ewha University Medical Center) ;
  • Park, Si-Hoon (Department of Cardiology, Ewah Womans University School of Medicine, Ewha University Medical Center)
  • 발행 : 2012.09.30
⟨ 이전 논문 다음 논문 ⟩

초록

Background and Objectives: Statin prevents atherosclerotic progression and helps to stabilize the plaque. According to a recent study, statin reduces inflammation in blood vessels. However, it has not been demonstrated to have any anti-inflammation reaction in patients who have been diagnosed as having a triple-vessel coronary artery disease (CAD). Subjects and Methods: This study included a total of thirty (30) patients who had been diagnosed by coronary angiogram as having a triple-vessel CAD. Patients who already had been taking statin were given doubled dosage. An interview, physical examination and blood test were performed at the beginning of this study and three months later. Results: After doubling the dose of statin, there was no statistically significant decrease in total cholesterol, low density lipoprotein-cholesterol, (increase in) high density lipoprotein-cholesterol and triglyceride in the blood test. C-reactive protein (CRP), an acute phase reactant, significantly decreased from 0.34 mg/dL at the beginning of the study to 0.12 mg/dL at the end of study (p<0.01). The interleukin-6 concentration also significantly decreased from 8.55 pg/dL to 4.81 pg/dL (p<0.001). No major cardiovascular events occurred and the dosage regimen was not modified during the close observation period. There was no difference in the symptoms of angina pectoris, established by World Health Organization Angina Questionnaires, before and after the dose increase. Liver enzymes remained within normal range with no significant increase before and after conducting this study. Conclusion: Doubling the dose of statin alone significantly lowers pro-inflammatory cytokine concentration, which is closely related to the potential acute coronary syndrome, and CRP, a marker of vascular inflammation.

키워드

참고문헌

  1. Libby P, Sasiela W. Plaque stabilization: can we turn theory into evidence? Am J Cardiol 2006;98(11A):26P-33P. https://doi.org/10.1016/j.amjcard.2006.09.017
  2. Danesh J, Wheeler JG, Hirschfield GM, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease. N Engl J Med 2004;350:1387-97. https://doi.org/10.1056/NEJMoa032804
  3. Ridker PM, Danielson E, Fonseca FA, et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N Engl J Med 2008;359:2195-207. https://doi.org/10.1056/NEJMoa0807646
  4. Biloglav Z, Ivankovic´ D, Campbell H, Rudan I. Performance of WHO Angina Questionnaire in measuring burden of coronary heart disease in human isolate populations. Coll Antropol 2004;28:205-13.
  5. Murphy NF, Stewart S, Hart CL, MacIntyre K, Hole D, McMurray JJ. A population study of the long-term consequences of Rose angina: 20- year follow-up of the Renfrew-Paisley Study. Heart 2006;92:1739- 46. https://doi.org/10.1136/hrt.2006.090118
  6. Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation: modification of Diet in Renal Disease Study Group. Ann Intern Med 1999;130:461-70. https://doi.org/10.7326/0003-4819-130-6-199903160-00002
  7. Mills R, Bhatt DL. The Yin and Yang of arterial inflammation. J Am Coll Cardiol 2004;44:50-2. https://doi.org/10.1016/j.jacc.2004.04.002
  8. Pradhan AD, Manson JE, Rifai N, Buring JE, Ridker PM. C-reactive protein, interleukin 6, and risk of developing type 2 diabetes mellitus. JAMA 2001;286:327-34. https://doi.org/10.1001/jama.286.3.327
  9. Apple FS, Wu AH, Mair J, et al. Future biomarkers for detection of ischemia and risk stratification in acute coronary syndrome. Clin Chem 2005;51:810-24. https://doi.org/10.1373/clinchem.2004.046292
  10. Shishehbor MH, Bhatt DL, Topol EJ. Using C-reactive protein to assess cardiovascular disease risk. Cleve Clin J Med 2003;70:634-40. https://doi.org/10.3949/ccjm.70.7.634
  11. Kofler S, Nickel T, Weis M. Role of cytokines in cardiovascular diseases: a focus on endothelial responses to inflammation. Clin Sci (Lond) 2005; 108:205-13. https://doi.org/10.1042/CS20040174
  12. LaRosa JC. Pleiotropic effects of statins and their clinical significance. Am J Cardiol 2001;88:291-3. https://doi.org/10.1016/S0002-9149(01)01643-5
  13. Shishehbor MH, Brennan ML, Aviles RJ, et al. Statins promote potent systemic antioxidant effects through specific inflammatory pathways. Circulation 2003;108:426-31. https://doi.org/10.1161/01.CIR.0000080895.05158.8B
  14. Ridker PM, Rifai N, Clearfield M, et al. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events. N Engl J Med 2001;344:1959-65. https://doi.org/10.1056/NEJM200106283442601
  15. Morrow DA, de Lemos JA, Sabatine MS, et al. Clinical relevance of Creactive protein during follow-up of patients with acute coronary syndromes in the Aggrastat-to-Zocor Trial. Circulation 2006;114:281-8. https://doi.org/10.1161/CIRCULATIONAHA.106.628909
  16. Ridker PM, Morrow DA, Rose LM, Rifai N, Cannon CP, Braunwald E. Relative efficacy of atorvastatin 80 mg and pravastatin 40 mg in achieving the dual goals of low-density lipoprotein cholesterol <70 mg/dl and C-reactive protein <2 mg/l: an analysis of the PROVE-IT TIMI-22 Trial. J Am Coll Cardiol 2005;45:1644-8. https://doi.org/10.1016/j.jacc.2005.02.080
  17. Ambrose JA, Martinez EE. A new paradigm for plaque stabilization. Circulation 2002;105:2000-4. https://doi.org/10.1161/01.CIR.0000012528.89469.8E
  18. Alsheikh-Ali AA, Maddukuri PV, Han H, Karas RH. Effect of the magnitude of lipid lowering on risk of elevated liver enzymes, rhabdomyolysis, and cancer: insights from large randomized statin trials. J Am Coll Cardiol 2007;50:409-18. https://doi.org/10.1016/j.jacc.2007.02.073
  19. Wenger NK, Lewis SJ, Herrington DM, Bittner V, Welty FK; the Treating to New Targets Study Steering Committee and Investigators. Outcomes of using high- or low- dose atorvastatin in patients 65 years age or older with stable coronary heart disease. Ann Intern Med 2007;147:1-9. https://doi.org/10.7326/0003-4819-147-1-200707030-00002

피인용 문헌

  1. Association between interleukin 6 and interleukin 16 gene polymorphisms and coronary heart disease risk in a Chinese population vol.41, pp.4, 2012, https://doi.org/10.1177/0300060513483405
  2. High-dose atorvastatin for preventing contrast-induced nephropathy in primary percutaneous coronary intervention : vol.16, pp.3, 2012, https://doi.org/10.2459/jcm.0000000000000157