THE CORRELATION BETWEEN INFLAMMATION MEdIATORS ANd MYOCARdIAL CONTRACTILITY IN PATIENTS WITH ACuTE CORONARY SYNdROME.THE IMPACT OF EARLY INTENSIVE STATIN THERAPY

Cover Page

Cite item

Full Text

Abstract

The article highlights the impact of early intensive statin therapy on myocardial contractility in patients with acute coronary syndrome. 303 patients with ACS were enrolled in the study. All patients were randomized into two groups. 156 of them received early statin therapy by atorvastastin (80 mg/ day) or simvastatin (40 mg/day) starting from the first day of hospitalization. 147 patients received standard therapy (the control group). The left ventricle ejection fraction was assessed by echocardiography on 12-14 day of disease and after 6 months. The first assessment reveаled no significant difference between groups, while the second examination found better EF results in patients treated with high doses of statins. The statistical analysis was performed to estimate the correlation between inflammation markers and myocardial function. The negative relationship between several inflammation markers and myocardial contractility was revealed. The most significant relationship was found between LV EF and CRP and IL-6 levels. The role of inflammation markers in pathogenesis of ACS and possible mechanisms of early intensive statin therapy effect on myocardial function are being discussed.

About the authors

V I Shalnev

North-Western State Medical university named after I.I. Mechnikov

V I Mazurov

North-Western State Medical university named after I.I. Mechnikov

References

  1. Early and late benefits of high-dose atorvastatin in patients with acute coronary syndromes: results from the PROVE IT-TIMI 22 trial / K. Ray [et al.] for PROVE IT-TIMI 22 Investigators. // J. Am. Coll. Cardiol. - 2005. - Vol. 118. - P. 1405-1410.
  2. Inflammatory biomarkers, death, and recurrent nonfatal coronary events after an acute coronary syndrome in the MIRACL study/ P. Zamani [et al.] // J. Am. Heart Assoc. - 2013. - V. 2 - e003103.
  3. Шальнев В.И. Влияние раннего применения симвастатина на уровень С-реактивного белка, липиды крови и клиническое течение при остром коронарном синдроме / В.И. Шальнев // Клиническая медицина. - 2007. - № 11. - С. 46-50.
  4. Шальнев В.И. Маркеры воспаления при остром коронарном синдроме: Роль в патогенезе и прогностическое значение / В.И. Шальнев, В.И. Мазуров // Скорая медицинская помощь. - 2012. - № 2. - С. 70-76.
  5. Шальнев В.И. Влияние ранней интенсивной терапии аторвастатином и симвастатином на клиническое течение острого коронарного синдрома / В.И. Шальнев, В.И. Мазуров // Вестник Северо-Западного государственного медицинского университета им. И.И. Мечникова. - 2013. - № 3. - С. 57-62.
  6. Proinflammatory cytokines in acute myocardial infarction with and without cardiogenic shock / M. Debrunner [et al.] // Clin. Res. Cardiol. - 2008. - Vol. 97. - P. 298-305.
  7. Armstrong E.J. Inflammatory Biomarkers in Acute Coronary Syndromes: Part I: Introduction and Cytokines / E. J. Armstrong, D. A. Morrow, M. S. Sabatine // Circulation. - 2006. - Vol. 113. - P. 72-75.
  8. Мазуров В.И. Иммунологические механизмы в патогенезе коронарного атеросклероза / В.И. Мазуров, С.В. Столов, М.И. Зарайский // Терапевтический архив. - 2005. - № 9. - С. 24-28.
  9. Mann D.L. Stress-activated cytokines and the heart: from adaptation to maladaptation / D.L. Mann // Ann. Rev. Physiol. - 2003. - Vol. 65. - P. 81-101.
  10. Ridker P.M. From C-Reactive Protein to Interleukin-6 to Interleukin-1: Moving Upstream To Identify Novel Targets for Atheroprotection / P.M. Ridker // Circulation Research. - 2016. - V. 118. - P. 145-156.
  11. Jialal I. The Role of C-Reactive Protein Activation of Nuclear Factor Kappa -B in the Pathogenesis of Unstable Angina. / I. Jialal, S. Devaraj // J. Am. Coll. Cardiol. - 2007. - V. 49. - P. 195-197.
  12. A self-fulfilling prophecy: C-reactive protein attenuates nitric oxide production and inhibits angiogenesis / S.Verma [et al.] // Circulation.- 2002. - V. 106. - P. 913-919.
  13. Kitsis R. Limiting Myocardial Damage during Acute Myocardial Infarction by Inhibiting C-Reactive Protein / R. Kitsis, I. Jialal // N. Engl. J. Med. - 2006. - Vol. 355. - P. 513-516.
  14. Role of interleukin-6 in regulation of immune responses to remodeling after myocardial infarction / M. Huang [et al.] // Heart Failure Rev. - 2015. - V. 20. - P. 23-34.
  15. Effect of a single dose of the interleukin-6 receptor antagonist tocilizumab on inflammation and troponin T release in patients with non-ST-elevation myocardial infarction: a double-blind, randomized, placebo-controlled phase 2 trial / O. Kleveland [et al.] // Eur. Heart J. - 2016. - V. 30 - P. 2406-2413.
  16. Relation between expression of TNF-alpha, iNOS, VEGF mRNA and development of heart failure after experimental myocardial infarction in rats / G. Heba [et al.] // J. Physiol. Pharmacol. - 2001. - Vol. 52. - P. 39-52.
  17. Bradham W.S. Tumor necrosis factor and myocardial remodeling in progression of heart failure: a current perspec-tive / W.S. Bradham, B. Bozkurt, H. Gunasinghe // Cardiovasc. Research - 2002. - Vol. 53. - P. 822-830.
  18. Шальнев В.И. Гранулоцитарно-макрофагальный колониестимулирующий фактор при остром коронарном синдроме: содержание в крови, роль в патогенезе и прогностическое значение / В.И. Шальнев, В.И. Мазуров // Интеграция знаний в кардиологии. Материалы российского национального конгресса кардиологов. - Москва, 2012. - С. 468-469.
  19. Antibody to GM-CSF reduce the number of activated macrophages and improve left ventricle function after myocardial infarction / R. S. Kеllar [et al.] // J. Cardiovasc. Pharmacol. - 2011. - Vol. 57. - P. 568-574.
  20. Subramanian M. Identification of a Non-Growth Factor Role of GM-CSF in Advanced Atherosclerosis. Promotion of Macrophage Apoptosis and Plaque Necrosis Through IL-23 Signaling / M. Subramanian, E. Thorp, I. Tabas // Circulation Research. - 2015. - V. 116. - P. 13-24.

Copyright (c) 2017 Shalnev V.I., Mazurov V.I.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies