Снижение концентрации С-реактивного белка, измеренного высокочувствительным методом, на фоне высокоинтенсивной терапии статинами перед коронарным стентированием: возможная связь с последующим прогрессированием атеросклероза
Снижение концентрации С-реактивного белка, измеренного высокочувствительным методом, на фоне высокоинтенсивной терапии статинами перед коронарным стентированием: возможная связь с последующим прогрессированием атеросклероза
Щинова А.М., Шлевкова Г.В., Филатова А.Ю. и др. Снижение концентрации С-реактивного белка, измеренного высокочувствительным методом, на фоне высокоинтенсивной терапии статинами перед коронарным стентированием: возможная связь с последующим прогрессированием атеросклероза. Терапевтический архив. 2019; 91 (9): 10–15. DOI: 10.26442/00403660.2019.09.000144
________________________________________________
Материалы доступны только для специалистов сферы здравоохранения. Авторизуйтесь или зарегистрируйтесь.
Аннотация
Провоспалительный статус является фактором риска прогрессии коронарного атеросклероза (АС) после коронарного стентирования (КС). Высокоинтенсивная терапия статинами ассоциирована со снижением концентрации С-реактивного белка, измеренного высокочувствительным методом (вчСРБ).
Цель исследования: определение прогностической значимости снижения предпроцедурного содержания вчСРБ на фоне высокоинтенсивной терапии статинами в отношении прогрессии коронарного АС в течение года после КС.
Материалы и методы. В исследование включено 102 пациента со стабильной стенокардией напряжения перед плановым КС. Группу I (n=37) составили пациенты, получавшие 80 мг аторвастатина в течение 7 сут перед и в течение 3 мес после КС с дальнейшей коррекцией дозы с учетом содержания липопротеинов низкой плотности (ЛПНП); группу II (n=65) – пациенты, получавшие 20–40 мг/сут аторвастатина с целью достижения оптимального уровня ЛПНП. Концентрация вчСРБ определялась исходно, перед КС и через 1, 3, 6 и 12 мес. Прогрессирование коронарного АС диагностировалось при выявлении нового стеноза (≥50%) или усугублении существовавшего (≥20%) как минимум на 30% при коронароангиографии (КАГ) через год после КС.
Результаты. Исходная концентрация вчСРБ была сопоставимой: 0,21 (0,13; 0,38) и 0,20 (0,1; 0,44) мг/дл (p>0,05) в группах I и II соответственно. В группе I значимое снижение вчСРБ наблюдалось после недели терапии: 0,14 (0,07;0,32) мг/дл перед КС (p<0,05). Прогрессия коронарного АС зарегистрирована у 10 (41%) пациентов группы I и у 20 (47%) – группы II при контрольной КАГ. Концентрация вчСРБ ≥0,26 мг/дл в предпроцедурном периоде ассоциировалась с прогрессированием коронарного АС в течение года (отношение шансов 4,2 для объединенной группы пациентов, 95% доверительный интервал 1,4–12,3; p=0,01).
Заключение. Высокий уровень вчСРБ перед КС ассоциирован с прогрессией коронарного АС в течение года. Высокоинтенсивная терапия аторвастатином в течение недели перед КС снижает предпроцедурный уровень вчСРБ.
Ключевые слова: атеросклероз, воспаление, коронарное стентирование, С-реактивный белок, измеренный высокочувствительным методом, холестерин липопротеинов низкой плотности.
Aim: to evaluate prognostic significance of preprocedural hsCRP level reduction with intensive statin regimen for coronary atherosclerosis progression during one year after CS.
Materials and methods. We enrolled 102 patients with stable angina who were on list for scheduled CS. Group I (n=37) patients received atorvastatin 80 mg for 7 days before and 3 months after CS with further dose adjustment according to LDL; group II (n=65) patients received atorvastatin 20–40 mg/day for LDL goal achievement. HsCRP level was assessed at baseline, before CS and after 1, 3, 6 and 12 months. Coronary atherosclerosis progression was defined as new ≥50% stenosis or ≥30% increase of ≥20% pre-existing stenosis according to coronary angiography (CA) 1 year after CS.
Results. Baseline concentration of hsCRP was comparable: 0.21 (0.13; 0.38) vs. 0.20 (0.1; 0.44) mg/dl in groups I и II, respectively (p>0.05). In group I significant hsCRP level decrease to 0.14 (0.07; 0.32) mg/dl (p<0.05) was determined after 7 days. Coronary atherosclerosis progression was revealed in 10 (41%) patients in group I and in 20 (47%) in group II according to CA. HsCRP level ≥0.26 was associated with coronary atherosclerosis progression during 12 months (OR 4.2 for total study group, 95% CI 1.4–12.3; р=0.01).
Conclusion. Elevated preprocedural hsCRP level is associated with coronary atherosclerosis progression after CS. Intensive atorvastatin regimen for one week before CS leads to preprocedural hsCRP level reduction.
Keywords: atherosclerosis, inflammation, coronary stenting, high-sensitivity C-reactive protein, low-density lipoproteins, hsCRP, LDL.
Цель исследования: определение прогностической значимости снижения предпроцедурного содержания вчСРБ на фоне высокоинтенсивной терапии статинами в отношении прогрессии коронарного АС в течение года после КС.
Материалы и методы. В исследование включено 102 пациента со стабильной стенокардией напряжения перед плановым КС. Группу I (n=37) составили пациенты, получавшие 80 мг аторвастатина в течение 7 сут перед и в течение 3 мес после КС с дальнейшей коррекцией дозы с учетом содержания липопротеинов низкой плотности (ЛПНП); группу II (n=65) – пациенты, получавшие 20–40 мг/сут аторвастатина с целью достижения оптимального уровня ЛПНП. Концентрация вчСРБ определялась исходно, перед КС и через 1, 3, 6 и 12 мес. Прогрессирование коронарного АС диагностировалось при выявлении нового стеноза (≥50%) или усугублении существовавшего (≥20%) как минимум на 30% при коронароангиографии (КАГ) через год после КС.
Результаты. Исходная концентрация вчСРБ была сопоставимой: 0,21 (0,13; 0,38) и 0,20 (0,1; 0,44) мг/дл (p>0,05) в группах I и II соответственно. В группе I значимое снижение вчСРБ наблюдалось после недели терапии: 0,14 (0,07;0,32) мг/дл перед КС (p<0,05). Прогрессия коронарного АС зарегистрирована у 10 (41%) пациентов группы I и у 20 (47%) – группы II при контрольной КАГ. Концентрация вчСРБ ≥0,26 мг/дл в предпроцедурном периоде ассоциировалась с прогрессированием коронарного АС в течение года (отношение шансов 4,2 для объединенной группы пациентов, 95% доверительный интервал 1,4–12,3; p=0,01).
Заключение. Высокий уровень вчСРБ перед КС ассоциирован с прогрессией коронарного АС в течение года. Высокоинтенсивная терапия аторвастатином в течение недели перед КС снижает предпроцедурный уровень вчСРБ.
Ключевые слова: атеросклероз, воспаление, коронарное стентирование, С-реактивный белок, измеренный высокочувствительным методом, холестерин липопротеинов низкой плотности.
________________________________________________
Aim: to evaluate prognostic significance of preprocedural hsCRP level reduction with intensive statin regimen for coronary atherosclerosis progression during one year after CS.
Materials and methods. We enrolled 102 patients with stable angina who were on list for scheduled CS. Group I (n=37) patients received atorvastatin 80 mg for 7 days before and 3 months after CS with further dose adjustment according to LDL; group II (n=65) patients received atorvastatin 20–40 mg/day for LDL goal achievement. HsCRP level was assessed at baseline, before CS and after 1, 3, 6 and 12 months. Coronary atherosclerosis progression was defined as new ≥50% stenosis or ≥30% increase of ≥20% pre-existing stenosis according to coronary angiography (CA) 1 year after CS.
Results. Baseline concentration of hsCRP was comparable: 0.21 (0.13; 0.38) vs. 0.20 (0.1; 0.44) mg/dl in groups I и II, respectively (p>0.05). In group I significant hsCRP level decrease to 0.14 (0.07; 0.32) mg/dl (p<0.05) was determined after 7 days. Coronary atherosclerosis progression was revealed in 10 (41%) patients in group I and in 20 (47%) in group II according to CA. HsCRP level ≥0.26 was associated with coronary atherosclerosis progression during 12 months (OR 4.2 for total study group, 95% CI 1.4–12.3; р=0.01).
Conclusion. Elevated preprocedural hsCRP level is associated with coronary atherosclerosis progression after CS. Intensive atorvastatin regimen for one week before CS leads to preprocedural hsCRP level reduction.
Keywords: atherosclerosis, inflammation, coronary stenting, high-sensitivity C-reactive protein, low-density lipoproteins, hsCRP, LDL.
Список литературы
1. Гребенщикова И.А. Эпидемиология ишемической болезни сердца и значение показателей периферического атеросклероза и функционального состояния почек в развитии коронарной болезни сердца у мужчин. Современные проблемы науки и образования. 2011;(5) [Grebenshchikova IA. Epidemiology of coronary artery disease and significance of indices of peripheral atherosclerosis and functional state of the kidneys in the development of ischemic heart disease in men. Sovremennye problemy nauki i obrazovaniya. 2011;(5) (In Russ.)].
2. Williams TN, Zhang CX, Game BA, He L, Huang Y. C-reactive protein stimulates MMP-1 expression in U937 histiocytes through Fc[gamma]RII and extracellular signal-regulated kinase pathway:: an implication of CRP involvement in plaque destabilization. Arterioscler Thromb Vasc Biol. 2004;24:61-6. doi: 10.1161/01.ATV.0000104014.24367.16
3. Wågsäter D, Zhu C, Björkegren J, Skogsberg J, Eriksson P. MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the Ldlr(-/-)Apob(100/100) mouse. Int J Mol Med. 2011;28:247-53. doi: 10.3892/ijmm.2011.693
4. Dabek J, Glogowska-Ligus J, Szadorska B. Transcription activity of MMP-2 and MMP-9 metalloproteinase genes and their tissue inhibitor (TIMP-2) in acute coronary syndrome patients. J Postgrad Med. 2013;59:115-20. doi: 10.4103/0022-3859.113836
5. Guo C, et al. Correlation between the severity of coronary artery lesions and levels of estrogen, hs-CRP and MMP-9. Exp Ther Med. 2014;7:1177-80. doi: 10.3892/etm.2014.1565
6. Szalai AJ, Agrawal A, Greenhough TJ, Volanakis, JE. C-reactive protein: structural biology, gene expression, and host defense function. Immunol Res. 1997;16:127-36. doi: 10.1007/BF02786357
7. Szmitko PE, Verma S. C-reactive protein and statins: IL-8 as a molecular link? Clin Sci Lond Engl. 2005;108:493-5. doi: 10.1042/CS20050093
8. Singh U, Devaraj S, Jialal I. C-reactive protein decreases tissue plasminogen activator activity in human aortic endothelial cells: evidence that C-reactive protein is a procoagulant. Arterioscler Thromb Vasc Biol. 2005;25:2216-21. doi: 10.1161/01.ATV.0000183718.62409.ea
9. Devaraj S, Xu DY, Jialal I. C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis. Circulation. 2003;107:398-404. doi: 10.1161/01.cir. 0000052617.91920.fd
10. Mirjanic-Azaric B, et al. Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: pleiotropic evidence from plasma mRNA analyses. Clin Biochem. 2013;46:1526-31. doi: 10.1016/j.clinbiochem.2013.06.006
11. Ferri C, et al. C-reactive protein: interaction with the vascular endothelium and possible role in human atherosclerosis. Curr Pharm Des. 2007;13:1631-45. doi: 10.2174/138161207780831301
12. Libby P, Ridker PM. Novel inflammatory markers of coronary risk: theory versus practice. Circulation. 1999;100:1148-50. doi: 10.1161/01.cir.100.11.1148
13. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005;352:20-8. doi: 10.1056/NEJMoa042378
14. Takemoto M, Liao JK. Pleiotropic effects of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712-9. doi: 10.1161/hq1101.098486
15. Mausner-Fainberg K, et al. The effect of HMG-CoA reductase inhibitors on naturally occurring CD4+CD25+ T-cells. Atherosclerosis. 2008;197:829-39. doi: 10.1016/j.atherosclerosis.2007.07.031
16. Nissen SE, et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA. 2004;291:1071-80. doi: 10.1001/jama.291.9.1071
17. Albert MA, Danielson E, Rifai N, Ridker PM. PRINCE Investigators. Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study. JAMA. 2001;286:64-70. doi: 10.1001/jama.286.1.64
18. Kim J-S, et al. Efficacy of high-dose atorvastatin loading before primary percutaneous coronary intervention in ST-segment elevation myocardial infarction: the STATIN STEMI trial. JACC Cardiovasc Interv. 2010;3:332-9. doi: 10.1016/j.jcin.2009.11.021
19. Isaacsohn JL, et al. Aggressive Lipid-Lowering Initiation Abates New Cardiac Events (ALLIANCE)-rationale and design of atorvastatin versus usual care in hypercholesterolemic patients with coronary artery disease. Am J Cardiol. 2000;86:250-2. doi: 10.1016/s0002-9149(00)00872-9
20. LaRosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352:1425-35. doi: 10.1056/NEJMoa050461
21. Рекомендации по лечению стабильной ишемической болезни сердца ESC. https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines
22. Kinlay S, et al. High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation. 2003;108:1560-6. doi: 10.1161/01.CIR.0000091404.09558.AF
23. Loppnow H, et al. Statins potently reduce the cytokine-mediated IL-6 release in SMC/MNC cocultures. J Cell Mol Med. 2011;15:994-1004. doi: 10.1111/j.1582-4934.2010.01036.x
24. Miyazaki Y, et al. Effect of statins on atherogenic serum amyloid A and α1-antitrypsin low-density lipoprotein complexes. Int J Cardiol. 2016;225:332-6. doi: 10.1016/j.ijcard.2016.09.116
25. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001;103:1813-8. doi: 10.1161/01.cir. 103.13.1813
26. Park D-W, et al. C-reactive protein and the risk of stent thrombosis and cardiovascular events after drug-eluting stent implantation. Circulation. 2009;120:1987-95. doi: 10.1161/CIRCULATIONAHA.109.876763
27. Delhaye C, et al. Long-term prognostic value of preprocedural C-reactive protein after drug-eluting stent implantation. Am J Cardiol. 2010;105:826-32. doi: 10.1016/j.amjcard.2009.10.064
28. Iijima R, et al. Pre-procedural C-reactive protein levels and clinical outcomes after percutaneous coronary interventions with and without abciximab: pooled analysis of four ISAR trials. Heart Br Card Soc. 2009;95:107-12. doi: 10.1136/hrt.2008.153635
29. Park D-W, et al. Prognostic impact of preprocedural C reactive protein levels on 6-month angiographic and 1-year clinical outcomes after drug-eluting stent implantation. Heart Br Card Soc. 2007;93:1087-92. doi: 10.1136/hrt.2006.099762
30. Ridker PM, et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial. Lancet Lond Engl. 2017. doi:10.1016/S0140-6736(17)32814-3.
31. Mor A, Luboshits G, Planer D, Keren G, George J. Altered status of CD4(+)CD25(+) regulatory T-cells in patients with acute coronary syndromes. Eur Heart J. 2006;27:2530-7. doi: 10.1093/eurheartj/ehl222
32. Kim YC, Kim KK, Shevach EM. Simvastatin induces Foxp3+ T regulatory cells by modulation of transforming growth factor-beta signal transduction. Immunology. 2010;130:484-93. doi: 10.1111/j.1365-2567.2010.03269.x
33. Meng X, et al. Statins induce the accumulation of regulatory T-cells in atherosclerotic plaque. Mol Med Camb Mass. 2012;18:598-605. doi: 10.2119/molmed.2011.00471
34. Filatova AYu, Kuznetsova GV, Shchinova AM, Osokina AK, Potekhina AV, et al. Influence of short-term intensive atorvastatin therapy on lymphocyte and monocyte subpopulations and CCR2, CCR5, CX3CR1 and TLR4 expression in blood of patients with stable angina. 85th EAS Congress, Prague, 2016.
35. Nabatov AA, Pollakis G, Linnemann T, Paxton WA, de Baar MP. Statins disrupt CCR5 and RANTES expression levels in CD4(+) T-lymphocytes in vitro and preferentially decrease infection of R5 versus X4 HIV-1. PloS One. 2007;(2):e470. doi: 10.1371/journal.pone.0000470
36. Veillard NR, et al. Simvastatin modulates chemokine and chemokine receptor expression by geranylgeranyl isoprenoid pathway in human endothelial cells and macrophages. Atherosclerosis. 2006;188:51-8. doi: 10.1016/j.atherosclerosis.2005.10.015
37. Martínez-González J, Alfón J, Berrozpe M, Badimon L. HMG-CoA reductase inhibitors reduce vascular monocyte chemotactic protein-1 expression in early lesions from hypercholesterolemic swine independently of their effect on plasma cholesterol levels. Atherosclerosis. 2001;159:27-33. doi: 10.1016/S0021-9150(01)00469-5
2. Williams TN, Zhang CX, Game BA, He L, Huang Y. C-reactive protein stimulates MMP-1 expression in U937 histiocytes through Fc[gamma]RII and extracellular signal-regulated kinase pathway:: an implication of CRP involvement in plaque destabilization. Arterioscler Thromb Vasc Biol. 2004;24:61-6. doi: 10.1161/01.ATV.0000104014.24367.16
3. Wågsäter D, Zhu C, Björkegren J, Skogsberg J, Eriksson P. MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the Ldlr(-/-)Apob(100/100) mouse. Int J Mol Med. 2011;28:247-53. doi: 10.3892/ijmm.2011.693
4. Dabek J, Glogowska-Ligus J, Szadorska B. Transcription activity of MMP-2 and MMP-9 metalloproteinase genes and their tissue inhibitor (TIMP-2) in acute coronary syndrome patients. J Postgrad Med. 2013;59:115-20. doi: 10.4103/0022-3859.113836
5. Guo C, et al. Correlation between the severity of coronary artery lesions and levels of estrogen, hs-CRP and MMP-9. Exp Ther Med. 2014;7:1177-80. doi: 10.3892/etm.2014.1565
6. Szalai AJ, Agrawal A, Greenhough TJ, Volanakis, JE. C-reactive protein: structural biology, gene expression, and host defense function. Immunol Res. 1997;16:127-36. doi: 10.1007/BF02786357
7. Szmitko PE, Verma S. C-reactive protein and statins: IL-8 as a molecular link? Clin Sci Lond Engl. 2005;108:493-5. doi: 10.1042/CS20050093
8. Singh U, Devaraj S, Jialal I. C-reactive protein decreases tissue plasminogen activator activity in human aortic endothelial cells: evidence that C-reactive protein is a procoagulant. Arterioscler Thromb Vasc Biol. 2005;25:2216-21. doi: 10.1161/01.ATV.0000183718.62409.ea
9. Devaraj S, Xu DY, Jialal I. C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis. Circulation. 2003;107:398-404. doi: 10.1161/01.cir. 0000052617.91920.fd
10. Mirjanic-Azaric B, et al. Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: pleiotropic evidence from plasma mRNA analyses. Clin Biochem. 2013;46:1526-31. doi: 10.1016/j.clinbiochem.2013.06.006
11. Ferri C, et al. C-reactive protein: interaction with the vascular endothelium and possible role in human atherosclerosis. Curr Pharm Des. 2007;13:1631-45. doi: 10.2174/138161207780831301
12. Libby P, Ridker PM. Novel inflammatory markers of coronary risk: theory versus practice. Circulation. 1999;100:1148-50. doi: 10.1161/01.cir.100.11.1148
13. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005;352:20-8. doi: 10.1056/NEJMoa042378
14. Takemoto M, Liao JK. Pleiotropic effects of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712-9. doi: 10.1161/hq1101.098486
15. Mausner-Fainberg K, et al. The effect of HMG-CoA reductase inhibitors on naturally occurring CD4+CD25+ T-cells. Atherosclerosis. 2008;197:829-39. doi: 10.1016/j.atherosclerosis.2007.07.031
16. Nissen SE, et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA. 2004;291:1071-80. doi: 10.1001/jama.291.9.1071
17. Albert MA, Danielson E, Rifai N, Ridker PM. PRINCE Investigators. Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study. JAMA. 2001;286:64-70. doi: 10.1001/jama.286.1.64
18. Kim J-S, et al. Efficacy of high-dose atorvastatin loading before primary percutaneous coronary intervention in ST-segment elevation myocardial infarction: the STATIN STEMI trial. JACC Cardiovasc Interv. 2010;3:332-9. doi: 10.1016/j.jcin.2009.11.021
19. Isaacsohn JL, et al. Aggressive Lipid-Lowering Initiation Abates New Cardiac Events (ALLIANCE)-rationale and design of atorvastatin versus usual care in hypercholesterolemic patients with coronary artery disease. Am J Cardiol. 2000;86:250-2. doi: 10.1016/s0002-9149(00)00872-9
20. LaRosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352:1425-35. doi: 10.1056/NEJMoa050461
21. Рекомендации по лечению стабильной ишемической болезни сердца ESC. https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines
22. Kinlay S, et al. High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation. 2003;108:1560-6. doi: 10.1161/01.CIR.0000091404.09558.AF
23. Loppnow H, et al. Statins potently reduce the cytokine-mediated IL-6 release in SMC/MNC cocultures. J Cell Mol Med. 2011;15:994-1004. doi: 10.1111/j.1582-4934.2010.01036.x
24. Miyazaki Y, et al. Effect of statins on atherogenic serum amyloid A and α1-antitrypsin low-density lipoprotein complexes. Int J Cardiol. 2016;225:332-6. doi: 10.1016/j.ijcard.2016.09.116
25. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001;103:1813-8. doi: 10.1161/01.cir. 103.13.1813
26. Park D-W, et al. C-reactive protein and the risk of stent thrombosis and cardiovascular events after drug-eluting stent implantation. Circulation. 2009;120:1987-95. doi: 10.1161/CIRCULATIONAHA.109.876763
27. Delhaye C, et al. Long-term prognostic value of preprocedural C-reactive protein after drug-eluting stent implantation. Am J Cardiol. 2010;105:826-32. doi: 10.1016/j.amjcard.2009.10.064
28. Iijima R, et al. Pre-procedural C-reactive protein levels and clinical outcomes after percutaneous coronary interventions with and without abciximab: pooled analysis of four ISAR trials. Heart Br Card Soc. 2009;95:107-12. doi: 10.1136/hrt.2008.153635
29. Park D-W, et al. Prognostic impact of preprocedural C reactive protein levels on 6-month angiographic and 1-year clinical outcomes after drug-eluting stent implantation. Heart Br Card Soc. 2007;93:1087-92. doi: 10.1136/hrt.2006.099762
30. Ridker PM, et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial. Lancet Lond Engl. 2017. doi:10.1016/S0140-6736(17)32814-3.
31. Mor A, Luboshits G, Planer D, Keren G, George J. Altered status of CD4(+)CD25(+) regulatory T-cells in patients with acute coronary syndromes. Eur Heart J. 2006;27:2530-7. doi: 10.1093/eurheartj/ehl222
32. Kim YC, Kim KK, Shevach EM. Simvastatin induces Foxp3+ T regulatory cells by modulation of transforming growth factor-beta signal transduction. Immunology. 2010;130:484-93. doi: 10.1111/j.1365-2567.2010.03269.x
33. Meng X, et al. Statins induce the accumulation of regulatory T-cells in atherosclerotic plaque. Mol Med Camb Mass. 2012;18:598-605. doi: 10.2119/molmed.2011.00471
34. Filatova AYu, Kuznetsova GV, Shchinova AM, Osokina AK, Potekhina AV, et al. Influence of short-term intensive atorvastatin therapy on lymphocyte and monocyte subpopulations and CCR2, CCR5, CX3CR1 and TLR4 expression in blood of patients with stable angina. 85th EAS Congress, Prague, 2016.
35. Nabatov AA, Pollakis G, Linnemann T, Paxton WA, de Baar MP. Statins disrupt CCR5 and RANTES expression levels in CD4(+) T-lymphocytes in vitro and preferentially decrease infection of R5 versus X4 HIV-1. PloS One. 2007;(2):e470. doi: 10.1371/journal.pone.0000470
36. Veillard NR, et al. Simvastatin modulates chemokine and chemokine receptor expression by geranylgeranyl isoprenoid pathway in human endothelial cells and macrophages. Atherosclerosis. 2006;188:51-8. doi: 10.1016/j.atherosclerosis.2005.10.015
37. Martínez-González J, Alfón J, Berrozpe M, Badimon L. HMG-CoA reductase inhibitors reduce vascular monocyte chemotactic protein-1 expression in early lesions from hypercholesterolemic swine independently of their effect on plasma cholesterol levels. Atherosclerosis. 2001;159:27-33. doi: 10.1016/S0021-9150(01)00469-5
2. Williams TN, Zhang CX, Game BA, He L, Huang Y. C-reactive protein stimulates MMP-1 expression in U937 histiocytes through Fc[gamma]RII and extracellular signal-regulated kinase pathway:: an implication of CRP involvement in plaque destabilization. Arterioscler Thromb Vasc Biol. 2004;24:61-6. doi: 10.1161/01.ATV.0000104014.24367.16
3. Wågsäter D, Zhu C, Björkegren J, Skogsberg J, Eriksson P. MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the Ldlr(-/-)Apob(100/100) mouse. Int J Mol Med. 2011;28:247-53. doi: 10.3892/ijmm.2011.693
4. Dabek J, Glogowska-Ligus J, Szadorska B. Transcription activity of MMP-2 and MMP-9 metalloproteinase genes and their tissue inhibitor (TIMP-2) in acute coronary syndrome patients. J Postgrad Med. 2013;59:115-20. doi: 10.4103/0022-3859.113836
5. Guo C, et al. Correlation between the severity of coronary artery lesions and levels of estrogen, hs-CRP and MMP-9. Exp Ther Med. 2014;7:1177-80. doi: 10.3892/etm.2014.1565
6. Szalai AJ, Agrawal A, Greenhough TJ, Volanakis, JE. C-reactive protein: structural biology, gene expression, and host defense function. Immunol Res. 1997;16:127-36. doi: 10.1007/BF02786357
7. Szmitko PE, Verma S. C-reactive protein and statins: IL-8 as a molecular link? Clin Sci Lond Engl. 2005;108:493-5. doi: 10.1042/CS20050093
8. Singh U, Devaraj S, Jialal I. C-reactive protein decreases tissue plasminogen activator activity in human aortic endothelial cells: evidence that C-reactive protein is a procoagulant. Arterioscler Thromb Vasc Biol. 2005;25:2216-21. doi: 10.1161/01.ATV.0000183718.62409.ea
9. Devaraj S, Xu DY, Jialal I. C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis. Circulation. 2003;107:398-404. doi: 10.1161/01.cir. 0000052617.91920.fd
10. Mirjanic-Azaric B, et al. Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: pleiotropic evidence from plasma mRNA analyses. Clin Biochem. 2013;46:1526-31. doi: 10.1016/j.clinbiochem.2013.06.006
11. Ferri C, et al. C-reactive protein: interaction with the vascular endothelium and possible role in human atherosclerosis. Curr Pharm Des. 2007;13:1631-45. doi: 10.2174/138161207780831301
12. Libby P, Ridker PM. Novel inflammatory markers of coronary risk: theory versus practice. Circulation. 1999;100:1148-50. doi: 10.1161/01.cir.100.11.1148
13. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005;352:20-8. doi: 10.1056/NEJMoa042378
14. Takemoto M, Liao JK. Pleiotropic effects of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712-9. doi: 10.1161/hq1101.098486
15. Mausner-Fainberg K, et al. The effect of HMG-CoA reductase inhibitors on naturally occurring CD4+CD25+ T-cells. Atherosclerosis. 2008;197:829-39. doi: 10.1016/j.atherosclerosis.2007.07.031
16. Nissen SE, et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA. 2004;291:1071-80. doi: 10.1001/jama.291.9.1071
17. Albert MA, Danielson E, Rifai N, Ridker PM. PRINCE Investigators. Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study. JAMA. 2001;286:64-70. doi: 10.1001/jama.286.1.64
18. Kim J-S, et al. Efficacy of high-dose atorvastatin loading before primary percutaneous coronary intervention in ST-segment elevation myocardial infarction: the STATIN STEMI trial. JACC Cardiovasc Interv. 2010;3:332-9. doi: 10.1016/j.jcin.2009.11.021
19. Isaacsohn JL, et al. Aggressive Lipid-Lowering Initiation Abates New Cardiac Events (ALLIANCE)-rationale and design of atorvastatin versus usual care in hypercholesterolemic patients with coronary artery disease. Am J Cardiol. 2000;86:250-2. doi: 10.1016/s0002-9149(00)00872-9
20. LaRosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352:1425-35. doi: 10.1056/NEJMoa050461
21. Рекомендации по лечению стабильной ишемической болезни сердца ESC. https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines
22. Kinlay S, et al. High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation. 2003;108:1560-6. doi: 10.1161/01.CIR.0000091404.09558.AF
23. Loppnow H, et al. Statins potently reduce the cytokine-mediated IL-6 release in SMC/MNC cocultures. J Cell Mol Med. 2011;15:994-1004. doi: 10.1111/j.1582-4934.2010.01036.x
24. Miyazaki Y, et al. Effect of statins on atherogenic serum amyloid A and α1-antitrypsin low-density lipoprotein complexes. Int J Cardiol. 2016;225:332-6. doi: 10.1016/j.ijcard.2016.09.116
25. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001;103:1813-8. doi: 10.1161/01.cir. 103.13.1813
26. Park D-W, et al. C-reactive protein and the risk of stent thrombosis and cardiovascular events after drug-eluting stent implantation. Circulation. 2009;120:1987-95. doi: 10.1161/CIRCULATIONAHA.109.876763
27. Delhaye C, et al. Long-term prognostic value of preprocedural C-reactive protein after drug-eluting stent implantation. Am J Cardiol. 2010;105:826-32. doi: 10.1016/j.amjcard.2009.10.064
28. Iijima R, et al. Pre-procedural C-reactive protein levels and clinical outcomes after percutaneous coronary interventions with and without abciximab: pooled analysis of four ISAR trials. Heart Br Card Soc. 2009;95:107-12. doi: 10.1136/hrt.2008.153635
29. Park D-W, et al. Prognostic impact of preprocedural C reactive protein levels on 6-month angiographic and 1-year clinical outcomes after drug-eluting stent implantation. Heart Br Card Soc. 2007;93:1087-92. doi: 10.1136/hrt.2006.099762
30. Ridker PM, et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial. Lancet Lond Engl. 2017. doi:10.1016/S0140-6736(17)32814-3.
31. Mor A, Luboshits G, Planer D, Keren G, George J. Altered status of CD4(+)CD25(+) regulatory T-cells in patients with acute coronary syndromes. Eur Heart J. 2006;27:2530-7. doi: 10.1093/eurheartj/ehl222
32. Kim YC, Kim KK, Shevach EM. Simvastatin induces Foxp3+ T regulatory cells by modulation of transforming growth factor-beta signal transduction. Immunology. 2010;130:484-93. doi: 10.1111/j.1365-2567.2010.03269.x
33. Meng X, et al. Statins induce the accumulation of regulatory T-cells in atherosclerotic plaque. Mol Med Camb Mass. 2012;18:598-605. doi: 10.2119/molmed.2011.00471
34. Filatova AYu, Kuznetsova GV, Shchinova AM, Osokina AK, Potekhina AV, et al. Influence of short-term intensive atorvastatin therapy on lymphocyte and monocyte subpopulations and CCR2, CCR5, CX3CR1 and TLR4 expression in blood of patients with stable angina. 85th EAS Congress, Prague, 2016.
35. Nabatov AA, Pollakis G, Linnemann T, Paxton WA, de Baar MP. Statins disrupt CCR5 and RANTES expression levels in CD4(+) T-lymphocytes in vitro and preferentially decrease infection of R5 versus X4 HIV-1. PloS One. 2007;(2):e470. doi: 10.1371/journal.pone.0000470
36. Veillard NR, et al. Simvastatin modulates chemokine and chemokine receptor expression by geranylgeranyl isoprenoid pathway in human endothelial cells and macrophages. Atherosclerosis. 2006;188:51-8. doi: 10.1016/j.atherosclerosis.2005.10.015
37. Martínez-González J, Alfón J, Berrozpe M, Badimon L. HMG-CoA reductase inhibitors reduce vascular monocyte chemotactic protein-1 expression in early lesions from hypercholesterolemic swine independently of their effect on plasma cholesterol levels. Atherosclerosis. 2001;159:27-33. doi: 10.1016/S0021-9150(01)00469-5
________________________________________________
2. Williams TN, Zhang CX, Game BA, He L, Huang Y. C-reactive protein stimulates MMP-1 expression in U937 histiocytes through Fc[gamma]RII and extracellular signal-regulated kinase pathway:: an implication of CRP involvement in plaque destabilization. Arterioscler Thromb Vasc Biol. 2004;24:61-6. doi: 10.1161/01.ATV.0000104014.24367.16
3. Wågsäter D, Zhu C, Björkegren J, Skogsberg J, Eriksson P. MMP-2 and MMP-9 are prominent matrix metalloproteinases during atherosclerosis development in the Ldlr(-/-)Apob(100/100) mouse. Int J Mol Med. 2011;28:247-53. doi: 10.3892/ijmm.2011.693
4. Dabek J, Glogowska-Ligus J, Szadorska B. Transcription activity of MMP-2 and MMP-9 metalloproteinase genes and their tissue inhibitor (TIMP-2) in acute coronary syndrome patients. J Postgrad Med. 2013;59:115-20. doi: 10.4103/0022-3859.113836
5. Guo C, et al. Correlation between the severity of coronary artery lesions and levels of estrogen, hs-CRP and MMP-9. Exp Ther Med. 2014;7:1177-80. doi: 10.3892/etm.2014.1565
6. Szalai AJ, Agrawal A, Greenhough TJ, Volanakis, JE. C-reactive protein: structural biology, gene expression, and host defense function. Immunol Res. 1997;16:127-36. doi: 10.1007/BF02786357
7. Szmitko PE, Verma S. C-reactive protein and statins: IL-8 as a molecular link? Clin Sci Lond Engl. 2005;108:493-5. doi: 10.1042/CS20050093
8. Singh U, Devaraj S, Jialal I. C-reactive protein decreases tissue plasminogen activator activity in human aortic endothelial cells: evidence that C-reactive protein is a procoagulant. Arterioscler Thromb Vasc Biol. 2005;25:2216-21. doi: 10.1161/01.ATV.0000183718.62409.ea
9. Devaraj S, Xu DY, Jialal I. C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis. Circulation. 2003;107:398-404. doi: 10.1161/01.cir. 0000052617.91920.fd
10. Mirjanic-Azaric B, et al. Atorvastatin in stable angina patients lowers CCL2 and ICAM1 expression: pleiotropic evidence from plasma mRNA analyses. Clin Biochem. 2013;46:1526-31. doi: 10.1016/j.clinbiochem.2013.06.006
11. Ferri C, et al. C-reactive protein: interaction with the vascular endothelium and possible role in human atherosclerosis. Curr Pharm Des. 2007;13:1631-45. doi: 10.2174/138161207780831301
12. Libby P, Ridker PM. Novel inflammatory markers of coronary risk: theory versus practice. Circulation. 1999;100:1148-50. doi: 10.1161/01.cir.100.11.1148
13. Ridker PM, et al. C-reactive protein levels and outcomes after statin therapy. N Engl J Med. 2005;352:20-8. doi: 10.1056/NEJMoa042378
14. Takemoto M, Liao JK. Pleiotropic effects of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitors. Arterioscler Thromb Vasc Biol. 2001;21:1712-9. doi: 10.1161/hq1101.098486
15. Mausner-Fainberg K, et al. The effect of HMG-CoA reductase inhibitors on naturally occurring CD4+CD25+ T-cells. Atherosclerosis. 2008;197:829-39. doi: 10.1016/j.atherosclerosis.2007.07.031
16. Nissen SE, et al. Effect of intensive compared with moderate lipid-lowering therapy on progression of coronary atherosclerosis: a randomized controlled trial. JAMA. 2004;291:1071-80. doi: 10.1001/jama.291.9.1071
17. Albert MA, Danielson E, Rifai N, Ridker PM. PRINCE Investigators. Effect of statin therapy on C-reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study. JAMA. 2001;286:64-70. doi: 10.1001/jama.286.1.64
18. Kim J-S, et al. Efficacy of high-dose atorvastatin loading before primary percutaneous coronary intervention in ST-segment elevation myocardial infarction: the STATIN STEMI trial. JACC Cardiovasc Interv. 2010;3:332-9. doi: 10.1016/j.jcin.2009.11.021
19. Isaacsohn JL, et al. Aggressive Lipid-Lowering Initiation Abates New Cardiac Events (ALLIANCE)-rationale and design of atorvastatin versus usual care in hypercholesterolemic patients with coronary artery disease. Am J Cardiol. 2000;86:250-2. doi: 10.1016/s0002-9149(00)00872-9
20. LaRosa JC, et al. Intensive lipid lowering with atorvastatin in patients with stable coronary disease. N Engl J Med. 2005;352:1425-35. doi: 10.1056/NEJMoa050461
21. Рекомендации по лечению стабильной ишемической болезни сердца ESC. https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines
22. Kinlay S, et al. High-dose atorvastatin enhances the decline in inflammatory markers in patients with acute coronary syndromes in the MIRACL study. Circulation. 2003;108:1560-6. doi: 10.1161/01.CIR.0000091404.09558.AF
23. Loppnow H, et al. Statins potently reduce the cytokine-mediated IL-6 release in SMC/MNC cocultures. J Cell Mol Med. 2011;15:994-1004. doi: 10.1111/j.1582-4934.2010.01036.x
24. Miyazaki Y, et al. Effect of statins on atherogenic serum amyloid A and α1-antitrypsin low-density lipoprotein complexes. Int J Cardiol. 2016;225:332-6. doi: 10.1016/j.ijcard.2016.09.116
25. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001;103:1813-8. doi: 10.1161/01.cir. 103.13.1813
26. Park D-W, et al. C-reactive protein and the risk of stent thrombosis and cardiovascular events after drug-eluting stent implantation. Circulation. 2009;120:1987-95. doi: 10.1161/CIRCULATIONAHA.109.876763
27. Delhaye C, et al. Long-term prognostic value of preprocedural C-reactive protein after drug-eluting stent implantation. Am J Cardiol. 2010;105:826-32. doi: 10.1016/j.amjcard.2009.10.064
28. Iijima R, et al. Pre-procedural C-reactive protein levels and clinical outcomes after percutaneous coronary interventions with and without abciximab: pooled analysis of four ISAR trials. Heart Br Card Soc. 2009;95:107-12. doi: 10.1136/hrt.2008.153635
29. Park D-W, et al. Prognostic impact of preprocedural C reactive protein levels on 6-month angiographic and 1-year clinical outcomes after drug-eluting stent implantation. Heart Br Card Soc. 2007;93:1087-92. doi: 10.1136/hrt.2006.099762
30. Ridker PM, et al. Relationship of C-reactive protein reduction to cardiovascular event reduction following treatment with canakinumab: a secondary analysis from the CANTOS randomised controlled trial. Lancet Lond Engl. 2017. doi:10.1016/S0140-6736(17)32814-3.
31. Mor A, Luboshits G, Planer D, Keren G, George J. Altered status of CD4(+)CD25(+) regulatory T-cells in patients with acute coronary syndromes. Eur Heart J. 2006;27:2530-7. doi: 10.1093/eurheartj/ehl222
32. Kim YC, Kim KK, Shevach EM. Simvastatin induces Foxp3+ T regulatory cells by modulation of transforming growth factor-beta signal transduction. Immunology. 2010;130:484-93. doi: 10.1111/j.1365-2567.2010.03269.x
33. Meng X, et al. Statins induce the accumulation of regulatory T-cells in atherosclerotic plaque. Mol Med Camb Mass. 2012;18:598-605. doi: 10.2119/molmed.2011.00471
34. Filatova AYu, Kuznetsova GV, Shchinova AM, Osokina AK, Potekhina AV, et al. Influence of short-term intensive atorvastatin therapy on lymphocyte and monocyte subpopulations and CCR2, CCR5, CX3CR1 and TLR4 expression in blood of patients with stable angina. 85th EAS Congress, Prague, 2016.
35. Nabatov AA, Pollakis G, Linnemann T, Paxton WA, de Baar MP. Statins disrupt CCR5 and RANTES expression levels in CD4(+) T-lymphocytes in vitro and preferentially decrease infection of R5 versus X4 HIV-1. PloS One. 2007;(2):e470. doi: 10.1371/journal.pone.0000470
36. Veillard NR, et al. Simvastatin modulates chemokine and chemokine receptor expression by geranylgeranyl isoprenoid pathway in human endothelial cells and macrophages. Atherosclerosis. 2006;188:51-8. doi: 10.1016/j.atherosclerosis.2005.10.015
37. Martínez-González J, Alfón J, Berrozpe M, Badimon L. HMG-CoA reductase inhibitors reduce vascular monocyte chemotactic protein-1 expression in early lesions from hypercholesterolemic swine independently of their effect on plasma cholesterol levels. Atherosclerosis. 2001;159:27-33. doi: 10.1016/S0021-9150(01)00469-5
Авторы
А.М. Щинова, Г.В. Шлевкова, А.Ю. Филатова, А.В. Потехина, А.К. Осокина, И.В. Ромасов, Е.А. Жарова, Е.А. Ноева, А.Н. Самко, В.П. Масенко, Т.И. Арефьева, С.И. Проваторов
ФГБУ «Национальный медицинский исследовательский центр кардиологии» Минздрава России, Москва, Россия
National Medical Research Center of Cardiology, Moscow, Russia
ФГБУ «Национальный медицинский исследовательский центр кардиологии» Минздрава России, Москва, Россия
________________________________________________
National Medical Research Center of Cardiology, Moscow, Russia
Цель портала OmniDoctor – предоставление профессиональной информации врачам, провизорам и фармацевтам.