Unmet needs in the management of atherosclerotic cardiovascular disease: Is there a role for emerging anti-inflammatory interventions?

International Journal of Cardiology

Volumn 221, Issue , 2016, Pages 581-586

  Lorenzatti, Alberto J ^a,b   Retzlaff, Brenda M ^c  

^a HOSPITAL PRIVADO   (Argentina)

^b Rusculleda Foundation for Research   (Argentina)

^c Unidad de Cirugía y Medicina Experimental   (Argentina)

Author keywords

Atherosclerosis; Cardiovascular; High sensitivity C reactive protein; Inflammation

Indexed keywords

ATORVASTATIN; C REACTIVE PROTEIN; CANAKINUMAB; COLCHICINE; EZETIMIBE; HYDROXYMETHYLGLUTARYL COENZYME A REDUCTASE INHIBITOR; LIPID; LOW DENSITY LIPOPROTEIN CHOLESTEROL; METHOTREXATE; MEVINOLIN; PLACEBO; PRAVASTATIN; ROSUVASTATIN; SIMVASTATIN; TOCILIZUMAB; ANTIINFLAMMATORY AGENT; AUTACOID;

ANTIINFLAMMATORY ACTIVITY; ATHEROGENESIS; ATHEROSCLEROSIS; CARDIOVASCULAR DISEASE; CLINICAL TRIAL (TOPIC); CORONARY ARTERY ATHEROSCLEROSIS; CORONARY ARTERY DISEASE; DRUG EFFICACY; DRUG SAFETY; DRUG WITHDRAWAL; ENDOPLASMIC RETICULUM STRESS; GASTROINTESTINAL SYMPTOM; HEART INFARCTION; HUMAN; INFLAMMATION; LIPID METABOLISM; LIPID STORAGE; LOW DRUG DOSE; META ANALYSIS (TOPIC); NON ST SEGMENT ELEVATION MYOCARDIAL INFARCTION; NONHUMAN; OUTCOME ASSESSMENT; PHAGOCYTOSIS; PRIMARY PREVENTION; PRIORITY JOURNAL; RANDOMIZED CONTROLLED TRIAL (TOPIC); REVIEW; RHEUMATOID ARTHRITIS; RISK REDUCTION; SECONDARY PREVENTION; SINGLE DRUG DOSE; SYSTEMATIC REVIEW (TOPIC); ANIMAL; BLOOD; MEDICATION THERAPY MANAGEMENT; PATHOPHYSIOLOGY; TRENDS;

ANIMALS; ANTI-INFLAMMATORY AGENTS; CORONARY ARTERY DISEASE; HUMANS; HYDROXYMETHYLGLUTARYL-COA REDUCTASE INHIBITORS; INFLAMMATION; INFLAMMATION MEDIATORS; MEDICATION THERAPY MANAGEMENT;

EID: 84978501305     PISSN: 01675273     EISSN: 18741754     Source Type: Journal    
DOI: 10.1016/j.ijcard.2016.07.061     Document Type: Review

References (63)

1. [1] World Health Organization, Global Health Observatory Data Repository—Mortality and Burden of Disease—WHO Regions. 2008, WHO, Geneva.
2. [2] Stone, G.W., Maehara, A., Lansky, A.J., de Bruyne, B., Cristea, E., Mintz, G.S., et al. A prospective natural-history study of coronary atherosclerosis. N. Engl. J. Med. 364:3 (2011), 226–235.
3. [3] Virchow, R., Osler, W., Welch, W.H., Cellular Pathology (Die Cellularpathologiein Ihrer Begründung Auf Physiologische Und pathologischeGewebelehre), Prof. Rudolf Virchow. 1978, Omaha, NE, Gryphon Editions/Classics of Medicine Library.
4. [4] Viola, J., Soehnlein, O., Atherosclerosis — a matter of unresolved inflammation. Semin. Immunol. 27:3 (2015), 184–193.
5. [5] Ross, R., Atherosclerosis—an inflammatory disease. N. Engl. J. Med. 340:2 (1999), 115–126.
6. [6] Ross, R., The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 362:6423 (1993), 801–809.
7. [7] Libby, P., Ridker, P.M., Hansson, G.K., Progress and challenges in translating the biology of atherosclerosis. Nature 473:7347 (2011), 317–325.
8. [8] Kwon, G.P., Schroeder, J.L., Amar, M.J., Remaley, A.T., Balaban, R.S., Contribution of macromolecular structure to the retention of low-density lipoprotein at arterial branch points. Circulation 117:22 (2008), 2919–2927.
9. [9] Mestas, J., Ley, K., Monocyte-endothelial cell interactions in the development of atherosclerosis. Trends Cardiovasc. Med. 18:6 (2008), 228–232.
10. [10] Liu, J., Thewke, D.P., Su, Y.R., Linton, M.F., Fazio, S., Sinensky, M.S., Reduced macrophage apoptosis is associated with accelerated atherosclerosis in low-density lipoprotein receptor-null mice. Arterioscler. Thromb. Vasc. Biol. 25:1 (2005), 174–179.
11. [11] Bentzon, J.F., Otsuka, F., Virmani, R., Falk, E., Mechanisms of plaque formation and rupture. Circ. Res. 114:12 (2014), 1852–1866.
12. [12] Libby, P., Mechanisms of acute coronary syndromes and their implications for therapy. N. Engl. J. Med. 368:21 (2013), 2004–2013.
13. [13] Hansson, G.K., Immune mechanisms in atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 21:12 (2001), 1876–1890.
14. [14] Duewell, P., Kono, H., Rayner, K.J., Sirois, C.M., Vladimer, G., Bauernfeind, F.G., et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature 464:7293 (2010), 1357–1361.
15. [15] Cassel, S.L., Joly, S., Sutterwala, F.S., The NLRP3 inflammasome: a sensor of immune danger signals. Semin. Immunol. 21:4 (2009), 194–198.
16. [16] Harris, T.B., Ferrucci, L., Tracy, R.P., Corti, M.C., Wacholder, S., Ettinger, W.H. Jr., et al. Associations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly. Am. J. Med. 106:5 (1999), 506–512.
17. [17] Libby, P., Inflammation in atherosclerosis. Nature 420:6917 (2002), 868–874.
18. [18] Haneklaus, M., O'Neill, L.A., Coll, R.C., Modulatory mechanisms controlling the NLRP3 inflammasome in inflammation: recent developments. Curr. Opin. Immunol. 25:1 (2013), 40–45.
19. [19] Tschopp, J., Schroder, K., NLRP3 inflammasome activation: the convergence of multiple signalling pathways on ROS production?. Nat. Rev. Immunol. 10:3 (2010), 210–215.
20. [20] Gilstrap, L.G., Wang, T.J., Biomarkers and cardiovascular risk assessment for primary prevention: an update. Clin. Chem. 58:1 (2012), 72–82.
21. [21] Ridker, P.M., Cushman, M., Stampfer, M.J., Tracy, R.P., Hennekens, C.H., Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N. Engl. J. Med. 336:14 (1997), 973–979.
22. [22] C. Emerging Risk Factors, Kaptoge, S., Di Angelantonio, E., Lowe, G., Pepys, M.B., Thompson, S.G., et al. C-reactive protein concentration and risk of coronary heart disease, stroke, and mortality: an individual participant meta-analysis. Lancet 375:9709 (2010), 132–140.
23. [23] Ridker, P.M., Inflammation, C-reactive protein, and cardiovascular disease: moving past the marker versus mediator debate. Circ. Res. 114:4 (2014), 594–595.
24. [24] Paffen, E., DeMaat, M.P., C-reactive protein in atherosclerosis: a causal factor?. Cardiovasc. Res. 71:1 (2006), 30–39.
25. [25] Zhang, Y.X., Cliff, W.J., Schoefl, G.I., Higgins, G., Coronary C-reactive protein distribution: its relation to development of atherosclerosis. Atherosclerosis 145:2 (1999), 375–379.
26. [26] Yousuf, O., Mohanty, B.D., Martin, S.S., Joshi, P.H., Blaha, M.J., Nasir, K., et al. High-sensitivity C-reactive protein and cardiovascular disease: a resolute belief or an elusive link?. J. Am. Coll. Cardiol. 62:5 (2013), 397–408.
27. [27] Ridker, P.M., Rifai, N., Pfeffer, M.A., Sacks, F.M., Moye, L.A., Goldman, S., et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) investigators. Circulation 98:9 (1998), 839–844.
28. [28] Ridker, P.M., Rifai, N., Clearfield, M., Downs, J.R., Weis, S.E., Miles, J.S., 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. 344:26 (2001), 1959–1965.
29. [29] Ridker, P.M., Danielson, E., Fonseca, F.A., Genest, J., Gotto, A.M. Jr., Kastelein, J.J., et al. Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein. N. Engl. J. Med. 359:21 (2008), 2195–2207.
30. [30] Ridker, P.M., MacFadyen, J., Libby, P., Glynn, R.J., Relation of baseline high-sensitivity C-reactive protein level to cardiovascular outcomes with rosuvastatin in the justification for use of statins in prevention: an intervention trial evaluating rosuvastatin (JUPITER). Am. J. Cardiol. 106:2 (2010), 204–209.
31. [31] Ridker, P.M., Cannon, C.P., Morrow, D., Rifai, N., Rose, L.M., McCabe, C.H., et al. C-reactive protein levels and outcomes after statin therapy. N. Engl. J. Med. 352:1 (2005), 20–28.
32. [32] Nissen, S.E., Tuzcu, E.M., Schoenhagen, P., Crowe, T., Sasiela, W.J., Tsai, J., et al. Statin therapy, LDL cholesterol, C-reactive protein, and coronary artery disease. N. Engl. J. Med. 352:1 (2005), 29–38.
33. [33] Bohula, E.A., Giugliano, R.P., Cannon, C.P., Zhou, J., Murphy, S.A., White, J.A., et al. Achievement of dual low-density lipoprotein cholesterol and high-sensitivity C-reactive protein targets more frequent with the addition of ezetimibe to simvastatin and associated with better outcomes in IMPROVE-IT. Circulation 132:13 (2015), 1224–1233.
34. [34] C Reactive Protein Coronary Heart Disease Genetics Collaboration (CCGC), Wensley, F., Gao, P., Burgess, S., Kaptoge, S., Di Angelantonio, E., et al. Association between C reactive protein and coronary heart disease: mendelian randomisation analysis based on individual participant data. BMJ, 342, 2011, d548.
35. [35] Zacho, J., Tybjaerg-Hansen, A., Jensen, J.S., Grande, P., Sillesen, H., Nordestgaard, B.G., Genetically elevated C-reactive protein and ischemic vascular disease. N. Engl. J. Med. 359:18 (2008), 1897–1908.
36. [36] IL6R Genetics Consortium Emerging Risk Factors Collaboration, Sarwar, N., Butterworth, A.S., Freitag, D.F., Gregson, J., Willeit, P., et al. Interleukin-6 receptor pathways in coronary heart disease: a collaborative meta-analysis of 82 studies. Lancet 379:9822 (2012), 1205–1213.
37. [37] C. Interleukin-6 Receptor Mendelian Randomisation Analysis, The interleukin-6 receptor as a target for prevention of coronary heart disease: a mendelian randomisation analysis. Lancet 379:9822 (2012), 1214–1224.
38. [38] Davignon, J., Beneficial cardiovascular pleiotropic effects of statins. Circulation 109:23 Suppl 1 (2004), III39–III43.
39. [39] Robinson, J.G., Smith, B., Maheshwari, N., Schrott, H., Pleiotropic effects of statins: benefit beyond cholesterol reduction? A meta-regression analysis. J. Am. Coll. Cardiol. 46:10 (2005), 1855–1862.
40. [40] Dong, Z.M., Chapman, S.M., Brown, A.A., Frenette, P.S., Hynes, R.O., Wagner, D.D., The combined role of P- and E-selectins in atherosclerosis. J. Clin. Invest. 102:1 (1998), 145–152.
41. [41] Yamashita, T., Sasaki, N., Kasahara, K., Hirata, K., Anti-inflammatory and immune-modulatory therapies for preventing atherosclerotic cardiovascular disease. J. Cardiol. 66:1 (2015), 1–8.
42. [42] Dinarello, C.A., A clinical perspective of IL-1beta as the gatekeeper of inflammation. Eur. J. Immunol. 41:5 (2011), 1203–1217.
43. [43] Dinarello, C.A., Simon, A., van der Meer, J.W., Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases. Nat. Rev. Drug Discov. 11:8 (2012), 633–652.
44. [44] Donath, M.Y., Weder, C., Brunner, A., Keller, C., Whitemore, J., Der, K., et al. XOMA 052, a potential disease modifying anti-1L-1beta antibody, shows sustained HbA1c reductions 3 months after a single injection with no increases in safety parameters in subjects with type 2 diabetes. Diabetes, 58, 2009, A30.
45. [45] Qamar, A., Rader, D.J., Effect of interleukin 1beta inhibition in cardiovascular disease. Curr. Opin. Lipidol. 23:6 (2012), 548–553.
46. [46] Arend, W.P., The balance between IL-1 and IL-1Ra in disease. Cytokine Growth Factor Rev. 13:4–5 (2002), 323–340.
47. [47] Dinarello, C.A., Anti-inflammatory agents: present and future. Cell 140:6 (2010), 935–950.
48. [48] Abbate, A., Kontos, M.C., Grizzard, J.D., Biondi-Zoccai, G.G., Van Tassell, B.W., Robati, R., et al. Interleukin-1 blockade with anakinra to prevent adverse cardiac remodeling after acute myocardial infarction (Virginia Commonwealth University Anakinra Remodeling Trial [VCU-ART] pilot study). Am. J. Cardiol. 105:10 (2010), 1371–1377, e1371.
49. [49] Abbate, A., Kontos, M.C., Abouzaki, N.A., Melchior, R.D., Thomas, C., Van Tassell, B.W., et al. Comparative safety of interleukin-1 blockade with anakinra in patients with ST-segment elevation acute myocardial infarction (from the VCU-ART and VCU-ART2 pilot studies). Am. J. Cardiol. 115:3 (2015), 288–292.
50. [50] Bastard, J.P., Jardel, C., Delattre, J., Hainque, B., Bruckert, E., Oberlin, F., Evidence for a link between adipose tissue interleukin-6 content and serum C-reactive protein concentrations in obese subjects. Circulation 99:16 (1999), 2221–2222.
51. [51] Kleveland, O., Kunszt, G., Bratlie, M., Ueland, T., Amundsen, B., Aakhus, S., et al. The interleukin-6 receptor antagonist tocilizumab reduces inflammation and myocardial damage in non-ST elevation myocardial infarction - a randomized, double-blind, placebo controlled study. Eur. Heart J., 36(Supplement 27), 2015.
52. [52] Ridker, P.M., Luscher, T.F., Anti-inflammatory therapies for cardiovascular disease. Eur. Heart J. 35:27 (2014), 1782–1791.
53. [53] Dalekos, G.N., Elisaf, M., Bairaktari, E., Tsolas, O., Siamopoulos, K.C., Increased serum levels of interleukin-1beta in the systemic circulation of patients with essential hypertension: additional risk factor for atherogenesis in hypertensive patients?. J. Lab. Clin. Med. 129:3 (1997), 300–308.
54. [54] Galea, J., Armstrong, J., Gadsdon, P., Holden, H., Francis, S.E., Holt, C.M., Interleukin-1 beta in coronary arteries of patients with ischemic heart disease. Arterioscler. Thromb. Vasc. Biol. 16:8 (1996), 1000–1006.
55. [55] Wang, L., Qu, P., Zhao, J., Chang, Y., NLRP3 and downstream cytokine expression elevated in the monocytes of patients with coronary artery disease. Arch. Med. Sci. 10:4 (2014), 791–800.
56. [56] Choi, H.K., Hernan, M.A., Seeger, J.D., Robins, J.M., Wolfe, F., Methotrexate and mortality in patients with rheumatoid arthritis: a prospective study. Lancet 359:9313 (2002), 1173–1177.
57. [57] Westlake, S.L., Colebatch, A.N., Baird, J., Kiely, P., Quinn, M., Choy, E., et al. The effect of methotrexate on cardiovascular disease in patients with rheumatoid arthritis: a systematic literature review. Rheumatology (Oxford) 49:2 (2010), 295–307.
58. [58] Micha, R., Imamura, F., Wyler von Ballmoos, M., Solomon, D.H., Hernan, M.A., Ridker, P.M., et al. Systematic review and meta-analysis of methotrexate use and risk of cardiovascular disease. Am. J. Cardiol. 108:9 (2011), 1362–1370.
59. [59] Ridker, P.M., Testing the inflammatory hypothesis of atherothrombosis: scientific rationale for the cardiovascular inflammation reduction trial (CIRT). J. Thromb. Haemost. 7:Suppl. 1 (2009), 332–339.
60. [60] Ridker, P.M., Thuren, T., Zalewski, A., Libby, P., Interleukin-1beta inhibition and the prevention of recurrent cardiovascular events: rationale and design of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS). Am. Heart J. 162:4 (2011), 597–605.
61. [61] Martinon, F., Petrilli, V., Mayor, A., Tardivel, A., Tschopp, J., Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 440:7081 (2006), 237–241.
62. [62] Nidorf, S.M., Eikelboom, J.W., Budgeon, C.A., Thompson, P.L., Low-dose colchicine for secondary prevention of cardiovascular disease. J. Am. Coll. Cardiol. 61:4 (2013), 404–410.
63. [63] Verma, S., Eikelboom, J.W., Nidorf, S.M., Al-Omran, M., Gupta, N., Teoh, H., et al. Colchicine in cardiac disease: a systematic review and meta-analysis of randomized controlled trials. BMC Cardiovasc. Disord., 15, 2015, 96.