Targeting Inflammation and Immune System in Acute Myocardial Infarction

Idrus Alwi


Over more than two decades, the concept of atherosclerosis has developed and lead to inflammatory hypothesis. Inflammation plays an important role on pathogenesis of atherothrombosis and coronary heart disease (CHD), including acute coronary syndrome (ACS). Although the management of ACS has been demonstrated to be beneficial for secondary prevention of coronary heart disease (such as using statin and aspirin) and also seemed to have positive effect on inflammation, the identification of effective management, specifically targeting inflammation, has been not been comprehensively understood.
The Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) supported targeting inflammation as a potential effective treatment for chronic coronary heart disease. In the CANTOS study, canakinumab, a monoclonal antibody that inhibits interleukin-1β, reduced the level of hsCRP and caused lower risk of composite endpoint of death due to cardiovascular diseases, myocardial infarct or stroke compared to placebo. However, non-specific anti-inflammatory treatment using methotrexate in the Cardiovascular Inflammation Reduction Trial (CIRT) study did not show any reduced hsCRP and demonstrated that there is no benefit associated with cardiovascular outcomes, which left us with a question whether direct intervention on inflammation could improve cardiovascular outcomes.


inflammation; immune system; acute myocardial infarction; acute coronary syndrome; coronary heart disease


Ross R. Atherosclerosis — an inflammatory disease. N Engl J Med. 1999;340:115-26.

Libby P, Hansson GK. From focal lipid storage to systemic inflammation. J Am Coll Cardiol. 2019;74:1594–607.

Bonaca MP, Morrow DA, Braunwald E, et al. Growth differentiation factor-15 and risk of recurrent events in patients stabilized after acute coronary syndrome. Arterioscler Thromb Vasc Biol. 2011;31:203–10.

Lukin A, Novak K, Polić S, Puljak L. Prognostic value of low and moderately elevated -reactive protein in acute coronary syndrome: a 2-year follow-up study. Med Sci Monit. 2013;19:777–86.

Bivona G, Bellia C, Lo Sasso B, et al. Short-term changes in gal 3 circulating levels after acute myocardial infarction. Arch Med Res. 2016;47:521–5.

Aldous SJ. Cardiac biomarkers in acute myocardial infarction. Int J Cardiol. 2013;164:282–94.

McCann CJ, Glover BM, Menown IB, et al. Prognostic value of a multimarker approach for patients presenting to hospital with acute chest pain. Am J Cardiol. 2009;103:22–8.

Schernthaner C, Lichtenauer M, Wernly B, et al. Multibiomarker analysis in patients with acute myocardial infarction. Eur J Clin Invest. 2017;47:638–48.

Rymer JA, Newby LK. Failure to launch: targeting inflammation in acute coronary syndromes. JACC Basic Transl Sci. 2017;2:484-97.

Ridker PM, Everett BM, Thuren T, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377:1119-31.

Ridker PM, Everett BM, Pradhan A, et al. Low-dose methotrexate for the prevention of atherosclerotic events. N Engl J Med. 2019;380:752-62.

Kelly GS. Clinical applications of N-acetylcysteine. Alt Med Rev. 1998;3(2):114-27.

Arstall MA, Yang J, Stafford I, Betts WH, Horowitz JD. N-acetylcysteine in combination with nitroglycerin and streptokinase for the treatment of evolving acute myocardial infarction. Safety and biochemical effects. Circulation. 1995;92:2855-62.

Sochman J, Vrbska J, Musilova B, Rocek M. Infarct size limitation: acute N-acetylcysteine defense (ISLAND trial): preliminary analysis and report after the first 30 patients. Clin Cardiol. 1996;19:94-100.

Wasyanto T, Yasa A, Jalaludinsyah A. Effect of oral N-acetylcysteine supplementation on the immunity system in patients with acute myocardial infarction. Acta Med Indones - Indones J Intern Med. 2019;51(4):219-25.

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