Targeting Inflammation and Immune System in Acute Myocardial Infarction

Idrus Alwi

Abstract


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.

Keywords


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

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