Local to Systemic Inflammation—From Generation to Prognosis in Acute Coronary Syndrome

Acute coronary syndromes (ACS) are a major cause of mortality worldwide, and although interventional treatment has significantly improved mortality and morbidity related to ischemic heart disease, there is constant concern about optimizing drug treatment. In this regard, multiple studies have been conducted on inflammation in myocardial infarction (MI), starting from its implications in the atherosclerosis process. The aim of this review is to analyse the current evidence related to the subject and the correlation between the inflammatory state at presentation and the prognosis of patients with MI, identifying key points, possible therapeutic limitations, and future research directions. Both innate and acquired immune components are involved in the inflammatory cascade, with an increase in inflammatory cell and cytokine levels. To analyse the degree of inflammation and determine when it is excessive, numerous inflammatory markers have been studied, from acute phase proteins such as high-sensitivity C-reactive protein (hsCRP) and fibrinogen, to the ratios between inflammatory cells and interleukins involved in the main inflammatory pathways. Their association with post-infarction mortality and morbidity has been observed, but they must be integrated into the clinical context for the selection of patients who would benefit most from their reduction. New anti-inflammatory therapies are being studied in light of these findings, and progress is expected. Early trials with non-selective anti-inflammatory drugs have highlighted the importance of selective inhibition so as not to disrupt healing, and drugs are now being studied that target specific pathways that are exacerbated in infarction and lead to excessive remodelling. Several inflammatory pathways have been investigated but the results are inconclusive in terms of improving prognosis, requiring further studies to formulate future therapeutic indications.