Immunomodulatory Effects of Ticagrelor in Myocardial Infarction: Shifting the Cytokine Balance Toward an Anti-Inflammatory Profile

Myocardial infarction (MI) triggers a systemic inflammatory response that influences cardiac recovery. Pharmacological therapies, including aspirin, β-blockers, Angiotensin-Converting Enzyme (ACE) inhibitors, statins, and P2Y12 inhibitors such as Ticagrelor, may have additional immunomodulatory effects beyond their primary cardiovascular benefits. This study evaluates the impact of different treatment regimens on inflammatory markers, immune cell phenotyping, and cardiac biomarkers in MI patients. A total of 78 MI patients were divided into three treatment groups: standard therapy (aspirin + β-blockers), enhanced therapy (aspirin, β-blockers, ACE inhibitors, and statins), and experimental therapy (Ticagrelor + standard therapy). Inflammatory cytokines (Interleukin (IL)-4, IL-6, IL-10, IL-17, Interferon (IFN)-γ, Tumor Necrosis Factor (TNF)-α, Transforming Growth Factor (TGF)-β), cardiac biomarkers [Troponin, B-type natriuretic peptide (BNP)], and immune cell profiles (Th1/Th2 balance) were assessed using Enzyme-Linked Immunosorbent Assay (ELISA), qPCR (Polymerase Chain Reaction), and flow cytometry before and after treatment. Pro-inflammatory markers (IL-6, TNF-α, IFN-γ, IL-17) significantly decreased, while anti-inflammatory cytokines (IL-4, IL-10, TGF-β) increased post-treatment ( P < 0.0001). Th1 cell proportions declined, with a concurrent rise in Th2 cells, particularly in enhanced and experimental therapy groups. Troponin and BNP levels decreased, indicating reduced myocardial stress. Pharmacological therapies effectively modulate immune responses, suppress inflammation, and promote myocardial recovery. Ticagrelor demonstrated additional anti-inflammatory benefits, suggesting potential for improved post-MI outcomes. Future studies should explore long-term clinical implications of immune-targeted cardiovascular therapy.