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Background: Despite significant progress in management of acute coronary syndromes (ACSs), they continue to be a major cause of death worldwide due to residual inflammatory risk (RIR). Aim: This study reviews existing clinical evidence for anti-inflammatory therapies in coronary heart disease (CHD) and assesses precision medicine in classifying patients from clinical, immunological, and genetic perspectives. Results: Large clinical trials confirm the inflammatory hypothesis of atherosclerosis. Therapies targeted at the specific NLRP3 inflammasome/interleukin-1β (IL-1β)/interleukin-6 (IL-6) pathway reduce major adverse cardiovascular events (MACEs), while broad immunosuppression fails. This highlights the need for molecular specificity. Precision cardiology aims to identify high-risk inflammatory phenotypes through clonal hematopoiesis of indeterminate potential (CHIP). Mutations in genes such as TET2 and ASXL1 lead to macrophage hyperreactivity and increased plaque vulnerability. Available data suggest that the effectiveness of immunomodulatory treatment strongly depends on timing. Starting therapy early with SGLT2 inhibitors (SGLT2is) or agents that target temporarily activated receptors like P2Y11 seems to be essential for managing harmful inflammation while supporting myocardial repair. Conclusions: Precision cardiology aims to integrate targeted anti-inflammatory therapies with established clinical markers, while future pathways may incorporate advanced immunophenotyping and genetic risk assessment as they undergo clinical validation.
Dudek et al. (Wed,) studied this question.