Key result
Post-MI patients show persistent systemic inflammation with a shift toward non-classical monocytes over 12 weeks.
Why the study?
The temporal changes in circulating monocyte subsets and their functional characteristics following myocardial infarction remain incompletely understood.
Observational (n=72)
Following myocardial infarction, patients exhibit a highly inflammatory monocyte profile in the acute phase that dynamically shifts towards non-classical monocytes over 12 weeks.
Following myocardial infarction (MI), recruited monocytes play an essential role in tissue repair and scar formation. However, the temporal changes in circulating monocyte subsets and their functional characteristics remain incompletely understood. We investigated systemic inflammation and circulating monocyte heterogeneity in 72 patients during the first 12 weeks after MI. Systemic inflammation was markedly increased immediately after MI, as reflected by significant elevated C-reactive protein and interleukin-6 (IL-6) levels. During follow-up, the proportion of classical monocytes decreased, whereas the relative abundance of non-classical monocytes increased. In the acute phase, cluster of differentiation 11b expression on intermediate monocytes was elevated, while peripheral blood mononuclear cells produced lower levels of the anti-inflammatory cytokines IL-10 and IL-1Ra. Together, the results support the presence of a relatively more inflammatory monocyte profile during the acute phase of MI.
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Los et al. (2026) conducted an observational in Myocardial infarction (n=72). Myocardial infarction (temporal changes post-MI) was evaluated on Temporal changes in circulating monocyte subsets, systemic inflammation, and cytokine production capacity. Following myocardial infarction, patients exhibited increased acute systemic inflammation, a decrease in classical monocytes, and an increase in non-classical monocytes over 12 weeks.
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