Key result
Impaired blood flow through the infarct-related artery (TIMI 0-1) in acute myocardial infarction was associated with significantly lower levels of IP-10 and higher levels of IL-10 and CRP compared to preserved blood flow.
Why the study?
Systemic inflammation correlates with AMI severity, and cytokines and endothelial dysfunction affect clot formation, but their relationship with IRA blood flow remained to be assessed.
Observational (n=75)
No
Answers are grounded in this paper and cite their sources.
Circulating inflammatory cytokines correlate with the type of myocardial infarction and the patency of the infarct-related artery, highlighting the link between inflammation, endothelial function, and thrombosis.
BACKGROUND: The level of systemic inflammation correlates with the severity of the clinical course of acute myocardial infarction (AMI). It has been shown that circulating cytokines and endothelial dysfunction play an important role in the process of clot formation. The aim of our study was to assess the concentration of various circulating cytokines, endothelial function and blood clotting in AMI patients depending on the blood flow through the infarction-related artery (IRA). METHODS: We included 75 patients with AMI. 58 presented with ST-elevation myocardial infarction (STEMI) and 17 had non-ST-elevation myocardial infarction (non-STEMI). A flow-mediated dilation test (FMD test), thrombodynamics and rotational thromboelastometry as well as assessment of 14 serum cytokines using xMAP technology were performed. FINDINGS: Non-STEMI-patients were characterized by higher levels of MDC, MIP-1β, TNF-α. Moreover, we observed that patients with impaired blood flow through the IRA (TIMI flow 0-1) had higher average and initial clot growth rates, earlier onset of spontaneous clots, C-reactive protein (CRP) and IL-10 compared to patients with preserved blood flow through the IRA (TIMI flow 2-3). Patients with TIMI 2-3 blood flow had higher level of IP-10. IL-10 correlated with CRP and pro-inflammatory cytokines levels, initial clot growth rate and clot lysis time in TIMI 0-1 patients. All these differences were statistically significant. INTERPRETATION: We demonstrated that concentrations of the inflammatory cytokines correlate not only with the form of myocardial infarction (STEMI or non-STEMI), but also with the blood flow through the infarct-related artery. Inflammatory response, functional state of endothelium, and clot formation are closely linked with each other. A combination of these parameters affects the patency of the infarct-related artery.
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Kalinskaya et al. (2022) conducted an observational in Acute Myocardial Infarction (n=75). Impaired blood flow (TIMI 0-1) vs. Preserved blood flow (TIMI 2-3) was evaluated on IP-10 concentration (pg/ml) (p=<0.05). Impaired blood flow through the infarct-related artery (TIMI 0-1) in acute myocardial infarction was associated with significantly lower levels of IP-10 and higher levels of IL-10 and CRP compared to preserved blood flow.
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