Key result
High day-1 thromboinflammation post-STEMI linked to ~157% higher major cardiovascular events risk.
Why the study?
Platelets and neutrophils drive postischemic thromboinflammation during STEMI, but whether circulating thromboinflammatory markers predict recurrent clinical events was unknown.
Does elevated thromboinflammation (H3Cit-DNA complexes) predict major adverse cardiac events in patients with STEMI?
Observational (n=361)
Yes
Does elevated thromboinflammation (H3Cit-DNA complexes) predict major adverse cardiac events in patients with STEMI?
Answers are grounded in this paper and cite their sources.
Elevated thromboinflammation (H3Cit-DNA complexes) at day 1 after STEMI is independently associated with an increased risk of major adverse cardiac events at 12 months.
Platelets are crucial in thrombus formation during ST-elevation myocardial infarction (STEMI). In addition, they also play an important role in postischemic thromboinflammation, which is determined by the interplay between activated platelets and neutrophils. The latter form neutrophil extracellular traps, which are detectable in plasma as citrullinated histone H3-deoxyribonucleic acid-DNA complexes. Prediction of the risk of recurrent events is important in precision medicine. Therefore, we investigated whether circulating thromboinflammatory markers predict clinical outcome after STEMI. We performed a prospective, multicentric, observational, all-comer study of patients with STEMI (n = 361). Thromboinflammation, measured as H3Cit-DNA complexes, was assessed on day 1 after presentation with STEMI as well as 5 days and 6 months after STEMI by enzyme-linked immunosorbent assay. Twelve months of clinical follow-up was conducted. Multivariate analysis was performed investigating which variables were independently associated with major adverse cardiac events (MACEs). Patients were aged 64 ± 12 years; 80% were male; and 40% had diabetes mellitus. Thromboinflammation was enhanced during index hospitalization compared with 6-months follow-up (137.4 ± 100.0 μg/L vs 53.7 ± 54.7 μg/L; P < .001). Additionally, patients within the highest tertile of thromboinflammation at day 1 after STEMI showed worse outcome during follow-up (hazard ratio, 2.57; 95% confidence interval, 1.72-3.85; P < .001). Receiver operating characteristic analysis revealed a cutoff value of 219.3 μg/L. In multivariate logistic regression analysis, thromboinflammation was independently associated with outcome after STEMI. To sum it up, thromboinflammation is enhanced in STEMI. It identifies patients at high risk of MACE. Therefore, thromboinflammation might be a promising target and marker in precision medicine. The trial was registered at www.clinicaltrials.gov as #NCT03539133.
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Benkhoff et al. (2024) conducted an observational in ST-elevation myocardial infarction (STEMI) (n=361). Thromboinflammation (H3Cit-DNA complexes) vs. Lower tertiles of thromboinflammation was evaluated on Major adverse cardiac events (MACEs) (HR 2.57, 95% CI 1.72-3.85, p=<.001). The highest tertile of thromboinflammation at day 1 after STEMI was associated with a higher risk of major adverse cardiac events.
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