ArticleESC heart failure2020
Coagulation factor XIII activity predicts left ventricular remodelling after acute myocardial infarction.
Article in ESC heart failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Linking factor XIII activity to all-cause mortality after myocardial infarction: the overlooked role of serum albumin.International journal of cardiology. Heart & vasculature · 2025Article
- Differential Role of Factor XIII in Acute Myocardial Infarction and Ischemic Stroke.Biomedicines · 2024Review
- Interaction between Acute Hepatic Injury and Early Coagulation Dysfunction on Mortality in Patients with Acute Myocardial Infarction.Journal of clinical medicine · 2023Article
- Use of serial changes in biomarkers vs. baseline levels to predict left ventricular remodelling after STEMI.ESC heart failure · 2023Article
- Sustained Increase in Serum Glial Fibrillary Acidic Protein after First ST-Elevation Myocardial Infarction.International journal of molecular sciences · 2022Article
- Coagulation factor XIII activity predicts left ventricular remodelling after acute myocardial infarction.ESC heart failure · 2020Article
- Machine Learning Analysis of the Cerebrovascular Thrombi Proteome in Human Ischemic Stroke: An Exploratory Study.Frontiers in neurology · 2020Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
aimsAcute myocardial infarction (MI) is the major cause of chronic heart failure. The activity of blood coagulation factor XIII (FXIIIa) plays an important role in rodents as a healing factor after MI, whereas its role in healing and remodelling processes in humans remains unclear. We prospectively evaluated the relevance of FXIIIa after acute MI as a potential early prognostic marker for adequate healing. METHODS AND
resultsThis monocentric prospective cohort study investigated cardiac remodelling in patients with ST-elevation MI and followed them up for 1 year. Serum FXIIIa was serially assessed during the first 9 days after MI and after 2, 6, and 12 months. Cardiac magnetic resonance imaging was performed within 4 days after MI (Scan 1), after 7 to 9 days (Scan 2), and after 12 months (Scan 3). The FXIII valine-to-leucine (V34L) single-nucleotide polymorphism rs5985 was genotyped. One hundred forty-six patients were investigated (mean age 58 ± 11 years, 13% women). Median FXIIIa was 118% (quartiles, 102-132%) and dropped to a trough on the second day after MI: 109% (98-109%; P < 0.001). FXIIIa recovered slowly over time, reaching the baseline level after 2 to 6 months and surpassed baseline levels only after 12 months: 124% (110-142%). The development of FXIIIa after MI was independent of the genotype. FXIIIa on Day 2 was strongly and inversely associated with the relative size of MI in Scan 1 (Spearman's ρ = -0.31; P = 0.01) and Scan 3 (ρ = -0.39; P < 0.01) and positively associated with left ventricular ejection fraction: ρ = 0.32 (P < 0.01) and ρ = 0.24 (P = 0.04), respectively.
conclusionsFXIII activity after MI is highly dynamic, exhibiting a significant decline in the early healing period, with reconstitution 6 months later. Depressed FXIIIa early after MI predicted a greater size of MI and lower left ventricular ejection fraction after 1 year. The clinical relevance of these findings awaits to be tested in a randomized trial.
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