Serum Talin-1 and Pentraxin-3 levels as biomarkers for vulnerable plaques in STEMI: Correlation with SYNTAX and Gensini scores

Cardiovascular diseases, especially ischemic heart diseases, are the leading cause of death globally, highlighting the need for improved diagnostic tools for vulnerable plaques. This study aimed to evaluate the potential of soluble Talin-1 (sTalin-1) and Pentraxin-3 (PTX-3) as biomarkers in patients with ST-elevation myocardial infarction (STEMI). Conducted as a single-center observational study, it included 40 STEMI patients and 30 controls with normal coronary arteries. Serum levels of sTalin-1 and PTX-3 were measured using enzyme-linked immunosorbent assays (ELISA), and disease severity was assessed with SYNTAX and Gensini scores. Results showed that STEMI patients had significantly lower levels of sTalin-1 and higher levels of PTX-3 compared to controls. ROC curve analysis revealed an area under the curve (AUC) of 0.785 for sTalin-1 and 0.702 for PTX-3 in differentiating between STEMI patients and controls. While sTalin-1 demonstrated high specificity but low sensitivity, PTX-3 exhibited moderate sensitivity and specificity. Talin-1 levels negatively correlated with SYNTAX and Gensini scores, suggesting its role in assessing disease severity. These findings suggest that decreased serum levels of sTalin-1 and increased levels of PTX-3 in STEMI patients could serve as potential biomarkers for identifying vulnerable plaques and assessing disease severity. The study supports the potential use of sTalin-1 and PTX-3 in the diagnostic and prognostic evaluation of acute coronary syndromes.

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Publication Details

Journal
Journal of Investigative Medicine
Published
2025-04-02
DOI
https://doi.org/10.1177/10815589251333444
Primary Topic
Biomarkers in Disease Mechanisms
Type
article
Field-Weighted Citation Impact
0.00
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article

Serum Talin-1 and Pentraxin-3 levels as biomarkers for vulnerable plaques in STEMI: Correlation with SYNTAX and Gensini scores

Sara Çetin Şanlıalp, Gökay Nar, Rukiye Nar, Işık Tekin et al.
Journal of Investigative Medicine
Biomarkers in Disease Mechanisms
article

Serum Talin-1 and Pentraxin-3 levels as biomarkers for vulnerable plaques in STEMI: Correlation with SYNTAX and Gensini scores

Sara Çetin Şanlıalp, Gökay Nar, Rukiye Nar, Işık Tekin, Gürsel Şen, Harun Akarsu
article en

Abstract

Cardiovascular diseases, especially ischemic heart diseases, are the leading cause of death globally, highlighting the need for improved diagnostic tools for vulnerable plaques. This study aimed to evaluate the potential of soluble Talin-1 (sTalin-1) and Pentraxin-3 (PTX-3) as biomarkers in patients with ST-elevation myocardial infarction (STEMI). Conducted as a single-center observational study, it included 40 STEMI patients and 30 controls with normal coronary arteries. Serum levels of sTalin-1 and PTX-3 were measured using enzyme-linked immunosorbent assays (ELISA), and disease severity was assessed with SYNTAX and Gensini scores. Results showed that STEMI patients had significantly lower levels of sTalin-1 and higher levels of PTX-3 compared to controls. ROC curve analysis revealed an area under the curve (AUC) of 0.785 for sTalin-1 and 0.702 for PTX-3 in differentiating between STEMI patients and controls. While sTalin-1 demonstrated high specificity but low sensitivity, PTX-3 exhibited moderate sensitivity and specificity. Talin-1 levels negatively correlated with SYNTAX and Gensini scores, suggesting its role in assessing disease severity. These findings suggest that decreased serum levels of sTalin-1 and increased levels of PTX-3 in STEMI patients could serve as potential biomarkers for identifying vulnerable plaques and assessing disease severity. The study supports the potential use of sTalin-1 and PTX-3 in the diagnostic and prognostic evaluation of acute coronary syndromes.

Journal of Investigative MedicineVol. 73(6)
Ministry of Health (TR), Isparta University of Applied Sciences (TR), Denizli Devlet Hastanesi (TR), Pamukkale University (TR)
Openalex Percentile: Top 93%
Biomarkers in Disease Mechanisms
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