Key result
Salivary hs-cTnI, Endoglin, and Irisin strongly correlate with blood levels in acute MI.
Why the study?
Acute myocardial infarction requires rapid biochemical confirmation, and saliva offers a potential non-invasive alternative to venous sampling for measuring hs-cTnI and an adipokine panel.
Do salivary assay signals of hs-cTnI and an adipokine panel (Apelin, Elabela, Endoglin, Irisin, IMA) correlate with blood concentrations and differ between acute myocardial infarction patients and healthy controls?
Cross-Sectional (n=90)
No
Do salivary assay signals of hs-cTnI and an adipokine panel (Apelin, Elabela, Endoglin, Irisin, IMA) correlate with blood concentrations and differ between acute myocardial infarction patients and healthy controls?
This exploratory study demonstrates that hs-cTnI, Endoglin, and Irisin generate measurable salivary signals that strongly correlate with blood concentrations in AMI patients, supporting future matrix validation for non-invasive diagnostics.
Salivary hs-cTnI and adipokine signals may support non-invasive AMI detection; leaves open prospective validation before clinical adoption.
Acute myocardial infarction (AMI) requires rapid biochemical confirmation, and saliva offers a non-invasive alternative to venous sampling. We measured high-sensitivity cardiac troponin I (hs-cTnI), Apelin, Elabela, Endoglin, Irisin and ischaemia-modified albumin (IMA) in paired blood and saliva from 60 selected AMI patients presenting within six hours of symptom onset and 30 healthy controls. In blood, Irisin, Elabela and Apelin were lower in patients and Endoglin higher (all p ≤ 0.020). In saliva, Endoglin was higher and Irisin lower (both p < 0.001), and only these differences survived Bonferroni correction and age restriction ( p ≤ 0.030); IMA differed in neither matrix. Blood and salivary values correlated strongly (Spearman rs 0.773–0.979, all p < 0.001), but Bland–Altman analysis showed proportional differences and wide limits of agreement. Salivary hs-cTnI assay signals completely separated the two groups; because elevated serum hs-cTnI was an inclusion criterion and no salivary assay was matrix-validated, this reflects case selection rather than diagnostic accuracy. The adipokine panel did not demonstrate an improvement over hs-cTnI in an exploratory cross-validation analysis. These findings provide preliminary evidence that the six analytes generate measurable assay signals in saliva and support further investigation, including matrix-specific validation and prospective evaluation in undifferentiated chest pain.
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Gül et al. (2026) conducted a cross-sectional in Acute myocardial infarction (STEMI and NSTEMI) (n=90). Acute myocardial infarction (evaluated via paired salivary and blood hs-cTnI, Apelin, Elabela, Endoglin, Irisin, and IMA) vs. Healthy controls without cardiovascular disease, hypertension, or diabetes was evaluated on Salivary and blood biomarker levels (hs-cTnI, Endoglin, Irisin, Apelin, Elabela, IMA) and blood-saliva correlation (p=<0.001). Salivary and blood levels of hs-cTnI, Endoglin, and Irisin correlated strongly (rs 0.773-0.979, p<0.001), with higher Endoglin and lower Irisin in AMI patients vs controls (p<0.001).
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