Key result
Serum midkine levels rise in DCM but fail to distinguish inflammatory from non-inflammatory subtypes.
Why the study?
Identifying a serological biomarker to distinguish dilated cardiomyopathy from inflammatory dilated cardiomyopathy is crucial for effective treatment of these two entities.
Can midkine serum levels reliably distinguish between inflammatory and non-inflammatory dilated cardiomyopathy in patients with heart failure?
Cohort (n=67)
No
Can midkine serum levels reliably distinguish between inflammatory and non-inflammatory dilated cardiomyopathy in patients with heart failure?
Midkine serum levels are markedly elevated in patients with severe dilated cardiomyopathy phenotypes compared to healthy controls but cannot serve as a serological biomarker to differentiate between inflammatory and non-inflammatory dilated cardiomyopathy.
Serum midkine should not guide DCM subtype differentiation; leaves open its role as a severity marker in heart failure.
Objectives: This retrospective study examines midkine, an inflammatory cytokine, as a potential serological biomarker to distinguish dilated cardiomyopathy (DCM) and inflammatory dilated cardiomyopathy (DCMi). Identifying such a biomarker is crucial for effective treatment of these two entities. Methods: The study included 54 patients with heart failure, reduced left ventricular systolic function, and suspected cardiac inflammation. Endomyocardial biopsies were obtained from all 54 patients to differentiate between DCM and DCMi. Blood sera were collected from these patients the same day the endomyocardial biopsy was performed and compared with those of 13 age-matched healthy individuals for different measurements such as midkine and NT-proBNP. Patients were followed up to a median of 194 days after the baseline visit. Results: Endomyocardial biopsies from patients with DCMi were associated with more infiltrating immune cells such as CD68+ macrophages and CD3+ T cells and a more frequent presence of a viral genome than those from patients with DCM. Both groups showed similar improvements in LV function and dimensions over time. MK serum levels were significantly higher in DCM/ DCMi patients than in healthy individuals but did not differ significantly between DCM and DCMi. MK levels did not significantly correlate with NYHA class, NT-proBNP, LVEDD, or LVEF, except for a weak correlation with LVEF at follow-up. Conclusions: Midkine serum levels were significantly higher in patients with a DCM phenotype and severely reduced systolic function. However, these levels could not distinguish between DCM and DCMi and showed no correlation with baseline or follow-up parameters. Therefore, midkine cannot be used as a biomarker to distinguish between DCM and DCMi.
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Grabmaier et al. (2025) conducted a cohort in Dilated cardiomyopathy (DCM) and inflammatory dilated cardiomyopathy (DCMi) (n=67). Midkine serum levels vs. Healthy controls and non-inflammatory DCM was evaluated on Differentiation between DCM and DCMi using midkine serum levels (AUC 0.512, 95% CI 0.356-0.668, p=0.883). Midkine serum levels were significantly elevated in patients with a dilated cardiomyopathy phenotype compared to healthy controls but failed to distinguish between inflammatory and non-inflammatory subtypes.
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