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Prognostic Value of Circulating Fibrosis Biomarkers in Dilated Cardiomyopathy (DCM): Insights into Clinical Outcomes

Overview
Journal Biomolecules
Publisher MDPI
Date 2024 Sep 28
PMID 39334904
Authors
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Abstract

Background: Dilated cardiomyopathy (DCM) involves myocardial remodeling, characterized by significant fibrosis and extracellular matrix expansion. These changes impair heart function, increasing the risk of heart failure and sudden cardiac death. This study investigates the prognostic value of circulating fibrosis biomarkers as a less invasive method in DCM patients.

Methods: Plasma samples from 185 patients with confirmed DCM were analyzed to measure 13 circulating biomarkers using Luminex bead-based multiplex assays and ELISA. The prognostic value of these biomarkers was evaluated concerning heart failure-associated events and all-cause mortality.

Results: Elevated MMP-2 levels (>1519.3 ng/mL) were linked to older age, higher diabetes prevalence, lower HDL, increased NT-proBNP and hs-TnT levels, and severe systolic dysfunction. High TIMP-1 levels (>124.9 ng/mL) correlated with elevated NT-proBNP, more atrial fibrillation, reduced exercise capacity, and larger right ventricles. Increased GDF-15 levels (>1213.9 ng/mL) were associated with older age, systemic inflammation, renal impairment, and poor exercise performance. Elevated OPN levels (>81.7 ng/mL) were linked to higher serum creatinine and NT-proBNP levels. Over a median follow-up of 32.4 months, higher levels of these biomarkers predicted worse outcomes, including increased risks of heart failure-related events and mortality.

Conclusions: Circulating fibrosis biomarkers, particularly MMP-2, TIMP-1, GDF-15, and OPN, are valuable prognostic tools in DCM. They reflect the severity of myocardial remodeling and systemic disease burden, aiding in risk stratification and therapeutic intervention. Integrating these biomarkers into clinical practice could improve DCM management and patient prognosis.

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References
1.
Krishnamurthy P, Thomas Peterson J, Subramanian V, Singh M, Singh K . Inhibition of matrix metalloproteinases improves left ventricular function in mice lacking osteopontin after myocardial infarction. Mol Cell Biochem. 2008; 322(1-2):53-62. PMC: 2711544. DOI: 10.1007/s11010-008-9939-6. View

2.
Spinale F, Coker M, Heung L, Bond B, Gunasinghe H, Etoh T . A matrix metalloproteinase induction/activation system exists in the human left ventricular myocardium and is upregulated in heart failure. Circulation. 2000; 102(16):1944-9. DOI: 10.1161/01.cir.102.16.1944. View

3.
Banfi C, Cavalca V, Veglia F, Brioschi M, Barcella S, Mussoni L . Neurohormonal activation is associated with increased levels of plasma matrix metalloproteinase-2 in human heart failure. Eur Heart J. 2004; 26(5):481-8. DOI: 10.1093/eurheartj/ehi073. View

4.
Lau C, Gul U, Liu B, Captur G, Hothi S . Cardiovascular Magnetic Resonance Imaging in Familial Dilated Cardiomyopathy. Medicina (Kaunas). 2023; 59(3). PMC: 10057087. DOI: 10.3390/medicina59030439. View

5.
Kempf T, Zarbock A, Widera C, Butz S, Stadtmann A, Rossaint J . GDF-15 is an inhibitor of leukocyte integrin activation required for survival after myocardial infarction in mice. Nat Med. 2011; 17(5):581-8. DOI: 10.1038/nm.2354. View