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Association of Low Ficolin-Lectin Pathway Parameters with Cardiac Syndrome X
Z Horváth1,2, D Csuka3, K Vargova2
1Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University, Budapest, Hungary.
Scandinavian Journal of Immunology
|June 18, 2016
Summary
Cardiac Syndrome X (CSX) patients show elevated terminal complement complex (TCC) levels, suggesting complement activation. However, reduced ficolin-lectin pathway components indicate complement consumption in CSX.
Area of Science:
- Immunology
- Cardiology
- Complement System
Background:
- Cardiac Syndrome X (CSX) is characterized by angina with normal coronary arteries.
- Elevated terminal complement complex (TCC) levels are observed in CSX patients.
- Classical and alternative complement pathways are not activated in CSX.
Purpose of the Study:
- To investigate the role of the ficolin-lectin pathway in the pathogenesis of CSX.
- To compare lectin pathway parameters in CSX patients, coronary heart disease (CHD) patients, and healthy controls (HC).
Main Methods:
- Serum levels of ficolin-2, ficolin-3, ficolin-3/MASP-2 complex, and ficolin-3-mediated TCC deposition (FCN3-TCC) were measured.
- Plasma TCC levels were determined.
- Patients with CSX (n=18), CHD (n=37), and HC (n=54) were analyzed.
Main Results:
- Plasma TCC levels were significantly higher in CSX patients compared to HC and CHD groups.
- Serum ficolin-2 and ficolin-3 levels were significantly lower in CSX patients versus HC and CHD groups.
- Ficolin-3/MASP-2 complex and FCN3-TCC deposition were significantly lower in CSX patients compared to HC and CHD groups.
Conclusions:
- CSX patients exhibit reduced levels of ficolin-lectin pathway components, suggesting complement activation and consumption.
- The ficolin-lectin pathway may play a role in the complex pathophysiology of Cardiac Syndrome X.
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