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Therefore, our aim was to clarify the role of the ficolin\u2013lectin pathway in CSX<\/jats:styled-content>. Eighteen patients with CSX<\/jats:styled-content>, 37 stable angina patients with significant coronary stenosis (CHD<\/jats:styled-content>) and 54 healthy volunteers (HC<\/jats:styled-content>) were enrolled. Serum levels of ficolin\u20102 and ficolin\u20103, ficolin\u20103\/MASP<\/jats:styled-content>\u20102 complex and ficolin\u20103\u2010mediated TCC<\/jats:styled-content> deposition (FCN<\/jats:styled-content>3\u2010TCC<\/jats:styled-content>) were determined. Plasma level of TCC<\/jats:styled-content> was significantly higher in the CSX<\/jats:styled-content> than in the HC<\/jats:styled-content> or CHD<\/jats:styled-content> group (5.45 versus 1.30 versus 2.04\u00a0AU<\/jats:styled-content>\/ml, P<\/jats:italic>\u00a0<\u00a00.001). Serum levels of ficolin\u20102 and ficolin\u20103 were significantly lower in the CSX<\/jats:styled-content> compared to the HC<\/jats:styled-content> or CHD<\/jats:styled-content> group (3.60 versus 5.80 or 5.20\u00a0\u03bc<\/jats:italic>g\/ml, P<\/jats:italic>\u00a0<\u00a00.05; 17.80 versus 24.10 or 26.80\u00a0\u03bc<\/jats:italic>g\/ml, P<\/jats:italic>\u00a0<\u00a00.05). The ficolin\u20103\/MASP<\/jats:styled-content>\u20102 complex was significantly lower in the CSX<\/jats:styled-content> group compared to the HC<\/jats:styled-content> group (92.90 versus 144.90\u00a0AU<\/jats:styled-content>\/ml, P<\/jats:italic>\u00a0=\u00a00.006). FCN<\/jats:styled-content>3\u2010TCC<\/jats:styled-content> deposition was significantly lower in the CSX<\/jats:styled-content> group compared to the HC<\/jats:styled-content> and CHD<\/jats:styled-content> groups (67.8% versus 143.3% or 159.7%, P<\/jats:italic>\u00a0<\u00a00.05). In the CSX<\/jats:styled-content> group, a significant correlation was found between TCC<\/jats:styled-content> and FCN<\/jats:styled-content>3\u2010TCC<\/jats:styled-content> level (r<\/jats:italic>\u00a0=\u00a00.507, P<\/jats:italic>\u00a0=\u00a00.032) and between ficolin\u20103\/MASP<\/jats:styled-content>\u20102 complex level and FCN<\/jats:styled-content>3\u2010TCC<\/jats:styled-content> deposition (r<\/jats:italic>\u00a0=\u00a00.651, P<\/jats:italic>\u00a0=\u00a00.003). In conclusion, in patients with typical angina and myocardial ischaemia despite macroscopically normal coronary arteries, low levels of several lectin pathway parameters were observed, indicating complement activation and consumption. Complement activation through the ficolin\u2013lectin pathway might play a role in the complex pathomechanism of CSX<\/jats:styled-content>.<\/jats:p>","DOI":"10.1111\/sji.12454","type":"journal-article","created":{"date-parts":[[2016,6,17]],"date-time":"2016-06-17T08:01:02Z","timestamp":1466150462000},"page":"174-181","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Association of Low Ficolin\u2013Lectin Pathway Parameters with Cardiac Syndrome X"],"prefix":"10.1111","volume":"84","author":[{"given":"Z.","family":"Horv\u00e1th","sequence":"first","affiliation":[{"name":"Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University Budapest Hungary"},{"name":"Department of Cardiology Hungarian Defence Forces Medical Centre Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"D.","family":"Csuka","sequence":"additional","affiliation":[{"name":"3rd Department of Internal Medicine Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"K.","family":"Vargova","sequence":"additional","affiliation":[{"name":"Department of Cardiology Hungarian Defence Forces Medical Centre Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S.","family":"Le\u00e9","sequence":"additional","affiliation":[{"name":"Department of Cardiology Hungarian Defence Forces Medical Centre Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L.","family":"Varga","sequence":"additional","affiliation":[{"name":"3rd Department of Internal Medicine Semmelweis University Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P.","family":"Garred","sequence":"additional","affiliation":[{"name":"Laboratory of Molecular Medicine Department of Clinical Immunology Section\u00a07631 Rigshospitalet Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"I.","family":"Pr\u00e9da","sequence":"additional","affiliation":[{"name":"Research Group for Inflammation Biology and Immunogenomics of Hungarian Academy of Sciences and Semmelweis University Budapest Hungary"},{"name":"Department of Cardiology Hungarian Defence Forces Medical Centre Budapest Hungary"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"E. 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