Association of low ficolin-lectin pathway parameters with Cardiac Syndrome X

In patients with typical angina pectoris, inducable myocardial ischaemia and macroscopically normal coronaries (Cardiac Syndrome X, CSX) significantly elevated plasma level of terminal complement complex (TCC), the common end-product of complement activation, has been observed without subsequent activation of the classical or the alternative pathways. Therefore, our aim was to clarify the role of the ficolin-lectin pathway in CSX. Eighteen CSX patients, 37 stable angina patients with significant coronary stenosis (CHD) and 54 healthy volunteers (HC) were enrolled. Serum levels of ficolin-2, ficolin-3, ficolin-3/MASP-2 complex and ficolin-3 mediated TCC deposition (FCN3-TCC) were determined. Plasma level of TCC was significantly higher in CSX than in HC or in CHD groups (5.45 vs. 1.30 vs. 2.04AU/ml, p<0.001). Serum levels of ficolin-2 and ficolin-3 were significantly lower in CSX compared to HC or to CHD groups (3.60 vs. 5.80 or 5.20mug/ml, p<0.05; 17.80 vs. 24.10 or 26.80mug/ml, p<0.05). The ficolin-3/MASP-2 complex was significantly lower in CSX group compared to HC (92.90 vs. 144.90AU/ml, p=0.006). FCN3-TCC deposition was significantly lower in the CSX group compared to HC and to CHD (67.8% vs.143.3% or 159.7%, p<0.05). In the CSX group, significant correlation was found between TCC and FCN3-TCC level (r=0.507, p=0.032) and ficolin-3/MASP-2 complex level and FCN3-TCC deposition (r=0.651, p=0.003). In conclusion, in patients with typical angina and myocardial ischemia despite macroscopically normal coronary arteries, low levels of several lectin-pathway parameters were observed, indicating complement activation and consumption. Complement activation through the ficolin-lectin pathway might play a role in the complex pathomechanism of CSX. This article is protected by copyright. All rights reserved