Association of Low Ficolin-Lectin Pathway Parameters with Cardiac Syndrome X
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Association of Low Ficolin-Lectin Pathway Parameters with Cardiac Syndrome X. / Horváth, Z; Csuka, Dorottya; Vargova, K; Leé, S; Varga, L; Garred, P; Préda, I; Zsámboki, E T; Prohászka, Zoltán; Kiss, Robert Gabor.
I: Scandinavian Journal of Immunology, Bind 84, Nr. 3, 09.2016, s. 174-81.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Association of Low Ficolin-Lectin Pathway Parameters with Cardiac Syndrome X
AU - Horváth, Z
AU - Csuka, Dorottya
AU - Vargova, K
AU - Leé, S
AU - Varga, L
AU - Garred, P
AU - Préda, I
AU - Zsámboki, E T
AU - Prohászka, Zoltán
AU - Kiss, Robert Gabor
N1 - © 2016 The Foundation for the Scandinavian Journal of Immunology.
PY - 2016/9
Y1 - 2016/9
N2 - In patients with typical angina pectoris, inducible myocardial ischaemia and macroscopically normal coronaries (cardiac syndrome X (CSX)), a significantly elevated plasma level of terminal complement complex (TCC), the common end product of complement activation, has been observed without accompanying activation of the classical or the alternative pathways. Therefore, our aim was to clarify the role of the ficolin-lectin pathway in CSX. Eighteen patients with CSX, 37 stable angina patients with significant coronary stenosis (CHD) and 54 healthy volunteers (HC) were enrolled. Serum levels of ficolin-2 and 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 the CSX than in the HC or CHD group (5.45 versus 1.30 versus 2.04 AU/ml, P < 0.001). Serum levels of ficolin-2 and ficolin-3 were significantly lower in the CSX compared to the HC or CHD group (3.60 versus 5.80 or 5.20 μg/ml, P < 0.05; 17.80 versus 24.10 or 26.80 μg/ml, P < 0.05). The ficolin-3/MASP-2 complex was significantly lower in the CSX group compared to the HC group (92.90 versus 144.90 AU/ml, P = 0.006). FCN3-TCC deposition was significantly lower in the CSX group compared to the HC and CHD groups (67.8% versus 143.3% or 159.7%, P < 0.05). In the CSX group, a significant correlation was found between TCC and FCN3-TCC level (r = 0.507, P = 0.032) and between 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 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-lectin pathway might play a role in the complex pathomechanism of CSX.
AB - In patients with typical angina pectoris, inducible myocardial ischaemia and macroscopically normal coronaries (cardiac syndrome X (CSX)), a significantly elevated plasma level of terminal complement complex (TCC), the common end product of complement activation, has been observed without accompanying activation of the classical or the alternative pathways. Therefore, our aim was to clarify the role of the ficolin-lectin pathway in CSX. Eighteen patients with CSX, 37 stable angina patients with significant coronary stenosis (CHD) and 54 healthy volunteers (HC) were enrolled. Serum levels of ficolin-2 and 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 the CSX than in the HC or CHD group (5.45 versus 1.30 versus 2.04 AU/ml, P < 0.001). Serum levels of ficolin-2 and ficolin-3 were significantly lower in the CSX compared to the HC or CHD group (3.60 versus 5.80 or 5.20 μg/ml, P < 0.05; 17.80 versus 24.10 or 26.80 μg/ml, P < 0.05). The ficolin-3/MASP-2 complex was significantly lower in the CSX group compared to the HC group (92.90 versus 144.90 AU/ml, P = 0.006). FCN3-TCC deposition was significantly lower in the CSX group compared to the HC and CHD groups (67.8% versus 143.3% or 159.7%, P < 0.05). In the CSX group, a significant correlation was found between TCC and FCN3-TCC level (r = 0.507, P = 0.032) and between 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 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-lectin pathway might play a role in the complex pathomechanism of CSX.
KW - Adult
KW - Case-Control Studies
KW - Complement Membrane Attack Complex
KW - Complement Pathway, Mannose-Binding Lectin
KW - Enzyme-Linked Immunosorbent Assay
KW - Female
KW - Gene Expression Regulation
KW - Glycoproteins
KW - Humans
KW - Lectins
KW - Male
KW - Mannose-Binding Protein-Associated Serine Proteases
KW - Microvascular Angina
KW - Middle Aged
KW - Signal Transduction
KW - Journal Article
U2 - 10.1111/sji.12454
DO - 10.1111/sji.12454
M3 - Journal article
C2 - 27312152
VL - 84
SP - 174
EP - 181
JO - Scandinavian Journal of Immunology, Supplement
JF - Scandinavian Journal of Immunology, Supplement
SN - 0301-6323
IS - 3
ER -
ID: 177522751