Figure 5
Figure 5. CAD patient plasma samples are hypocomplementemic for upstream CP components. (A) C4, (B) C2, (C) C5, and (D) C1s concentrations were determined in CAD (solid bars) and healthy (open bars) plasma samples by using plate-based ELISAs. Plasma concentrations of complement components were natural log transformed to yield normal distributions for statistical analysis. C4 was significantly reduced in CAD samples compared with healthy samples (e4.24 ± 0.24 vs e5.98 ± 0.35; n = 28 and 12, respectively). C2 also was reduced in CAD vs healthy samples (e3.40 ± 0.07 vs e3.94 ± 0.13; n = 37 and 12, respectively). By contrast, there was no difference in the C5 plasma concentrations between CAD and healthy samples (e4.50 ± 0.03 vs e4.37 ± 0.06; n = 37 and 12, respectively). Finally, C1s levels in CAD plasma samples were significantly reduced compared with healthy samples (e3.91 ± 0.07 vs e4.24 ± 0.12; n = 40 and 13, respectively). *P < .05; ***P < .001.

CAD patient plasma samples are hypocomplementemic for upstream CP components. (A) C4, (B) C2, (C) C5, and (D) C1s concentrations were determined in CAD (solid bars) and healthy (open bars) plasma samples by using plate-based ELISAs. Plasma concentrations of complement components were natural log transformed to yield normal distributions for statistical analysis. C4 was significantly reduced in CAD samples compared with healthy samples (e4.24 ± 0.24 vs e5.98 ± 0.35; n = 28 and 12, respectively). C2 also was reduced in CAD vs healthy samples (e3.40 ± 0.07 vs e3.94 ± 0.13; n = 37 and 12, respectively). By contrast, there was no difference in the C5 plasma concentrations between CAD and healthy samples (e4.50 ± 0.03 vs e4.37 ± 0.06; n = 37 and 12, respectively). Finally, C1s levels in CAD plasma samples were significantly reduced compared with healthy samples (e3.91 ± 0.07 vs e4.24 ± 0.12; n = 40 and 13, respectively). *P < .05; ***P < .001.

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