Although CRP was previously treated simply as a marker of inflammation, evidences have been presented that, like the proinflammatory cytokines, CRP exerts detrimental effect on the heart by amplifying the inflammatory response responsible for adverse ventricular remodeling, which could explain especially a significant difference of CRP levels between chronic types of CRS and control group in our study [19, 20]. This evidence concerns the gene CRP and congenital rubella syndrome.