This seems plausible: mitral regurgitation burdens the left ventricle with inflammation (mirrored by hsCRP and sST2) and fibrosis (mirrored by Galectin-3) in the early clinical course, but these mechanisms are gradually replaced by chronic remodelling processes with enlargement of the LV chamber, which are more appropriately represented by natriuretic peptides. This evidence concerns the gene LGALS3 and mitral valve insufficiency.