This could lead to fibrin deposition and aortic valve calcification.[9] A further mechanism suggests that Lp(a) may bind to fibrin and deliver cholesterol to sites of tissue injury, thus promoting calcification in patients with mild aortic stenosis.[10,11] In addition, it has recently been proposed that autotaxin derived from Lp(a) could promote inflammation and mineralisation promoting valve stenosis.[12]. Here, LPA is linked to aortic valve calcification.