Morten Kaltoft (Denmark)
Copenhagen University Hospital - Herlev and Gentofte Department of Clinical BiochemistryAuthor Of 1 Presentation
O055 - Elevated lipoprotein(a) in mitral and aortic valve calcification and stenosis: The Copenhagen General Population Study (ID 464)
Abstract
Background and Aims
We tested the hypotheses (i) that elevated lipoprotein(a) is causally associated with both mitral and aortic valve calcification, and (ii) that aortic valve calcification mediates the effect of elevated lipoprotein(a) on aortic valve stenosis.
Methods
From the Copenhagen General Population study, we included 12,006 individuals who underwent cardiac computed tomography to measure mitral and aortic valve calcification. Participants had information on plasma lipoprotein(a), LPA kringle IV type 2 number of repeats; and two single nucleotide polymorphisms (LPA rs10455872 and rs3798220); genetic instruments known to be associated with plasma lipoprotein(a). These instruments were used to investigate the genetic association of lipoprotein(a) with mitral and aortic valve calcification to indicate causality.
Results
At age 70-79, 29% and 54% had mitral and aortic valve calcification. For 10-fold higher lipoprotein(a) levels, multifactorially adjusted odds ratios for mitral and aortic valve calcification were 1.26 (95% CI: 1.13-1.41) and 1.65 (1.50-1.81). Correspondingly, for ≤23 versus ≥36 kringle IV type 2 number of repeats the age and sex adjusted odds ratios for mitral and aortic valve calcification were 1.53 (1.18-1.99) and 2.23 (1.81-2.76). For carriers versus non-carriers of LPA rs10455872, odds ratios for mitral and aortic valve calcification were 1.33 (1.13-1.57) and 1.86 (1.64-2.13). For aortic valve stenosis, 20% (95% CI: 12%-28%) of the effect of lipoprotein(a) was mediated through calcification.
Conclusions
Elevated lipoprotein(a) was causally from human genetics and observationally associated with both mitral and aortic valve calcification. Aortic valve calcification mediated 20% of the effect of elevated lipoprotein(a) on aortic valve stenosis.
Presenter of 1 Presentation
O055 - Elevated lipoprotein(a) in mitral and aortic valve calcification and stenosis: The Copenhagen General Population Study (ID 464)
Abstract
Background and Aims
We tested the hypotheses (i) that elevated lipoprotein(a) is causally associated with both mitral and aortic valve calcification, and (ii) that aortic valve calcification mediates the effect of elevated lipoprotein(a) on aortic valve stenosis.
Methods
From the Copenhagen General Population study, we included 12,006 individuals who underwent cardiac computed tomography to measure mitral and aortic valve calcification. Participants had information on plasma lipoprotein(a), LPA kringle IV type 2 number of repeats; and two single nucleotide polymorphisms (LPA rs10455872 and rs3798220); genetic instruments known to be associated with plasma lipoprotein(a). These instruments were used to investigate the genetic association of lipoprotein(a) with mitral and aortic valve calcification to indicate causality.
Results
At age 70-79, 29% and 54% had mitral and aortic valve calcification. For 10-fold higher lipoprotein(a) levels, multifactorially adjusted odds ratios for mitral and aortic valve calcification were 1.26 (95% CI: 1.13-1.41) and 1.65 (1.50-1.81). Correspondingly, for ≤23 versus ≥36 kringle IV type 2 number of repeats the age and sex adjusted odds ratios for mitral and aortic valve calcification were 1.53 (1.18-1.99) and 2.23 (1.81-2.76). For carriers versus non-carriers of LPA rs10455872, odds ratios for mitral and aortic valve calcification were 1.33 (1.13-1.57) and 1.86 (1.64-2.13). For aortic valve stenosis, 20% (95% CI: 12%-28%) of the effect of lipoprotein(a) was mediated through calcification.
Conclusions
Elevated lipoprotein(a) was causally from human genetics and observationally associated with both mitral and aortic valve calcification. Aortic valve calcification mediated 20% of the effect of elevated lipoprotein(a) on aortic valve stenosis.