Abstract
Background and aimsWe tested the hypotheses (i) that elevated lipoprotein(a) is causally associated with both mitral and aortic valve calcification and disease, and (ii) that aortic valve calcification mediates the effect of elevated lipoprotein(a) on aortic valve stenosis. MethodsFrom the Copenhagen General Population study, we included 12,006 individuals who underwent cardiac computed tomography to measure mitral and aortic valve calcification and 85,884 to examine risk of heart valve disease. Participants had information on plasma lipoprotein(a) and genetic instruments associated with plasma lipoprotein(a) to investigate potential causality. ResultsAt age 70–79 years, 29% and 54% had mitral and aortic valve calcification, respectively. For 10-fold higher lipoprotein(a) levels, multifactorially adjusted odds ratios for mitral and aortic valve calcification were 1.26 (95% confidence interval: 1.13–1.41) and 1.62 (1.48–1.77). For mitral and aortic valve stenosis, corresponding hazard ratios were 0.93 (95%CI:0.40–2.15, 19 events) and 1.54 (1.38–1.71, 1158 events), respectively. 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, 31% (95%CI:16%–76%) of the effect of lipoprotein(a) was mediated through calcification. ConclusionsElevated lipoprotein(a) was genetically and observationally associated with mitral and aortic valve calcification and aortic valve stenosis. Aortic valve calcification mediated 31% of the effect of elevated lipoprotein(a) on aortic valve stenosis.
Highlights
Aortic and mitral valve calcification has increasing prevalence with age, and due to higher life expectancies in the future, prevalence is ex pected to rise even further [1,2]
From the Copenhagen General Population Study, we examined 12,006 individuals who un derwent cardiac computed tomography to measure mitral and aortic valve calcification, and 85,884 to examine risk of mitral and aortic valve disease, that is, stenosis or regurgitation
In the Danish general population, elevated plasma lipoprotein(a) was observationally and genetically, causally associated with increased risk of mitral and aortic valve calcification. These findings suggest that li poprotein(a) is one of several factors that facilitate the evolution of mitral and aortic valve calcification
Summary
Aortic and mitral valve calcification has increasing prevalence with age, and due to higher life expectancies in the future, prevalence is ex pected to rise even further [1,2]. Both aortic and mitral valve calcifi cations may impact risk of heart valve disease and death [3,4,5,6,7]. We tested the hypotheses (i) that elevated lipoprotein(a) is causally associated with both mitral and aortic valve calcification and disease, and (ii) that aortic valve calcification mediates the effect of elevated lipoprotein(a) on aortic valve stenosis. Conclusions: Elevated lipoprotein(a) was genetically and observationally associated with mitral and aortic valve calcification and aortic valve stenosis. Aortic valve calcification mediated 31% of the effect of elevated lipo protein(a) on aortic valve stenosis
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