Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Elevated lipoprotein(a) in mitral and aortic valve calcification and disease : The Copenhagen General Population Study. / Kaltoft, Morten; Sigvardsen, Per E.; Afzal, Shoaib; Langsted, Anne; Fuchs, Andreas; Kühl, Jørgen Tobias; Køber, Lars; Kamstrup, Pia R.; Kofoed, Klaus F.; Nordestgaard, Børge G.

I: Atherosclerosis, Bind 349, 2022, s. 166-174.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Kaltoft, M, Sigvardsen, PE, Afzal, S, Langsted, A, Fuchs, A, Kühl, JT, Køber, L, Kamstrup, PR, Kofoed, KF & Nordestgaard, BG 2022, 'Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study', Atherosclerosis, bind 349, s. 166-174. https://doi.org/10.1016/j.atherosclerosis.2021.11.029

APA

Kaltoft, M., Sigvardsen, P. E., Afzal, S., Langsted, A., Fuchs, A., Kühl, J. T., Køber, L., Kamstrup, P. R., Kofoed, K. F., & Nordestgaard, B. G. (2022). Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study. Atherosclerosis, 349, 166-174. https://doi.org/10.1016/j.atherosclerosis.2021.11.029

Vancouver

Kaltoft M, Sigvardsen PE, Afzal S, Langsted A, Fuchs A, Kühl JT o.a. Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study. Atherosclerosis. 2022;349:166-174. https://doi.org/10.1016/j.atherosclerosis.2021.11.029

Author

Kaltoft, Morten ; Sigvardsen, Per E. ; Afzal, Shoaib ; Langsted, Anne ; Fuchs, Andreas ; Kühl, Jørgen Tobias ; Køber, Lars ; Kamstrup, Pia R. ; Kofoed, Klaus F. ; Nordestgaard, Børge G. / Elevated lipoprotein(a) in mitral and aortic valve calcification and disease : The Copenhagen General Population Study. I: Atherosclerosis. 2022 ; Bind 349. s. 166-174.

Bibtex

@article{e8e4cb69b8f540718eca18c4a5ea3bd8,
title = "Elevated lipoprotein(a) in mitral and aortic valve calcification and disease: The Copenhagen General Population Study",
abstract = "Background and aims: 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. Methods: From 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. Results: At 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. 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 lipoprotein(a) on aortic valve stenosis.",
keywords = "Heart valve, Lp(a), Stenosis",
author = "Morten Kaltoft and Sigvardsen, {Per E.} and Shoaib Afzal and Anne Langsted and Andreas Fuchs and K{\"u}hl, {J{\o}rgen Tobias} and Lars K{\o}ber and Kamstrup, {Pia R.} and Kofoed, {Klaus F.} and Nordestgaard, {B{\o}rge G.}",
note = "Publisher Copyright: {\textcopyright} 2021 The Authors",
year = "2022",
doi = "10.1016/j.atherosclerosis.2021.11.029",
language = "English",
volume = "349",
pages = "166--174",
journal = "Atherosclerosis",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",

}

RIS

TY - JOUR

T1 - Elevated lipoprotein(a) in mitral and aortic valve calcification and disease

T2 - The Copenhagen General Population Study

AU - Kaltoft, Morten

AU - Sigvardsen, Per E.

AU - Afzal, Shoaib

AU - Langsted, Anne

AU - Fuchs, Andreas

AU - Kühl, Jørgen Tobias

AU - Køber, Lars

AU - Kamstrup, Pia R.

AU - Kofoed, Klaus F.

AU - Nordestgaard, Børge G.

N1 - Publisher Copyright: © 2021 The Authors

PY - 2022

Y1 - 2022

N2 - Background and aims: 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. Methods: From 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. Results: At 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. 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 lipoprotein(a) on aortic valve stenosis.

AB - Background and aims: 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. Methods: From 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. Results: At 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. 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 lipoprotein(a) on aortic valve stenosis.

KW - Heart valve

KW - Lp(a)

KW - Stenosis

U2 - 10.1016/j.atherosclerosis.2021.11.029

DO - 10.1016/j.atherosclerosis.2021.11.029

M3 - Journal article

C2 - 34903381

AN - SCOPUS:85121273008

VL - 349

SP - 166

EP - 174

JO - Atherosclerosis

JF - Atherosclerosis

SN - 0021-9150

ER -

ID: 288185435