Cargando…
Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases?
Cardiovascular diseases are prevalent in patients with chronic obstructive pulmonary disease (COPD). Their coexistence implies that many COPD patients require anticoagulation therapy. Although more and more replaced by direct oral anticoagulants, vitamin K antagonists (VKAs) are still widely used. V...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5683584/ https://www.ncbi.nlm.nih.gov/pubmed/29132356 http://dx.doi.org/10.1186/s12931-017-0673-z |
_version_ | 1783278316788121600 |
---|---|
author | Piscaer, Ianthe Wouters, Emiel F. M. Vermeer, Cees Janssens, Wim Franssen, Frits M. E. Janssen, Rob |
author_facet | Piscaer, Ianthe Wouters, Emiel F. M. Vermeer, Cees Janssens, Wim Franssen, Frits M. E. Janssen, Rob |
author_sort | Piscaer, Ianthe |
collection | PubMed |
description | Cardiovascular diseases are prevalent in patients with chronic obstructive pulmonary disease (COPD). Their coexistence implies that many COPD patients require anticoagulation therapy. Although more and more replaced by direct oral anticoagulants, vitamin K antagonists (VKAs) are still widely used. VKAs induce profound deficiency of vitamin K, a key activator in the coagulation pathway. It is recognized however that vitamin K is also an essential cofactor in the activation of other extrahepatic proteins, such as matrix Gla protein (MGP), a potent inhibitor of arterial calcification. No or insufficient MGP activation by the use of VKAs is associated with a rapid progression of vascular calcification, which may enhance the risk for overt cardiovascular disease. Vitamin K consumption, on the other hand, seems to have a protective effect on the mineralization of arteries. Furthermore, vascular calcification mutually relates to elastin degradation, which is accelerated in patients with COPD associating with impaired survival. In this commentary, we hypothesize that vitamin K is a critical determinant to the rate of elastin degradation. We speculate on the potential link between poor vitamin K status and crucial mechanisms of COPD pathogenesis and raise concerns about the use of VKAs in patients with this disease. Future intervention studies are needed to explore if vitamin K supplementation is able to reduce elastin degradation and vascular calcification in COPD patients. |
format | Online Article Text |
id | pubmed-5683584 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-56835842017-11-20 Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? Piscaer, Ianthe Wouters, Emiel F. M. Vermeer, Cees Janssens, Wim Franssen, Frits M. E. Janssen, Rob Respir Res Commentary Cardiovascular diseases are prevalent in patients with chronic obstructive pulmonary disease (COPD). Their coexistence implies that many COPD patients require anticoagulation therapy. Although more and more replaced by direct oral anticoagulants, vitamin K antagonists (VKAs) are still widely used. VKAs induce profound deficiency of vitamin K, a key activator in the coagulation pathway. It is recognized however that vitamin K is also an essential cofactor in the activation of other extrahepatic proteins, such as matrix Gla protein (MGP), a potent inhibitor of arterial calcification. No or insufficient MGP activation by the use of VKAs is associated with a rapid progression of vascular calcification, which may enhance the risk for overt cardiovascular disease. Vitamin K consumption, on the other hand, seems to have a protective effect on the mineralization of arteries. Furthermore, vascular calcification mutually relates to elastin degradation, which is accelerated in patients with COPD associating with impaired survival. In this commentary, we hypothesize that vitamin K is a critical determinant to the rate of elastin degradation. We speculate on the potential link between poor vitamin K status and crucial mechanisms of COPD pathogenesis and raise concerns about the use of VKAs in patients with this disease. Future intervention studies are needed to explore if vitamin K supplementation is able to reduce elastin degradation and vascular calcification in COPD patients. BioMed Central 2017-11-13 2017 /pmc/articles/PMC5683584/ /pubmed/29132356 http://dx.doi.org/10.1186/s12931-017-0673-z Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Commentary Piscaer, Ianthe Wouters, Emiel F. M. Vermeer, Cees Janssens, Wim Franssen, Frits M. E. Janssen, Rob Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? |
title | Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? |
title_full | Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? |
title_fullStr | Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? |
title_full_unstemmed | Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? |
title_short | Vitamin K deficiency: the linking pin between COPD and cardiovascular diseases? |
title_sort | vitamin k deficiency: the linking pin between copd and cardiovascular diseases? |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5683584/ https://www.ncbi.nlm.nih.gov/pubmed/29132356 http://dx.doi.org/10.1186/s12931-017-0673-z |
work_keys_str_mv | AT piscaerianthe vitaminkdeficiencythelinkingpinbetweencopdandcardiovasculardiseases AT woutersemielfm vitaminkdeficiencythelinkingpinbetweencopdandcardiovasculardiseases AT vermeercees vitaminkdeficiencythelinkingpinbetweencopdandcardiovasculardiseases AT janssenswim vitaminkdeficiencythelinkingpinbetweencopdandcardiovasculardiseases AT franssenfritsme vitaminkdeficiencythelinkingpinbetweencopdandcardiovasculardiseases AT janssenrob vitaminkdeficiencythelinkingpinbetweencopdandcardiovasculardiseases |