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Proteoglycan Remodeling Is Accelerated in Females with Angina Pectoris and Diffuse Myocardial Fibrosis: the iPOWER Study

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review


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Vis graf over relationer

Angina and no obstructive coronary artery disease (CAD) have an unfavorable prognosis, possibly due to diffuse myocardial fibrosis (DMF). In DMF the proteoglycans biglycan and versican are actively remodeled by matrix metalloproteinase. We investigated biglycan and versican in females with angina and possible DMF assessed by cardiac magnetic resonance (CMR). Seventy-one females with angina and no obstructive CAD were included. Asymptomatic females served as controls. Versican and biglycan were measured and CMR was performed measuring extracellular volume. Biglycan and versican levels were higher in symptomatic females compared with controls; 31.4 ng/mL vs. 16.4 ng/mL (p < 0.001) and 2.1 ng/mL vs. 1.8 ng/mL (p < 0.001) and moderately correlated to extracellular volume (r 2 = 0.38, p<0.001 and r 2 = 0.26, p = 0.015). Turnover of biglycan and versican was increased in angina females compared with controls and associated with extracellular volume, supporting a link between angina with no obstructive CAD and fibrotic remodeling. Graphical abstract: [Figure not available: see fulltext.]

TidsskriftJournal of Cardiovascular Translational Research
Udgave nummer5
Sider (fra-til)921-929
Antal sider9
StatusUdgivet - okt. 2021

Bibliografisk note

Funding Information:
The authors would like to thank the Danish Heart Foundation, the University of Copenhagen, The Innovation Foundation, and the Danish Research Fund (Den Danske Forskningsfond) for financial support and all collaborators in the iPOWER group. We also thank the Department of Cardiology at Bispebjerg Hospital and the Department of Radiology at Rigshospitalet where the examinations have taken place. A special thanks to the CMR technicians Birte Kjærulff, Jesper Kromann, Andrija Srkoc, and Torben Vaaben for assisting in scanning the participants. Finally, we thank all the participants for their time and willingness to contribute to the research.

Funding Information:
This work was supported by The Danish Heart Foundation (grant number: 11-10-R87-B-A3628-22678), the Danish Research Fund (Den Danske Forskningsfond), and the University of Copenhagen.

ID: 64081685