Coronary artery- and aortic valve calcifications in patients with Philadelphia-negative myeloproliferative neoplasms

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Background: Patients with the hematological cancers Philadelphia-negative Myeloproliferative Neoplasms (MPNs) have an increased risk of cardiovascular disease. However, whether MPNs have an increased burden of cardiac calcification has not been thoroughly investigated. Our aim is to investigate whether patients with MPNs have an increased burden of cardiac calcification that could help explain their increased risk of cardiovascular disease. Methods and results: We recruited 161 patients (mean age 65 years, 52% men) with an MPN diagnosis between 2016 and 2018. Coronary artery calcium score (CACS) and aortic valve calcification (AVC) were measured by cardiac computer tomography, and detailed information on cardiovascular risk factors was recorded. MPNs were matched on age and sex, with 805 controls from the Copenhagen General Population Study. A CACS>400 was present in 26% of MPNs and 19% of controls (p = 0.031). AVC was present in 58% of MPNs and 34% of controls (p < 0.0001). After adjustment for cardiovascular risk factors, the odds ratio (OR) of a CACS>400 was 1.9 (95% CI 1.2–3.1, p = 0.008) in MPNs compared to controls, and the OR of AVC was 4.4 (95% CI 2.9–6.9, p < 0.0001) in MPNs compared to controls. Conclusion: Patients with MPNs have a significantly higher prevalence of a CACS >400 and AVC, compared to controls from the general population. The association between MPN and a CACS>400 or AVC remains significant after adjustment for cardiovascular risk factors. These novel data support the hypothesis that MPNs have an increased burden of cardiac calcifications, independent of other cardiovascular risk factors.

OriginalsprogEngelsk
TidsskriftInternational Journal of Cardiology
Vol/bind364
Sider (fra-til)112-118
Antal sider7
ISSN0167-5273
DOI
StatusUdgivet - 2022

Bibliografisk note

Funding Information:
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper: PES reports consultancies for Novo Nordisk and Actelion. NEB has received investigator initiated founding from The Novo Nordisk Foundation, The Kaj Hansens Foundation, The Augustinus Foundation, Health Insurance Denmark, Copenhagen University, and Region South. KFK reports grants from the A.P Møller and wife Chastine McKinney Møller foundation, the Danish Heart Association, The Danish Agency for Science, Technology and Innovation by The Danish Council for Strategic Research, Health Insurance Denmark, Canon Medical Corporation, and GE Healthcare.

Funding Information:
This work was supported by Region Sjællands Sundhedsvidenskabelige Forskningsfond [grant number RSSF2017000654 ]; The A.P Møller Foundation for the Advancement of Medical Science [Grant number 17-L-0517 ]; University of Copenhagen Cancer Research Foundation [Grant number 2021–0004 ]; Fabrikant Einar Willumsens Mindelegat [Grant number 20844469 ]; Direktør Kurt Bønnelycke og hustru Grethe Bønnelyckes Fond [Grant number 10053–030 ]; Tømrermester Jørgen Holm og hustru Elisa F. Hansens Mindelegat [Grant number 20006–1952 ]; Aase og Ejnar Danielsens Fond ; Trigon Fonden and A.V. Lyckfeldt og hustrus legat.

Publisher Copyright:
© 2022 The Author(s)

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