Heart failure is associated with accelerated age related metabolic bone disease

Abstract

Background

The heart failure (HF)-syndrome is associated with neuro-hormonal activation, chronic kidney disease (CKD), inflammation and alterations in the phosphorus-metabolism, all of which are involved in regulation of mineral bone density. However, the role of HF as an independent factor associated with metabolic bone disease (MBD) remains unclear.

Methods

HF-patients undergoing dual X-ray absorptiometry (DEXA) were matched in a 1:2 fashion against age and gender matched controls without HF, to determine the proportion of osteoporosis (T-score < −2.5). HF-status was tested against known predictors of MBD. Correlation analysis and Z-score analysis were used to assess the impact of HF on age-related bone demineralisation.

Results

A total of 190 HF-patients (age = 80 ± 10 years, female = 61%) were age and gender matched to 380 controls. HF-patients had a higher proportion of osteoporosis (26 vs 17%; p = .007). HF patients had a lower averaged mineral bone density expressed in g/cm² (p = .030), T-scores (p = .001) and Z-scores (p < .001). After adjusting for the individual osteoporosis risk-factors of the FRAX-score, difference in baseline features, kidney function and phosphorus-metabolism alterations, heart failure remained independently associated with a lower averaged T-score (Adjusted β = –0.189; p = .017). Heart failure was associated with an accelerated age-related decline in mineral bone density (p = .0418). Therapies with ACE-I or ARBs and beta-blockers associated with ameliorated bone demineralisation (p = .023, respectively p = .029), while loop diuretic associated with worsened bone demineralization (p < .001).

Conclusion

Heart failure independently associates with MBD and higher prevalence of osteoporosis. Heart failure aggravates the aged related loss in mineral bone density while treatment with neuro-hormonal blockers seemed to ameliorate this finding.

Keywords:

• Heart failure
• comorbidities
• geriatrics
• osteoporosis
• metabolic bone disease

Acknowledgements

Pieter Martens and Wilfried Mullens are researchers for the Limburg Clinical Research Centre (LCRC) UHasselt-ZOL-Jessa, supported by the foundation Limburg Sterk Merk (LSM), Hasselt University, Ziekenhuis Oost-Limburg and Jessa Hospital.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

Pieter Martens is supported by a doctoral fellowship by the Research Foundation – Flanders [FWO, grant-number: 11,27,917 N].