Abstract 828: Plasma Parathyroid Hormone and Risk of Congestive Heart Failure in the Community
Background Patients with diseases with increased levels of parathyroid hormone (PTH), such as primary hyperparathyroidism or secondary hyperparathyroidism due to chronic renal failure, have a higher risk of developing ischemic heart disease and heart failure (HF). Moreover, in patients with HF, increasing levels of PTH have been associated with worse prognosis. Levels of PTH have in experimental and clinical studies been associated with left ventricular hypertrophy and myocardial fibrosis, two causes of non-ischemic HF. However, the association between circulating PTH levels and the incidence of HF has not been reported in the general population.
Methods In a prospective, community-based study of 864 men (mean age 71 years, the ULSAM study, Uppsala, Sweden) without HF or valvular disease at baseline, plasma PTH was analyzed together with established risk factors for HF (prior myocardial infarction, hypertension, diabetes, electrocardiographic left ventricular hypertrophy, smoking, serum cholesterol level and lipid-lowering treatment) and variables reflecting mineral metabolism (serum calcium, serum phosphate, plasma vitamin D and glomerular filtration rate).
Results During a mean follow-up of eight years, 75 individuals developed HF. In multivariable Cox proportional hazard analyses adjusting for established risk factors for HF and variables reflecting mineral metabolism, higher levels of PTH were associated with higher risk for HF (hazard ratio for 1-SD increase of PTH 1.40, 95% CI 1.13–1.74, p=0.003). PTH also predicted HF in participants without apparent ischemic causes of HF and in participants with plasma PTH within the normal range.
Conclusions In a large community-based sample of elderly men, plasma PTH predicted total HF and non-ischemic HF incidence, also after accounting for established risk factors and for variables of the mineral metabolism. Our data suggest a role for PTH in the development of heart failure even in the absence of overt hyperparathyroidism. Additional investigations are warranted to confirm these findings and to assess the clinical utility of our data.