Introduction In patients with heart failure with reduced ejection fraction (HFrEF), a raised serum parathyroid hormone (PTH) level is associated with increased morbidity and mortality. Previous studies suggest that PTH levels correlate with peak VO2 and markers of endothelial dysfunction in HFrEF. We examined the role of PTH in the pathophysiological difference between response and non-response to cardiac resynchronisation therapy (CRT) in HFrEF.
Methods All patients met National Institute for Health and Care Excellence criteria for CRT implantation and were prospectively recruited from a single centre. A positive response to CRT was defined as an improvement in all four of the following domains: 1) a greater than 1ml/kg/min increase in peak VO2; 2) a 10% reduction in left ventricular end-systolic volume (LVESV); 3) a 10% reduction in symptoms as measured by the Minnesota living with heart failure questionnaire (MLWHFQ); 4); over 10% increase in 6 minute walk distance (6MWD). PTH levels were measured at baseline and at 6 months following CRT. Percentage change in PTH level was calculated as (6 month PTH level – baseline PTH level)/(baseline PTH level). Data are presented as mean ± standard error of the mean. Analyses were performed using IBM SPSS version 24. Paired continuous data were compared with paired t test; unpaired continuous data with independent sample t test. Tests were 2-tailed. p<0.05 was considered statistically significant.
Results A total of 19 patients were studied (9 responders, 10 non-responders; 95% male, age 70 ± 1.9 years). At baseline, there was no significant difference in estimated glomerular filtration rate (64.1 ± 3.2 ml/min/1.73m2 in responders, 58.3 ± 3.9 ml/min/1.73m2 in non-responders; p=0.27), corrected serum calcium level (2.31 ± 0.02 mg/dL in responders, 2.36 ± 0.02 mg/dL in non-responders; p=0.13), or serum 25-hydroxy vitamin D levels (56.5 ± 6.8 ng/mL in responders and 45.1 ± 12 ng/mL in non-responders; p=0.44) in between the two groups. At baseline, PTH levels in responders were 85.4 ± 9.9 pg/mL, compared to 63.4 ± 9.8 pg/mL in non-responders (p=0.06). At 6 months, PTH levels in responders were 72.3 ± 11.5 pg/mL, compared to 87.8 ± 10.7 pg/mL in non-responders (p=0.2). There was a significant difference in the percentage change in PTH levels between responders (an average reduction of 16 ± 3.6 %) and non-responders (an average increase of 38 ± 3.4 %) (p=0.002) (figure 1A). All responders had a decrease in serum PTH level at 6 months, whereas 8 out of 10 non-responders had an increase in serum PTH levels at 6 months (figure 1B).
Conclusion This small, single-centre study suggests that a positive response to CRT is associated with a reduction in serum PTH levels at 6 months following the procedure. Conversely, non-response to CRT is generally characterised by an increase in PTH levels at 6 months. The pathophysiological role of PTH in CRT response warrants further investigation.
Conflict of Interest Nil.
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