N-Terminal-Pro-B-type Natriuretic Peptide in Acute Hyperthyroidism

Abstract

Objective: Serum N-terminal-pro-B-type natriuretic peptide (NT-proBNP) is elevated in systolic heart failure due to volume expansion and pressure overload. Recent data suggest a direct stimulatory effect of thyroid hormones on NT-proBNP synthesis. We examined the influence of acutely induced hyperthyroidism on serum levels of NT-proBNP. Design: Forty-three healthy women were evaluated before and after treatment with 60 μg triiodothyronine (T₃) daily for 7 days in a noncontrolled study. Main outcome: Before treatment, NT-proBNP was independently and inversely associated with thyrotropin (TSH), (r = −0.34, p = 0.02). T₃ therapy induced an increase in free T₃ (3.3 times, p < 0.0001) and suppression of TSH ( p < 0.0001). Heart rate increased by 14% ( p < 0.0001); weight decreased 0.6 kg ( p < 0.0001). Median NT-proBNP increased from 53 to 66 pg/mL ( p < 0.0001). The increase in NT-proBNP levels was independently associated with increase in free T₃ ( p = 0.05) and with reduction in TSH ( p = 0.04), without any association to the changes in cardiac workload. Conclusions: NT-proBNP is influenced by thyroid function among healthy women, as demonstrated by an inverse association between TSH and NT-proBNP. Induction of an acute hyperthyroid state resulted in an increase in NT-proBNP, which seems to reflect a direct action of T₃ on the NT-proBNP secretion rather than an effect of increased cardiac workload.