TY - JOUR
T1 - N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism
AU - Schultz, M
AU - Kistorp, C
AU - Corell, P
AU - Andersen, H U
AU - Jarlov, A
AU - Faber, J
N1 - Keywords: Adult; Denmark; Female; Heart Rate; Humans; Hyperthyroidism; Middle Aged; Natriuretic Peptide, Brain; Thyroid Function Tests; Verapamil; Young Adult
PY - 2009
Y1 - 2009
N2 - We hypothesized that elevated N-terminal-pro-B-type natriuretic peptide levels in hyperthyroidism are mainly driven by increased metabolism due to excess thyroid hormones. Therefore, serum levels of N-terminal-pro-B-type natriuretic peptide were studied during reduced cardiac work load by means of pharmacologically induced heart rate reduction in untreated hyperthyroidism. We designed a noncontrolled interventional study. Eighteen women with newly diagnosed hyperthyroidism were evaluated (including an echocardiography) before and after pharmacological heart rate reduction with 360 mg verapamil daily for 6 days. Before treatment, N-terminal-pro-B-type natriuretic peptide was independently associated with thyroid function (free triiodothyronine-index, r=0.64, p=0.001) and the hemoglobin concentration (r=-0.36, p=0.031). The verapamil treatment induced a decrease in parameters reflecting cardiac function; resting heart rate [from mean 97 to 80 beats per min (17.5%), p<0.001] and mean arterial pressure (8.5%, p=0.001). Median N-terminal-pro-B-type natriuretic peptide increased insignificantly from 224 to 240 pg/ml (p=0.31). Thyrotrotrophin levels were totally suppressed (<0.001 mU/l), free thyroxine-index decreased from median 319 to 315 arbitrary units (p=0.039) and free triiodothyronine-index increased from 8.6 to 9.9 arbitrary units (p=0.010). No changes in echocardiographic parameters were observed. A decrease in resting heart rate in untreated hyperthyroidism due to verapamil treatment did not result in decreasing N-terminal-pro-B-type natriuretic peptide levels. Thus elevated N-terminal-pro-B-type natriuretic peptide in hyperthyroidism seems mainly a result of high metabolism due to excess thyroid hormones rather than increased cardiac work load.
AB - We hypothesized that elevated N-terminal-pro-B-type natriuretic peptide levels in hyperthyroidism are mainly driven by increased metabolism due to excess thyroid hormones. Therefore, serum levels of N-terminal-pro-B-type natriuretic peptide were studied during reduced cardiac work load by means of pharmacologically induced heart rate reduction in untreated hyperthyroidism. We designed a noncontrolled interventional study. Eighteen women with newly diagnosed hyperthyroidism were evaluated (including an echocardiography) before and after pharmacological heart rate reduction with 360 mg verapamil daily for 6 days. Before treatment, N-terminal-pro-B-type natriuretic peptide was independently associated with thyroid function (free triiodothyronine-index, r=0.64, p=0.001) and the hemoglobin concentration (r=-0.36, p=0.031). The verapamil treatment induced a decrease in parameters reflecting cardiac function; resting heart rate [from mean 97 to 80 beats per min (17.5%), p<0.001] and mean arterial pressure (8.5%, p=0.001). Median N-terminal-pro-B-type natriuretic peptide increased insignificantly from 224 to 240 pg/ml (p=0.31). Thyrotrotrophin levels were totally suppressed (<0.001 mU/l), free thyroxine-index decreased from median 319 to 315 arbitrary units (p=0.039) and free triiodothyronine-index increased from 8.6 to 9.9 arbitrary units (p=0.010). No changes in echocardiographic parameters were observed. A decrease in resting heart rate in untreated hyperthyroidism due to verapamil treatment did not result in decreasing N-terminal-pro-B-type natriuretic peptide levels. Thus elevated N-terminal-pro-B-type natriuretic peptide in hyperthyroidism seems mainly a result of high metabolism due to excess thyroid hormones rather than increased cardiac work load.
U2 - 10.1055/s-0028-1112125
DO - 10.1055/s-0028-1112125
M3 - Journal article
C2 - 19140095
SN - 0018-5043
VL - 41
SP - 302
EP - 307
JO - Hormone and Metabolic Research
JF - Hormone and Metabolic Research
IS - 4
ER -