N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism

Research output: Contribution to journal › Journal article › Research › peer-review

Standard

N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism. / Schultz, M; Kistorp, C; Corell, P; Andersen, H U; Jarlov, A; Faber, J.

In: Hormone and Metabolic Research, Vol. 41, No. 4, 2009, p. 302-7.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Schultz, M, Kistorp, C, Corell, P, Andersen, HU, Jarlov, A & Faber, J 2009, 'N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism', Hormone and Metabolic Research, vol. 41, no. 4, pp. 302-7. https://doi.org/10.1055/s-0028-1112125

APA

Schultz, M., Kistorp, C., Corell, P., Andersen, H. U., Jarlov, A., & Faber, J. (2009). N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism. Hormone and Metabolic Research, 41(4), 302-7. https://doi.org/10.1055/s-0028-1112125

Vancouver

Schultz M, Kistorp C, Corell P, Andersen HU, Jarlov A, Faber J. N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism. Hormone and Metabolic Research. 2009;41(4):302-7. https://doi.org/10.1055/s-0028-1112125

Author

Schultz, M ; Kistorp, C ; Corell, P ; Andersen, H U ; Jarlov, A ; Faber, J. / N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism. In: Hormone and Metabolic Research. 2009 ; Vol. 41, No. 4. pp. 302-7.

Bibtex

@article{780c5a8077ac11df928f000ea68e967b,
title = "N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism",
abstract = "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.",
author = "M Schultz and C Kistorp and P Corell and Andersen, {H U} and A Jarlov and J Faber",
note = "Keywords: Adult; Denmark; Female; Heart Rate; Humans; Hyperthyroidism; Middle Aged; Natriuretic Peptide, Brain; Thyroid Function Tests; Verapamil; Young Adult",
year = "2009",
doi = "10.1055/s-0028-1112125",
language = "English",
volume = "41",
pages = "302--7",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "GeorgThieme Verlag",
number = "4",

}

RIS

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

VL - 41

SP - 302

EP - 307

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 4

ER -

ID: 20296161