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

M Schultz; C Kistorp; P Corell; H U Andersen; A Jarlov; J Faber

doi:10.1055/s-0028-1112125

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

M Schultz, C Kistorp, P Corell, H U Andersen, A Jarlov, J Faber

IKM

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

5 Citationer (Scopus)

Abstract

Udgivelsesdato: 2009-Apr

Originalsprog	Engelsk
Tidsskrift	Hormone and Metabolic Research
Vol/bind	41
Udgave nummer	4
Sider (fra-til)	302-7
Antal sider	6
ISSN	0018-5043
DOI	https://doi.org/10.1055/s-0028-1112125
Status	Udgivet - 2009

Bibliografisk note

Keywords: Adult; Denmark; Female; Heart Rate; Humans; Hyperthyroidism; Middle Aged; Natriuretic Peptide, Brain; Thyroid Function Tests; Verapamil; Young Adult

Adgang til dokumentet

10.1055/s-0028-1112125

Citationsformater

@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",

}

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 -