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N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism.
- Source :
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Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme [Horm Metab Res] 2009 Apr; Vol. 41 (4), pp. 302-7. Date of Electronic Publication: 2009 Jan 12. - Publication Year :
- 2009
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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.
Details
- Language :
- English
- ISSN :
- 1439-4286
- Volume :
- 41
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
- Publication Type :
- Academic Journal
- Accession number :
- 19140095
- Full Text :
- https://doi.org/10.1055/s-0028-1112125