首页> 外文期刊>Hormone and Metabolic Research >N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism.
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N-terminal-pro-B-type natriuretic peptide during pharmacological heart rate reduction in hyperthyroidism.

机译:甲亢中药理心率降低过程中的N端B型促利尿钠前体肽。

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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.
机译:我们假设甲亢中N端B型利尿钠肽水平的升高主要是由于过量的甲状腺激素引起的代谢增加所致。因此,在未经治疗的甲状腺功能亢进症中,通过药理学诱导的心率降低,在降低的心脏工作负荷期间研究了N末端B型前利尿钠肽的血清水平。我们设计了一项非对照干预研究。在每天360 mg维拉帕米降低药理心率之前和之后,对18名新诊断为甲状腺功能亢进的妇女进行了评估(包括超声心动图检查),持续6天。在治疗前,N端前B型利尿钠肽与甲状腺功能(游离三碘甲状腺素指数,r = 0.64,p = 0.001)和血红蛋白浓度(r = -0.36,p = 0.031)独立相关。维拉帕米治疗引起反映心脏功能的参数降低;静息心率[平均每分钟97至80次跳动(17.5%),p <0.001]和平均动脉压(8.5%,p = 0.001)。 N端前B型利尿钠肽的中位数从224 pg / ml微升至240 pg / ml(p = 0.31)。促甲状腺激素水平被完全抑制(<0.001 mU / l),游离甲状腺素指数从319个任意单位降低到315个任意单位(p = 0.039),游离三碘甲状腺素指数从8.6个任意单位增加到9.9个任意单位(p = 0.010)。没有观察到超声心动图参数的变化。由于维拉帕米治疗,未经治疗的甲状腺功能亢进症患者静息心率的降低并未导致N端前B型利尿钠肽水平降低。因此,甲亢中N端B型利尿钠原肽水平升高似乎主要归因于过量的甲状腺激素引起的高代谢,而不是心脏工作负荷增加。

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