Faber J, Wiinberg N, Schifter S, Mehlsen J
Department of Endocrinology E, Frederiksberg Hospital, DK-2000, Denmark.
Eur J Endocrinol. 2001 Oct;145(4):391-6. doi: 10.1530/eje.0.1450391.
Hyperthyroidism has profound effects on the cardiovascular system, including reduced systemic vascular resistance (SVR) due to relaxation of vascular smooth muscle cells, enhanced heart rate (HR) and cardiac output (CO) due to an increase in cardiac diastolic relaxation, contractility and heart rate. Subclinical hyperthyroidism is characterised by reduced serum TSH levels despite free thyroxine (T4) and tri-iodothyronine (T3) estimates within the reference range, in subjects with no obvious symptoms of hyperthyroidism. We measured haemodynamic changes (using impedance cardiography) in subjects with endogenous subclinical hyperthyroidism in order to elucidate whether these patients had signs of excess thyroid hormone at the tissue level.
The patients were otherwise healthy women with a multinodular goitre (n=6; age 47-81 years; serum TSH 0.006-0.090 mU/l and normal free T4 and T3 estimates), studied before and after normalisation of TSH (0.280-1.120 mU/l) by means of radioiodine treatment, and they were compared with 9 overt hyperthyroid patients (2 with multinodular goitre and 7 with Graves' disease) in the untreated state and after euthyroidism had been obtained.
Treatment of the subclinical hyperthyroid women resulted in 11% reduction in HR (P<0.02), 19% reduction in CO from (means+/-s.d.) 6.93+/-2.15 l/min to 5.58+/-1.94 l/min (P<0.05), and 30% increase in SVR (P<0.02). Similar but more pronounced changes were seen in the hyperthyroid group: 17% reduction in HR, 25% reduction in CO and 46% increase in SVR (all at least P<0.05). Taking all 15 patients together, thyroid function (as measured by free T3 index (FT3I) or TSH) correlated significantly to the haemodynamic parameters as follows: the higher the thyroid function the lower the mean arterial pressure and SVR, and the higher the CO and central aortic compliance (stroke volume/pulse pressure) (P<0.05). Plasma norepinephrine increased significantly after treatment of the overt hyperthyroid patients, whereas epinephrine did not change, and no changes were seen among subclinical hyperthyroid patients.
Treatment of endogenous subclinical hyperthyroidism resulted in significant changes in several haemodynamic parameters regarding the heart and the vascular system, compatible with some degree of excess tissue exposure to thyroid hormones in the untreated state. Our data favour more aggressive treatment of these patients, and endogenous subclinical hyperthyroidism might be regarded as a mild form of hyperthyroidism.
甲状腺功能亢进对心血管系统有深远影响，包括由于血管平滑肌细胞舒张导致全身血管阻力（SVR）降低，以及由于心脏舒张期松弛、收缩力和心率增加导致心率（HR）和心输出量（CO）升高。亚临床甲状腺功能亢进的特征是血清促甲状腺激素（TSH）水平降低，尽管游离甲状腺素（T4）和三碘甲状腺原氨酸（T3）在参考范围内，且患者无明显甲状腺功能亢进症状。我们测量了内源性亚临床甲状腺功能亢进患者的血流动力学变化（使用阻抗心动图），以阐明这些患者在组织水平上是否有甲状腺激素过量的迹象。
患者为患有多结节性甲状腺肿的健康女性（n = 6；年龄47 - 81岁；血清TSH 0.006 - 0.090 mU/l，游离T4和T3正常），在通过放射性碘治疗使TSH正常化（0.280 - 1.120 mU/l）之前和之后进行研究，并与9例显性甲状腺功能亢进患者（2例多结节性甲状腺肿和7例格雷夫斯病）在未治疗状态和达到甲状腺功能正常后进行比较。
亚临床甲状腺功能亢进女性患者治疗后，心率降低11%（P < 0.02），心输出量从（均值±标准差）6.93 ± 2.15 l/min降至5.58 ± 1.94 l/min，降低19%（P < 0.05），全身血管阻力增加30%（P < 0.02）。在甲状腺功能亢进组中观察到类似但更明显的变化：心率降低17%，心输出量降低25%，全身血管阻力增加46%（均至少P < 0.05）。将所有15例患者综合起来，甲状腺功能（通过游离T3指数（FT3I）或TSH测量）与血流动力学参数显著相关，如下：甲状腺功能越高，平均动脉压和全身血管阻力越低，心输出量和中心主动脉顺应性（每搏量/脉压）越高（P < 0.05）。显性甲状腺功能亢进患者治疗后血浆去甲肾上腺素显著增加，而肾上腺素未改变，亚临床甲状腺功能亢进患者未见变化。
内源性亚临床甲状腺功能亢进的治疗导致心脏和血管系统的几个血流动力学参数发生显著变化，这与未治疗状态下组织一定程度的甲状腺激素过量暴露相符。我们的数据支持对这些患者进行更积极的治疗，内源性亚临床甲状腺功能亢进可能被视为一种轻度的甲状腺功能亢进形式。
