Wustmann K, Kucera J P, Zanchi A, Burow A, Stuber T, Chappuis B, Diem P, Delacrétaz E
Department of Cardiovascular Medicine, Swiss Cardiovascular Center Bern, University Hospital, CH-3010 Bern, Switzerland.
J Clin Endocrinol Metab. 2008 Jun;93(6):2104-8. doi: 10.1210/jc.2008-0092. Epub 2008 Mar 18.
A shortening of the atrial refractory period has been considered as the main mechanism for the increased risk of atrial fibrillation in hyperthyroidism. However, other important factors may be involved.
Our objective was to determine the activity of abnormal supraventricular electrical depolarizations in response to elevated thyroid hormones in patients without structural heart disease.
Twenty-eight patients (25 females, three males, mean age 43+/-11 yr) with newly diagnosed and untreated hyperthyroidism were enrolled in a prospective trial after exclusion of heart disease. Patients were followed up for 16 +/- 6 months and studied at baseline and 6 months after normalization of serum TSH levels.
The incidence of abnormal premature supraventricular depolarizations (SVPD) and the number of episodes of supraventricular tachycardia was defined as primary outcome measurements before the start of the study. In addition, heart rate oscillations (turbulence) after premature depolarizations and heart rate variability were compared at baseline and follow-up.
SVPDs decreased from 59 +/- 29 to 21 +/- 8 per 24 h (P = 0.003), very early SVPDs (so called P on T) decreased from 36 +/- 24 to 3 +/- 1 per 24 h (P < 0.0001), respectively, and nonsustained supraventricular tachycardias decreased from 22 +/- 11 to 0.5 +/- 0.2 per 24 h (P = 0.01) after normalization of serum thyrotropin levels. The hyperthyroid phase was characterized by an increased heart rate (93 +/- 14 vs. 79 +/- 8 beats/min, P < 0.0001) and a decreased turbulence slope (3.6 vs. 9.2, P = 0.003), consistent with decreased vagal tone. This was confirmed by a significant decrease of heart rate variability.
Hyperthyroidism is associated with an increased supraventricular ectopic activity in patients with normal hearts. The activation of these arrhythmogenic foci by elevated thyroid hormones may be an important causal link between hyperthyroidism and atrial fibrillation.
心房不应期缩短被认为是甲状腺功能亢进症患者心房颤动风险增加的主要机制。然而，可能还涉及其他重要因素。
我们的目的是确定无结构性心脏病患者对甲状腺激素升高时异常室上性电去极化的活动情况。
28例新诊断且未治疗的甲状腺功能亢进症患者（25例女性，3例男性，平均年龄43±11岁）在排除心脏病后纳入一项前瞻性试验。对患者进行了16±6个月的随访，并在基线和血清促甲状腺激素水平正常化后6个月进行研究。
异常室上性早搏去极化（SVPD）的发生率和室上性心动过速的发作次数在研究开始前被定义为主要观察指标。此外，在基线和随访时比较了早搏去极化后的心率振荡（湍流）和心率变异性。
血清促甲状腺激素水平正常化后，每24小时SVPD从59±29次降至21±8次（P = 0.003），极早期SVPD（所谓的T波上P波）从每24小时36±24次降至3±1次（P < 0.0001），非持续性室上性心动过速从每24小时22±11次降至0.5±0.2次（P = 0.01）。甲状腺功能亢进期的特征是心率增加（93±14次/分钟对79±8次/分钟，P < 0.0001）和湍流斜率降低（3.6对9.2，P = 0.003），这与迷走神经张力降低一致。心率变异性显著降低证实了这一点。
甲状腺功能亢进症与正常心脏患者的室上性异位活动增加有关。甲状腺激素升高激活这些致心律失常灶可能是甲状腺功能亢进症与心房颤动之间的重要因果联系。
