Effects of thyroid hormone on the arrhythmogenic activity of pulmonary vein cardiomyocytes
Effects of thyroid hormone on the arrhythmogenic activity of pulmonary vein cardiomyocytes
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DOI：
10.1016/s0735-1097(01)01731-4
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发表时间：
2002-01-16
影响因子：
24
通讯作者：
Lin, CI
中科院分区：
文献类型：
--
作者：
Chen, YC;Chen, SA;Lin, CI
目的探讨甲状腺激素对肺静脉心肌细胞电生理特性的影响。背景：甲状腺功能亢进是阵发性心房颤动（AF）的重要病因。方法应用全细胞钳夹技术，观察单家兔PV和心房心肌细胞（甲状腺功能亢进）和未（对照）l -三碘甲状腺原氨酸孵育的动作电位和离子电流。结果与对照心肌细胞相比，甲亢型PV和心房心肌细胞的动作电位持续时间较短。甲状腺功能亢进的PV心肌细胞有更快的心率（1.82 +/- 0.13 Hz vs 1.03 +/- 0.15 Hz, p < 0.005）和更高的延迟去极化发生率（跳动：92% vs. 6%, p < 0.0001；不跳动：45% vs. 3%, p < 0.005）。然而，只有甲状腺功能亢进的PV跳动心肌细胞在去极化后早期有更高的发生率（46%比0%，p < 0.0001）。离子电流的实验表明,甲状腺亢进PV击败心肌细胞有更大的整体缓慢的向内的密度(2.72 + / - 0.21 pA / pF与2.07 + / - 0.19 pA / pF, p < 0.05),整体向外瞬态(1.39 + / - 0.21 pA / pF与0.48 + / - 0.08 pA / pF, p < 0.001)和向外稳态电流(0.78 + / - 0.06 pA / pF与0.58 + / - 0.04 pA / pF, p < 0.05)在去极化和大的瞬态内(0.021 + / - 0.004 pA / pF与0.005 + / - 0.001 pA / pF, p + / - 0.001)复极化。相比之下，甲状腺功能亢进的PV非跳动心肌细胞具有更大的总瞬时向外电流密度（1.01 +/- 0.14 pA/pF vs. 0.37 +/- 0.07 pA/pF, p < 0.001）、稳态向外电流密度（0.61 +/- 0.06 pA/pF vs. 0.44 +/- 0.04 pA/pF, p < 0.05）和瞬时向内电流密度（0.011 +/- 0.002 pA/pF vs. 0.003 +/- 0.001 pA/pF, p < 0.05）。结论甲状腺激素可改变PV心肌细胞的电生理活性。自动性的增强和触发活性的增强可能会增加甲亢患者pv的致心律失常活性。(C) 2002年由美国心脏病学会提出。
OBJECTIVES This study was conducted to investigate the effects of thyroid hormone on the electrophysiological characteristics of pulmonary vein (PV) cardiomyocytes.BACKGROUND Hyperthyroidism is an important etiology of paroxysmal atrial fibrillation (AF). Pulmonary veins are known to initiate paroxysmal AF.METHODS The action potential and ionic currents were investigated in single rabbit PV and atrial cardiomyocytes with (hyperthyroid) and without (control) incubation of L-triiodothyronine using the whole-cell clamp technique.RESULTS Compared with the control cardiomyocytes, hyperthyroid PV and atrial cardiomyocytes had shorter action potential duration. Hyperthyroid PV cardiomyocytes had faster beating rates (1.82 +/- 0.13 Hz vs. 1.03 +/- 0.15 Hz, p < 0.005) and a higher incidence of delayed afterdepolarization (beating: 92% vs. 6%, p < 0.0001; non-beating: 45% vs. 3%, p < 0.005). However, only, hyperthyroid PV beating cardiomyocytes had a higher incidence of early afterdepolarization (46% vs. 0%, p < 0.0001). The ionic current experiments showed that hyperthyroid PV beating cardiomyocytes had larger densities of over-all slow inward (2.72 +/- 0.21 pA/pF vs. 2.07 +/- 0.19 pA/pF, p < 0.05), overall transient outward (1.39 +/- 0.21 pA/pF vs. 0.48 +/- 0.08 pA/pF, p < 0.001) and steady state outward currents (0.78 +/- 0.06 pA/pF vs. 0.58 +/- 0.04 pA/pF, p < 0.05) on depolarization and larger transient inward (0.021 +/- 0.004 pA/pF vs. 0.005 +/- 0.001 pA/pF, p +/- 0.001) on repolarization. By contrast, the hyperthyroid PV non-beating cardiomyocytes had larger densities of overall transient out-ward (1.01 +/- 0.14 pA/pF vs. 0.37 +/- 0.07 pA/pF, p < 0.001), steady state outward (0.61 +/- 0.06 pA/pF vs. 0.44 +/- 0.04 pA/pF, p < 0.05) and transient inward currents (0.011 +/- 0.002 pA/pF vs. 0.003 +/- 0.001 pA/pF, p < 0.05).CONCLUSIONS Thyroid hormone changes the electrophysiological activity of the PV cardiomyocytes. Increased automaticity and enhanced triggered activity may increase the arrhythmogenic activity of PVs in hyperthyroidism. (C) 2002 by the American College of Cardiology.