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J Am Coll Cardiol, 2002; 39:366-372 © 2002 by the American College of Cardiology Foundation |
,*
* Department of Biomedical Engineering and Institute of Pharmacology, National Defense Medical Center, Taipei, Taiwan, Republic of China
Division of Cardiology, Veterans General Hospital-Taipei and Institute of Clinical Medicine, National Yang-Ming University School of Medicine, Taipei, Taiwan, Republic of China
Taipei Medical University Wan-Fang Hospital, Taipei, Taiwan, Republic of China
Manuscript received January 31, 2001; revised manuscript received August 28, 2001, accepted October 17, 2001.
* Reprint requests and correspondence: Dr. Yi-Jen Chen, Taipei Medical University, Wan-Fang Hospital, 111, Sec 3, Hsin-Lung Road, Wen Shan, Taipei, Taiwan, Republic of China.
yjchen{at}tmc.edu.tw
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 overall 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 outward (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.
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