Key result
L-triiodothyronine increases beating rates by ~77% and triggers delayed afterdepolarizations in rabbit pulmonary vein cardiomyocytes.
Why the study?
Hyperthyroidism is an important etiology of paroxysmal AF, which is known to be initiated by pulmonary veins, but the electrophysiological effects of thyroid hormone on pulmonary vein cardiomyocytes were not well defined.
Does L-triiodothyronine incubation alter the electrophysiological characteristics of rabbit pulmonary vein cardiomyocytes?
Does L-triiodothyronine incubation alter the electrophysiological characteristics of rabbit pulmonary vein cardiomyocytes?
Answers are grounded in this paper and cite their sources.
Thyroid hormone increases automaticity and enhances triggered activity in pulmonary vein cardiomyocytes, providing a potential mechanism for arrhythmogenesis in hyperthyroidism.
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 after depolarization (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 after depolarization (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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Chen et al. (2002) studied Hyperthyroidism / Paroxysmal atrial fibrillation. L-triiodothyronine vs. Without incubation (control) was evaluated on Beating rates (Hz) (p=<0.005). Incubation of rabbit pulmonary vein cardiomyocytes with L-triiodothyronine increased beating rates (1.82 vs 1.03 Hz, p<0.005) and the incidence of delayed afterdepolarizations (92% vs 6%, p<0.0001).
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