Abstract
Atrial fibrillation (AF) is a complex condition with several possible contributing factors. The rapid and irregular heartbeat produced by AF increases the risk of blood clot formation inside the heart. These clots may eventually become dislodged, causing embolism, stroke and other disorders. AF occurs in up to 15% of patients with hyperthyroidism compared to 4% of people in the general population and is more common in men and in patients with triiodothyronine (T3) toxicosis. The incidence of AF increases with advancing age. Also, subclinical hyperthyroidism is a risk factor associated with a 3-fold increase in development of AF. Thyrotoxicosis exerts marked influences on electrical impulse generation (chronotropic effect) and conduction (dromotropic effect). Several potential mechanisms could be invoked for the effect of thyroid hormones on AF risk, including elevation of left atrial pressure secondary to increased left ventricular mass and impaired ventricular relaxation, ischemia resulting from increased resting heart rate, and increased atrial eopic activity. Reentry has been postulated as one of the main mechanisms leading to AF. AF is more likely if effective refractory periods are short and conduction is slow. Hyperthyroidism is associated with shortening of action potential duration which may also contribute to AF.
Highlights
Atrial fibrillation (AF) is a common dysrrhythmia representing an independent risk factor for cardiovascular events [1]
Several potential mechanisms could be invoked for the effect of thyroid hormones on AF risk, including elevation of left atrial pressure secondary to increased left ventricular mass (LVM) and impaired ventricular relaxation [28], ischemia resulting from raised resting heart rate, and increased atrial ectopic activity [39]
Previous studies in humans or in isolated canine pulmonary vein tissues have demonstrated that triggered activities may underlie the arrhythmogenic activity of pulmonary veins [55,56]. These findings suggest that thyroid hormones may induce the occurrence of paroxysmal AF through the increase of triggered activity in pulmonary veins
Summary
Atrial fibrillation (AF) is a common dysrrhythmia representing an independent risk factor for cardiovascular events [1]. Overt hyperthyroidism induces a hyperdynamic cardiovascular state (high cardiac output with low systemic vascular resistance), which is associated with a faster heart rate, enhanced left ventricular systolic and diastolic function, and increased prevalence of supraventricular tachyarrhythmias [28]. The TSH-producing cells of the anterior pituitary are sensitive to minor changes in circulating thyroid hormones and absent or subnormal TSH concentrations may be found in hyperthyroid patients in whom the T3 and T4 concentrations are higher than normal for the individual but within or at the upper end of the accepted reference range. In the studies by Chen et al [54,55,56] both the beating and non-beating hyperthyroid pulmonary vein cardiomyocytes had greater transient inward currents after being incubated with thyroid hormones, which may underlie the high incidence of DAD in these cells. P maximum and P wave dispersion were significant predictors of paroxysmal AF [60,61,62]
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