The corrected QT (QTc) prolongation in hyperthyroidism and the association of thyroid hormone with the QTc interval

Abstract

PurposeVentricular repolarization is assessed using the QT interval corrected by the heart rate (QTc) via an electrocardiogram (ECG). Prolonged QTc is associated with an increased risk of arrhythmias and cardiac mortality. As there have been few reports regarding the effects of hyperthyroidism on ventricular repolarization, we studied the association between serum free thyroxine (free T4 [fT4]) and thyroid stimulating hormone (TSH) levels and the QTc interval.MethodsThirty-eight patients with hyperthyroidism (<30 years old) were included, and we used their clinical records and available ECGs (between August 2003 and August 2011) to evaluate the association between their fT4 and TSH levels and their QTc interval. In addition, we studied the ECGs of 72 age-matched patients with no hyperthyroidism (control group) and compared their data with that from the patients group.ResultsThe QTc duration in patients with hyperthyroidism was significantly prolonged compared to that in the control subjects (P<0.001). In addition, the number of hyperthyroid patients with abnormal prolonged QTc was significantly higher than that in the control group (P<0.001). Among the patients with hyperthyroidism, patients with prolonged QTc and borderline QTc had higher fT4 levels and there was positive correlation between their fT4 levels and their QTc interval (P<0.05). However, no correlation was observed between their TSH levels and their QTc interval.ConclusionWe report that hyperthyroidism is associated with QTc prolongation. The correlation between the fT4 levels and the QTc interval suggests that thyroid status is associated with QTc values and the risk of cardiac mortality.

Ventricular Fibrillation: Potential Deadly Consequence of Discontinuation of Methimazole Prior to Radioiodine Ablation

“…Numerous studies have shown a strong association between hyperthyroidism and QTc prolongation. A positive correlation between free T4 and the degree of QT prolongation was seen; patients with higher levels of free T4 had longer QTc duration [1,[3][4][5][6][7][8]. This positive correlation was present with our patient: as free T4 increased, QTc also increased ( Table 1).…”

“…Factors that contribute to a fatal arrhythmia are thyrotoxicosis in the setting of an already weakened heart, seen in our patient. Literature review shows that ventricle repolarization is greatly affected in hyperthyroidism [3][4][5]. Ventricular repolarization is assessed using the QT interval corrected for the heart rate (QTc) on an electrocardiogram (ECG).…”

“…Research shows a significant positive correlation between QTc and thyroid hormones, especially free T4 levels. However, the mechanism and pathophysiology are not well understood [4][5][6][7][8]. The correlation has even been reported in patients with subclinical hyperthyroidism [7].…”

An unusual cause of polymorphic ventricular tachycardia: Acquired long QT syndrome from atypical variant of stress-induced cardiomyopathy

“…16 Though hyperthyroidism has been previously implicated in QTc prolongation, the association only held true for high fT4 (hers was normal) and not for suppressed levels of TSH. 17 Overall, we think that here an atypical stress-induced cardiomyopathy was responsible for the multifactorial QT interval prolongation and that the heterogeneity in dispersion of repolarization may have led to phase 2 reentry and the polymorphic VT. This is in keeping with similar reports recognizing the role of classical Takotsubo as a cause of acquired and often transient LQTS in the setting of multiple risk factors.…”

Thyroid and Cardiovascular Disease

“…Hyperthyroidism has been associated with both QTc prolongation 21 and short QTc intervals, 22 and hypothyroidism with QTc prolongation and a heightened risk for torsades de pointes. 23 These observations may be attributed to the net effect in context of sympathetic tone, genetic and other medical characteristics of the patient, which determines whether and how a hypo-or hyperthyroid state might provoke either brady-or tachyarrhythmias.…”