In this study, we found that preeclampsia increased QTcD, which indicates regional heterogeneity in myocardial repolarization, while magnesium administered in treatment significantly decreased QTc dispersion. The autonomic, hemodynamic, and hormonal changes that occur during pregnancy, especially the increase in blood volume and the increase in estrogen hormone levels, may trigger arrhythmias by stretching the myocardium and increasing sympathetic tone
14-17. These physiopathological changes may contribute to the occurrence of cardiac arrhythmias by directly affecting myocardial repolarization
17. In addition, many studies have shown the presence of various steroidal sex hormone receptors in the heart. The effect of hormonal changes during pregnancy on the heart suggests that pregnancy may contribute to the proarrhythmic effect of pregnancy
16,17. QT and QTc, which indicate cardiac repolarization, are longer in women compared to men in adulthood
18. Therefore, women are more prone to arrhythmogenic conditions, especially torsades de pointes
19. These sex differences are thought to be caused by the effect of sex hormones, especially androgens, on ventricular repolarization. Moreover, virilized women exhibited QTc intervals similar to those of healthy men, while castrated men had QTc intervals similar to normal women
20. These results explain why the repolarization time in women is longer. For this reason, female sex is an independent risk factor in terms of syncope and “torsade de pointes” in patients with hereditary long QT syndrome
14. It is possible that preeclampsia has a significant effect on ventricular repolarization. However, a previous prospective study showed a markedly longer QTc interval in women who developed eclampsia
21. The heterogeneity of the ventricular repolarization phase underlies the electrophysiological changes that occur during preeclampsia, even in the absence of symptoms. Previous studies have focused on the effect of preeclampsia on heart rate variability and have shown a state of sympathetic hyperactivity, especially before the onset of symptoms
22. Electrophysiologic cardiac changes may result from increased hemodynamic stress on the cardiovascular system due to elevated systolic blood pressure. However, high levels of circulating mediators may also have a specific role during preeclampsia
23. In this study, both QT and QTc intervals were longer in preeclamptic women than in the control group. Magnesium sulfate is an ideal drug for the prevention and treatment of eclampsia
11,14. To the best of our knowledge, this is the first study to investigate the effect of magnesium sulfate given during preeclampsia on QTcD. Serum magnesium and potassium levels may affect QTcD, but no electrolyte imbalance was observed between the groups in our study. Some studies have reported conflicting results of magnesium sulfate on QTcD. Nakaigawa et al.
24 and Grin J et al.
25 claimed that magnesium sulfate affects cardiac repolarization by causing hypokalemia. In our study, hypokalemia was not observed in patients that were administered magnesium sulfate.
Gurfinkel et al.26 reported that magnesium sulfate improved myocardial heterogeneity and prevented proarrhythmia. Changing ECG parameters such as QTc and QTcD with treatment will have a positive effect on placental blood flow in preeclamptic women and prevent maternal and fetal complications.
As a result, preeclampsia causes alteration of ventricular repolarization as evidenced by prolongation of ECG parameters such as QT and QTcD. Preeclampsia appears to be the only determinant of increased QTcD. Although these changes are mostly asymptomatic, clinical assessment of ventricular repolarization in preeclamptic women can be performed simply with a non-invasive 12-lead ECG. In these cases, magnesium sulfate corrects ventricular repolarization abnormalities and improves placental blood flow.