Abstract
Significant variations from the normal QT interval range of 350 to 450 milliseconds (ms) in men and 360 to 460 ms in women increase the risk for ventricular arrhythmias. This difference in the QT interval between men and women has led to the understanding of the influence of sex hormones on the role of gender-specific channelopathies and development of ventricular arrhythmias. The QT interval, which represents the duration of ventricular repolarization of the heart, can be affected by androgen levels, resulting in a sex-specific predilection for acquired and inherited channelopathies such as acquired long QT syndrome in women and Brugada syndrome and early repolarization syndrome in men. Manipulation of the homeostasis of these sex hormones as either hormonal therapy for certain cancers, recreational therapy or family planning and in transgender treatment has also been shown to affect QT interval duration and increase the risk for ventricular arrhythmias. In this review, we highlight the effects of endogenous and exogenous sex hormones in the physiological and pathological states on QTc variation and predisposition to gender-specific pro-arrhythmias.
Highlights
The QT interval of the electrocardiogram, which represents the total duration of ventricular depolarization and repolarization [1], is measured from the initiation of the QRS complex to the termination of the T wave
In a case series of seven consecutive men prospectively admitted for torsade de pointes (TdP), we showed that all had acquired hypogonadism and that normalization of testosterone levels shortened QT interval corrected for heart rate (QTc) and prevented recurrence of TdP [17]
Exogenous use of hormonal therapies such as medroxyprogesterone acetate (MPA) for contraception may exert similar antiproliferative effects to progesterone on the endometrium, it does not appear to affect the non-genomic eNOS pathway of cardiac ion current regulation and in patients with cLQTs, and use of MPA may increase the risk for TdP and sudden cardiac death (SCD) [108]
Summary
The QT interval of the electrocardiogram, which represents the total duration of ventricular depolarization and repolarization [1], is measured from the initiation of the QRS complex to the termination of the T wave. The QTc interval is the QT interval corrected for heart rate and normally ranges between 350 and 450 milliseconds (ms) in men and 360 to 460 ms in women [2] (Figure 1). There are many widely used rate correction formulas to calculate QTc, namely, Bazett’s, Fridericia’s, Framingham’s and Hodge’s, all with their own merits and disadvantages, that normalize the QT interval obtained at a given cycle length to 60 beats/min [4]. The QTc interval is a widely used marker of ventricular arrhythmia risk. Prolonged QTc is associated with a higher risk of ventricular arrhythmias, Int. J.
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