Many drugs, particularly antidepressants related to tricyclics can increase the repolarization time for the heart’s ventricles and prolong the QT interval, which can lead to ventricular tachycardia and arrhythmia, and in sever cases death in the form of torsades de pointes.
Magnesium has been showed to shorten the QT and can potentially protect against the negative effects of these drugs on the heart:
Mg(++) rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg(++) caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg(++) injection. However, this effect was transient, and, at 120 seconds after Mg(++) administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 +/- 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg(++) in this model.
SOURCE: Effects of intravenous magnesium in a prolonged QT interval model of polymorphic ventricular tachycardia focus on transmural ventricular repolariza… – PubMed – NCBI
Hypothyroidism can also trigger QT prolongation and torsades de pointes:
“Hypothyroidism can manifest with myriad cardiac abnormalities, often consisting of a combination of morphologic and functional changes. Low voltage, sinus bradycardia, and slowed conduction are usually found on electrocardiography. We describe a patient with severe hypothyroidism who presented with presyncope, prolongation of the QT interval, and polymorphic ventricular tachycardia (torsades de pointes). No other cause for the malignant ventricular ectopy was evident. With levothyroxine therapy, the QT interval normalized and the ventricular tachycardia was abolished. In addition to its commonly known cardiac effects, myxedema can predispose to the potentially life-threatening arrhythmia of torsades de pointes. Conversely, in patients presenting with QT interval prolongation and polymorphic ventricular tachycardia, hypothyroidism should be considered in the differential diagnosis.”
SOURCE: Severe primary hypothyroidism manifesting with torsades de pointes. – PubMed – NCBI
Estrogen prolongs the QT interval, whereas testosterone and progesterone shortens it:
“A prolonged QT interval is a marker for an increased risk of ventricular tachyarrhythmias. Both endogenous and exogenous sex hormones have been shown to affect the QT interval. Endogenous testosterone and progesterone shorten the action potential, and estrogen lengthens the QT interval. During a single menstrual cycle, progesterone levels, but not estrogen levels, have the dominant effect on ventricular repolarization in women. Studies of menopausal hormone therapy (MHT) in the form of estrogen-alone therapy (ET) and estrogen plus progesterone therapy (EPT) have suggested a counterbalancing effect of exogenous estrogen and progesterone on the QT. Specifically, ET lengthens the QT, whereas EPT has no effect. To date, there are no studies on oral contraception (OC) and the QT interval, and future research is needed. This review outlines the current literature on sex hormones and QT interval, including the endogenous effects of estrogen, progesterone, and testosterone and the exogenous effects of estrogen and progesterone therapy in the forms of MHT and hormone contraception. Further, we review the potential mechanisms and pathophysiology of sex hormones on the QT interval.
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