Evolution of Electrocardiographic Repolarization Parameters During Antiandrogen Therapy in Patients with Prostate Cancer and Hypogonadism

Gheorghe, Andrei Cristian Dan; Ciobanu, Ana; Hodorogea, Andreea Simona; Rădăvoi, George Daniel; Jinga, Viorel; Nanea, Ioan Tiberiu; Gheorghe, Gina

doi:10.1007/s12012-020-09566-6

Cited by 15 publications

(10 citation statements)

References 33 publications

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“…This is the first study to assess the influence of testosterone on drug‐induced lengthening of J‐T peak and T peak ‐T end . However, Gheorge et al 23 . reported that 6 months of antiandrogen therapy was associated with significant increases in QT interval, maximum T peak ‐T end , mean T peak ‐T end /QT, and T peak ‐T end dispersion in patients with prostate cancer and hypogonadism.…”

Section: Discussionmentioning

confidence: 99%

Transdermal Testosterone Attenuates Drug‐Induced Lengthening of Both Early and Late Ventricular Repolarization in Older Men

Muensterman

Jaynes

Sowinski

et al. 2020

Clin Pharma and Therapeutics

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We have previously reported that transdermal testosterone attenuates drug‐induced QT interval lengthening in older men. However, it is unknown whether this is due to modulation of early ventricular repolarization, late repolarization, or both. In a secondary analysis of a prospective, randomized, double‐blind, placebo‐controlled three‐way crossover study, we determined if transdermal testosterone and oral progesterone attenuate drug‐induced lengthening of early and late ventricular repolarization, represented by the electrocardiographic measurements J‐Tpeakc and Tpeak‐Tend, respectively, as well as Tpeak‐Tend/QT, a measure of transmural dispersion of repolarization. Male volunteers ≥ 65 years of age (n = 14) were randomized to receive transdermal testosterone 100 mg, oral progesterone 400 mg, or matching transdermal/oral placebo daily for 7 days. On the morning following the seventh day, subjects received intravenous ibutilide 0.003 mg/kg, after which electrocardiograms were performed serially. One subject was excluded due to difficulty in T‐wave interpretation. Pre‐ibutilide J‐Tpeakc was lower during the testosterone phase than during progesterone and placebo (216 ± 23 vs. 227 ± 28 vs. 227 ± 21 ms, P = 0.002). Maximum post‐ibutilide J‐Tpeakc was also lower during the testosterone phase (233 ± 22 vs. 246 ± 29 vs. 248 ± 23 ms, P < 0.0001). Pre‐ibutilide Tpeak‐Tend was not significantly different during the three phases, but maximum post‐ibutilide Tpeak‐Tend was lower during the testosterone phase (80 ± 12 vs. 89 ± 18 vs. 86 ± 15 ms, P = 0.002). Maximum Tpeak‐Tend/QT was also lower during the testosterone phase (0.199 ± 0.023 vs. 0.216 ± 0.035 vs. 0.209 ± 0.031, P = 0.005). Progesterone exerted minimal effect on drug‐induced lengthening of J‐Tpeakc, and no effect on Tpeak‐Tend or Tpeak‐Tend/QT. Transdermal testosterone attenuates drug‐induced lengthening of both early and late ventricular repolarization in older men.

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Section: Discussionmentioning

confidence: 99%

Transdermal Testosterone Attenuates Drug‐Induced Lengthening of Both Early and Late Ventricular Repolarization in Older Men

Muensterman

Jaynes

Sowinski

et al. 2020

Clin Pharma and Therapeutics

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“…The adipose tissue accumulates mainly subcutaneously without changes in waist-hip ratio. ADT can also induce fatal ventricular arrhythmia by lengthening Q-T interval on ECG [ 38 , 39 , 40 ] due to hypogonadism but also by a direct effect on I k currents in myocardial cells, described experimentally for some ADT [ 38 ] ( Figure 3 ). ADT raises the thrombotic risk by increasing the serum level of fibrinogen, as demonstrated by Ziaran et al [ 41 ] in 97 patients with locally advanced prostate cancer after 12 months of treatment, but not the serum level of CRP [ 16 , 42 ].…”

Section: Cardiovascular Effects Of Adtmentioning

confidence: 99%

“…In a recent study [ 39 ] which included 35 patients with advanced prostate cancer and secondary hypogonadism induced by 6 months ADT, there was a significant alteration of ECG parameters associated with arrhythmic risk: prolongations of QT interval corrected to the cardiac rate, QT dispersion, maximal value of Tpeak-Tend interval, mean ratio Tpe/QT and maximal ratio Tpe/QT, Tped. In patients which undergone an echocardiographic study there was also a subclinical alteration of global longitudinal strain and mechanical dispersion evaluated by echocardiography [ 67 ].…”

Section: Cardiovascular Effects Of Adtmentioning

confidence: 99%

Androgen Deprivation Therapy, Hypogonadism and Cardiovascular Toxicity in Men with Advanced Prostate Cancer

et al. 2021

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Androgen deprivation therapy (ADT) is successfully used in patients with advanced prostatic cancer, but there are many concerns about its systemic side effects, especially due to advanced age and frequent comorbidities in most patients. In patients treated with ADT there are metabolic changes involving the glycaemic control and lipid metabolism, increased thrombotic risk, an increased risk of myocardial infarction, severe arrhythmia and sudden cardiac death. Still, these adverse effects can be also due to the subsequent hypogonadism. Men with heart failure or coronary artery disease have a lower level of serum testosterone than normal men of the same age, and hypogonadism is related to higher cardiovascular mortality. Many clinical studies compared the cardiovascular effects of hypogonadism post orchiectomy or radiotherapy with those of ADT but their results are controversial. However, current data suggest that more intensive treatment of cardiovascular risk factors and closer cardiological follow-up of older patients under ADT might be beneficial. Our paper is a narrative review of the literature data in this field.

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“…Acquired male hypogonadism in patients receiving ADT for prostate cancer therapy has been reported as a risk factor for acquired LQTS and TdP [ 17 , 85 , 90 , 91 , 92 ] and normalization of the testosterone level by HRT attenuates the modification of QTc duration in hypogonadal males [ 85 , 93 , 94 ]. In a case series of seven consecutive men prospectively admitted for TdP, we showed that all had acquired hypogonadism and that normalization of testosterone levels shortened QTc and prevented recurrence of TdP [ 17 ].…”

Section: Exogenous Hormonal Therapy and Its Effect On Qtc Variatiomentioning

confidence: 99%

Sexual Dimorphisms, Anti-Hormonal Therapy and Cardiac Arrhythmias

Grouthier

Moey

Gandjbakhch

et al. 2021

IJMS

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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.

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Evolution of Electrocardiographic Repolarization Parameters During Antiandrogen Therapy in Patients with Prostate Cancer and Hypogonadism

Cited by 15 publications

References 33 publications

Transdermal Testosterone Attenuates Drug‐Induced Lengthening of Both Early and Late Ventricular Repolarization in Older Men

Transdermal Testosterone Attenuates Drug‐Induced Lengthening of Both Early and Late Ventricular Repolarization in Older Men

Androgen Deprivation Therapy, Hypogonadism and Cardiovascular Toxicity in Men with Advanced Prostate Cancer

Sexual Dimorphisms, Anti-Hormonal Therapy and Cardiac Arrhythmias

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