期刊
JOURNAL OF THE AMERICAN HEART ASSOCIATION
卷 10, 期 5, 页码 -出版社
WILEY
DOI: 10.1161/JAHA.120.017267
关键词
medical castration; prostate cancer; QT prolongation; torsade de pointes; ventricular fibrillation
资金
- Akaeda Medical Research Foundation
- Japan Society for the Promotion of Science KAKENHI [JP19K19553]
Medical castration can prolong QT/QTc intervals in prostate cancer patients, and may cause TdP/VFs even in patients without risk of QT prolongation before therapy. An increase in QTc interval >50 ms from baseline could be a predictor of TdP/VF. Close attention to QTc interval throughout medical castration is crucial in preventing malignant arrhythmias.
Background Medical castration, gonadotropin-releasing hormone agonists, and antiandrogens have been widely applied as a treatment for prostate cancer. Sex steroid hormones influence cardiac ion channels. However, few studies have examined the proarrhythmic properties of medical castration. Methods and Results This study included 149 patients who underwent medical castration using gonadotropin-releasing hormones with/without antiandrogen for prostate cancer. The changes in the ECG findings during the therapy and associations of the electrocardiographic findings with malignant arrhythmias were studied. The QT and corrected QT (QTc) intervals prolonged during the therapy compared with baseline (QT, 394 +/- 32 to 406 +/- 39 ms [P<0.001]; QTc, 416 +/- 27 to 439 +/- 31 ms [P<0.001]). The QTc interval was prolonged in 119 (79.9%) patients during the therapy compared with baseline. In 2 (1.3%) patients who had no structural heart disease, torsade de pointes (TdP) and ventricular fibrillation (VF) occurred >= 6 months after starting the therapy. In patients with TdP/VF, the increase in the QTc interval from the pretreatment value was >80 ms. However, in patients without TdP/VF, the prevalence of an increase in the QTc interval from the pretreatment value of >50 ms was 11%, and an increase in the QTc interval from the pretreatment value >80 ms was found in only 4 (3%) patients. Conclusions Medical castration prolongs the QT/QTc intervals in most patients with prostate cancer, and it could cause TdP/VFs even in patients with no risk of QT prolongation before the therapy. An increase in the QTc interval from the pretreatment value >50 ms might become a predictor of TdP/VF. Much attention should be paid to the QTc interval throughout all periods of medical castration to prevent malignant arrhythmias.
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