Subclinical left ventricular dysfunction in men under androgen deprivation therapy for prostate cancer, revealed by speckle‐tracking‐derived parameters, repolarization, and myocardial injury markers

OBJECTIVE: To analyze global left ventricular longitudinal strain (GLS), mechanical dispersion (MD), electrocardiographic repolarization, and myocardial injury markers changes during androgen deprivation therapy (ADT) and subsequent hypogonadism in men with advanced prostate cancer. METHODS: We included 31 patients 69.7 ± 7.3 years old, in sinus rhythm, with stable cardiac conditions and evaluated them by echocardiography, electrocardiography, and blood sampling for high sensitivity cardiac troponin I (hs‐cTnI), and N‐terminal pro‐brain natriuretic peptide (NTproBNP), at ADT initiation (M0) and after 6 months of treatment (M1). Peak longitudinal strain by speckle‐tracking echocardiography was assessed in 17 left ventricular segments and averaged to GLS. Standard deviation of time intervals from the start of Q/R on electrocardiogram to peak longitudinal strain in the 17 segments (MD(SD)), and the difference between the longest and shortest time‐to‐peak strain intervals (MD(delta)) were calculated as indices of MD. Fridericia corrected electrocardiographic repolarization parameters were analyzed as follows: QT interval (QTc), mean and maximum values of Tpeak‐Tend interval (Tpe), and Tpe/QT ratio, Tpe dispersion (Tped). RESULTS: Significant impairments of the following parameters were registered between M0 and M1: GLS (%) (−16.93 ± 3.89; −14.43 ± 3.57, P < .001), MD(SD) (ms) (77.4 ± 21.4; 89 ± 27, P = .004), MD(delta) (ms) (225.3 ± 78.3; 259.9 ± 108.4, P = .02), QTc (ms) (458.8 ± 43.4; 485.6 ± 45.1, P = .01), maxTpe/QT (0.246 ± 0.04; 0.268 ± 0.04, P = .01), maxTpe (ms) (105.4 ± 23.2; 119.5 ± 26.4 P = .01), meanTpe (ms) (83.3 ± 16.8; 90.7 ± 19.3, P = .02), and hs‐cTnI (ng/mL) (4.6 ± 5.4; 5.4 ± 6.4, P = .01). Mean serum testosterone level at M1 was 0.1 ± 0.13 ng/mL. The patients’ clinical cardiological status remained stable during follow‐up. CONCLUSIONS: ADT and subsequent hypogonadism induce subclinical alterations in GLS, MD, electrocardiographic repolarization parameters, and hs‐cTnI during the first 6 months of treatment.