Cardiovascular effects of hormone therapy for prostate cancer

Lester, J.F.; Mason, Malcolm David

doi:10.2147/dhps.s50549

Cited by 14 publications

(11 citation statements)

References 76 publications

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“…Our results show a negative association between concentrations of T/DHT and cholesterol subfractions, and this confirms previous outcomes suggesting that increased concentrations of T/DHT lead to decreased concentrations of total cholesterol and LDL cholesterol [ 6 ]. Similar trends in the relationships between total cholesterol or LDL cholesterol and T concentrations have been observed in hypogonadal men treated with T/DHT replacement therapy [ 4 ]. This further confirms that T/DHT may have a beneficial impact on lipid profile, even in subjects not receiving hormonal replacement therapies.…”

Section: Discussionsupporting

confidence: 67%

“…In addition, some men undergoing androgen deprivation therapy due to prostate cancer present an increased risk of impaired glucose and/or lipid metabolism, often contributing to cardiovascular ischaemic events [ 4 ]. This implies that T may be somehow involved in carbohydrate and lipid metabolism and thus, may indirectly contribute to the ongoing onset of atherogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Testosterone and dihydrotestosterone reduce platelet activation and reactivity in older men and women

Karolczak

Konieczna

Kostka

et al. 2018

Aging

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The cardiovascular effects of testosterone and dihydrotestosterone are generally attributed to their modulatory action on lipid and glucose metabolism. However, no ex vivo studies suggest that circulating androgen levels influence the activation and reactivity of blood platelets – one of the main components of the haemostasis system directly involved in atherosclerosis. The levels of testosterone, dihydrotestosterone and oestradiol in plasma from men and women aged from 60 to 65 years were measured by LC-MS; the aim was to identify any potential relationships between sex steroid levels and the markers of platelet activation (surface membrane expression of GPII/IIIa complex and P-selectin) and platelet reactivity in response to arachidonate, collagen or ADP, monitored with whole blood aggregometry and flow cytometry. The results of the ex vivo part of the study indicate that the concentrations of testosterone and its reduced form, dihydrotestosterone are significantly negatively associated with platelet activation and reactivity. These observations were confirmed in an in vitro model: testosterone and dihydrotestosterone significantly inhibited platelet aggregation triggered by arachidonate or collagen. Our findings indicate that testosterone and dihydrotestosterone are significant haemostatic steroids with inhibitory action on blood platelets in older people.

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Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 99%

Testosterone and dihydrotestosterone reduce platelet activation and reactivity in older men and women

Karolczak

Konieczna

Kostka

et al. 2018

Aging

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“…Many studies assess the occurrence of cardiovascular adverse events in patients with prostate cancer on androgen deprivation therapy [13][14][15][16][17], but data regarding the risk of sudden cardiac death in these patients are inconclusive. An analysis of the Surveillance, Epidemiology and End Results Medicare database which includes 73,196 patients with locoregional prostate cancer showed that the use of gonadotropin-releasing hormone receptor agonists was associated with a higher risk of coronary heart disease, sudden cardiac death, and myocardial infarction compared to orchiectomy [17,18].…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2020

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We assessed the effects of antiandrogen therapy on ECG parameters of ventricular repolarization related to arrhythmic risk in 35 patients aged 70.3 ± 7 years with advanced prostate cancer treated with degarelix associated with enzalutamide (group A, 26 patients) or degarelix monotherapy (group B, 9 patients). We analyzed Fridericia corrected Q-T interval (QTc), Q-T dispersion (QTd), J-Tpeak interval (JTp), mean and maximum Tpeak-Tend interval (Tpe) and Tpe/QT ratio, Tpeak-Tend dispersion (Tped), index of cardio-electrophysiological balance (iCEB) from ECG tracings, and occurrence of ventricular premature beats (VPB) recorded by Holter ECG, before initiation of medication (M0) and after 6 months of treatment (M1). The groups had similar demographics except for a higher prevalence of prior myocardial infarction in group B (p = 0.01). All patients had low serum testosterone at M1. Baseline QTc, QTd, maxTpe/QT, meanTpe, maxTpe, Tped values were higher in B compared to A. They had a significant prolongation at M1 only in A. 20 patients in A and 6 in B had a 10% prolongation or decrease of iCEB (p = 0.66). In 5 patients, VPB severity increased from non-complex to complex: 3 in A and 2 in B (p = 0.31), but no sustained ventricular arrhythmia was registered. In conclusion, after 6 months of treatment, patients with hypogonadism on degarelix associated with enzalutamide had significant prolongation of QTc, QTd, maxTpe, meanTpe/ QT, maxTpe/QT, Tped compared to patients on degarelix alone. The proportion of patients with 10% iCEB variation was similar between groups. There was no record of severe arrhythmias during the first 6 months of treatment.

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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%

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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Cardiovascular effects of hormone therapy for prostate cancer

Cited by 14 publications

References 76 publications

Testosterone and dihydrotestosterone reduce platelet activation and reactivity in older men and women

Testosterone and dihydrotestosterone reduce platelet activation and reactivity in older men and women

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

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

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