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It is important to note that SCD may occur during early, clinically occult stage of ARVC, which still bears the pathological hallmarks of progressive cardiomyocyte loss and fibrofatty infiltration. These findings have recently been validated in another study by Ren et al. (53) in a different ARVC cohort. While risk stratification traditionally relied on measurements of structural dysfunction and electrophysiological indices (51), there have been recent attempts to identify circulating biomarkers for prediction of arrhythmic risk. The role of testosterone during cardiac ischemia and in the prevention of reperfusion arrhythmias is controversial. In the context of an ischemic insult to the heart, reperfusion that accompanies the opening of a blocked coronary artery may trigger arrhythmias and result in SCD. It was shown that estrogen has beneficial effects by improving cardiac function, preserving calcium homeostasis and inhibiting the mitochondrial apoptotic pathway (44).
This genetically-determined disease is characterized by the appearance of a coved-type ST segment elevation in the right precordial ECG leads, and puts the patients at significant risk for SCD in the absence of an underlying structural heart disease (61). As mentioned previously, estrogen, progesterone and testosterone have varying effects on these currents, which could explain the gender differences (7). Female sex is known to be an independent risk factor, as females have 10–20 ms longer QTc intervals. Likewise, testosterone replacement was shown to exert cardioprotective effects in orchiectomized rats (48). In fact, there are reports of increased (29), decreased (32), or indifferent calcium currents (ICa) in females as compared to males (27).
Cumulative incidence did not differ between the 2 groups.47 These studies led the American Health Association, the American Cancer Society, and the American Urological Association48 to issue a joint statement in 2010, declaring it to be "appropriate to state that there may be a relation between ADT and cardiovascular risk." Soon after, the FDA also mandated the addition of warnings of increased risk of diabetes and CVD as a result of GnRH agonist use in men with prostate cancer.49 The effects of the artificial lowering of testosterone levels by ADT on an individual's overall health has also been studied extensively. Adequately powered randomized clinical trials designed to assess cardiovascular events are required to definitively determine the effect of testosterone therapy on cardiovascular risk. In contrast to these studies, others have reported a protective effect of testosterone therapy on cardiovascular health. The indication of an association between testosterone therapy and risk for adverse cardiovascular events prompted the US Food and Drug Administration (FDA) to issue a safety warning on testosterone therapy for older men, which was followed by a reduction in testosterone prescriptions.30 The safety warning cautioned against the use of testosterone therapy for aging-related decline and reinforced the current approval of testosterone products for hypogonadal men only.30 However, it is important to note that the methodology and reliability of the aforementioned studies have since been questioned.
Prostate cancer is the second most frequent malignancy in men worldwide.4 In 1941, Huggins and Hodges37 were the first to demonstrate the beneficial effects of castration and estrogen injections in men with metastatic prostate cancer. In contrast to the use of TRT in hypogonadal men, androgen deprivation therapy (ADT) is commonly used in the treatment of advanced prostate cancer. Questions also have been raised regarding the methodological validity and statistical analysis techniques in the study by Vigen et al.27 Some systematic reviews and meta-analyses have suggested that the conflicting associations, and subsequent lack of firm conclusions, may be due to study heterogeneity and low-quality evidence. Testosterone can be converted to dihydrotestosterone (DHT) or 17β-estradiol (E2).
Female sex hormones have well-documented effects on HRV that fluctuate throughout the menstrual cycle. While many of the compounded creams do not have published bone and breast data, subcutaneous pellet therapy studies have been published in peer-reviewed scientific journals. Whereas some compounded hormones have not been tested, others have had extensive testing, and have published data and FDA regulation of their outsource manufacturing. I find this perplexing, as it is the unopposed estrogen, rather than the testosterone, that can lead to the increased incidence of adenocarcinoma of the endometrium . Dunsmoor-Su et al. claim that their group of obstetrician gynecologists "diagnose several endometrial cancers a year from the use of estrogen and testosterone pellets that result in super-physiologic hormone levels without adequate progesterone use". Unfortunately, when we see outliers who have had complications, it is easy to extrapolate and reach conclusions about the therapy that are not supported by the larger group of patients whose health and quality of life have benefited from testosterone therapy. The goal should be to individualize the dosing to resolve the clinical symptoms, while keeping serum levels low enough to minimize androgenic side effects.
A recent publication on the complications of subcutaneous hormone-pellet therapy, looking at a large cohort of patients over 7 years, demonstrated long-term safety. There is growing evidence to support the use of physiologic doses of testosterone for sexual function, osteoporosis prevention, brain protection, and breast protection. By taking steps to monitor the heart and manage risk factors, TRT can be made safer for those who need it. The risk depends on personal health, the form and dose of TRT, and how the body responds. Eating a healthy diet, staying active, avoiding smoking, and managing stress can support heart health while taking TRT. There are steps that can help reduce the risk of side effects. This may include blood tests, blood pressure checks, and heart monitoring.
Monitoring helps identify early signs of unwanted effects and allows for safe adjustments to the therapy plan. Because of this, doctors often monitor heart health during treatment, especially during the first few months. Overall, current research does not show strong or consistent evidence that TRT causes dangerous heart rate changes in most patients. The authors concluded that more long-term studies are needed to fully understand how TRT affects the heart over time. It also noted that heart rate changes, when reported, were usually mild and temporary. While this does not happen in every patient, it may explain why some people feel jittery or experience palpitations after starting therapy.
The inconsistent findings to date and lack of standardized approach to TRT administration in these studies mandate a large-scale randomized controlled trial to better define the cardiovascular effects of TRT. This raises the possibility that these reductions in HDL-c do not confer increased CVD risk at all and conceivably could reflect a protective effect. In parallel to these clinical investigations, ongoing research efforts have been invested in better understanding the mechanisms by which T may influence cardiovascular health. The study endpoints include coronary artery plaque volume as measured by CT scan as well as serum lipids; thus, although resultant data merit interest, this study is underpowered to provide additional information regarding cardiovascular events. In a second study, Finkle et al. used a large healthcare database and also reported an association between T prescriptions and myocardial infarction in older men in the immediate 90-day postprescription period .
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