An update on heart disease risk associated with testosterone boosting medications

ABSTRACT

Introduction: The cardiovascular (CV) safety of testosterone replacement therapy (TRT) remains a crucial issue in the management of subjects with late-onset hypogonadism. The authors systematically reviewed and discussed the available evidence focusing our analysis on heart-related issues.

Areas covered: All the available data from prospective observational studies evaluating the role endogenous T levels on the risk of acute myocardial infarction (AMI) were collected and analyzed. In addition, the impact of TRT on heart-related diseases, as derived from pharmaco-epidemiological studies as well as from randomized placebo-controlled trials (RCTs), was also investigated.

Expert opinion: Available evidence indicates that endogenous low T represents a risk factor of AMI incidence and its related mortality. TRT in hypogonadal patients is able to improve angina symptoms in subjects with ischemic heart diseases and exercise ability in patients with heart failure (HF). In addition, when prescribed according to the recommended dosage, TRT does not increase the risk of heart-related events.

KEYWORDS:

• Testosterone
• cardiovascular diseases
• heart failure
• ischemic heart diseases

Article highlights

• Low endogenous testosterone (T) is associated with an increased risk of acute myocardial infarction (AMI)-related mortality and AMI incidence.

• Testosterone replacement therapy (TRT) in hypogonadal patients is able to improve angina symptoms in subjects with ischemic heart diseases and exercise ability in patients with heart failure.

• In 2014, the European Medical Agency (EMA) did not share the FDA’s opinion of an increased CV risk linked to T medication, because of the lack of convincing evidence.

• The analysis of all randomized placebo-controlled trials showed that when prescribed according to the recommended dosage, TRT does not increase the risk of heart-related events.

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Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

A reviewer on this manuscript has received research grants and lecture honoraria from Bayer and Besins. A reviewer on this manuscript has served on an advisory board for Ferring. All other peer reviewers on this manuscript have no other relevant financial relationships or otherwise to disclose.

Additional information

Funding

This paper was not funded.