Androgenic steroids dysregulation and the risk of coronary artery disease

ABSTRACT

Introduction

Endogenous testosterone deficiency or excess anabolic-androgenic steroids (AAS) have been linked to alter the physiology of different organs in the body, more specifically, the vasculature of coronary arteries. Despite the health-related concerns of using synthetic testosterone derivatives, such as AAS, there has been a tremendous increase in the use of AAS among athletes and bodybuilders.

Areas covered

We have highlighted the three main mechanisms that AAS increase the risk of coronary artery disease (CAD): altering the homeostasis of lipid metabolism which results in dyslipidemia and subsequently atherosclerosis, disturbing the function of platelet which results in platelet aggregation and subsequent thrombosis, and increasing the risk of coronary vasospasm by affecting the physiological function of vascular bed.

Expert opinion

Despite the restriction of AAS in specific clinical conditions such as testosterone deficiency and cancer therapy, many amateurs’ athletes misuse the AAS. Although there has been a strong association between the AAS misuse and risk of developing CAD, the more valued approach would be a randomized clinical double-blind trial. The suggested primary endpoint would be an occurrence of adverse cardiovascular events, such as myocardial infarction, cerebrovascular accidents, and death. Increasing awareness of the risk of missing AAS among high-risk groups is imperative.

KEYWORDS:

• Testosterone
• Anabolic-androgenic steroids
• coronary artery disease

Article highlights

• The use of anabolic-androgenic steroids (AAS) for recreation purposes is associated with diverse multi-systems adverse effects; notably increasing the risk of coronary artery disease (CAD).

• AAS increases the risk of CAD by three main mechanisms: dyslipidemia and subsequent atherosclerosis, platelet dysfunction, and a higher likelihood of coronary vasospasm.

• AAS alters the homeostasis of lipid metabolism, increases low-density lipoprotein and decreases higher-density lipoprotein.

• Platelet dysfunction promoted by alteration of fibrinogen, plasminogen activator inhibitor-1, and alpha-2- antiplasmin leads to vascular thrombosis and early onset of CAD.

• Dysregulation of the second messenger for production of the main vasodilator neurotransmitter (i.e. cyclic guanosine monophosphate) leads to lower production of nitric oxide and subsequently higher likelihood of coronary artery vasospasm.

• Easy access to AAS by bodybuilders and armature athlete increases the chance of early occurrence of CAD, thus, increasing the awareness among high-risk population is imperative.

Abbreviations

AASAnabolic-androgenic steroids

ATPAdenosine diphosphate

CADCoronary artery disease

cGMPcyclic guanosine monophosphate

HDLHigh-density lipoprotein

LDLLow-density lipoprotein

TG Triglycerides

TXA2Thromboxane A2 receptors

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

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.