Impact of Anabolic-Androgenic Steroids on Coronary Artery Disease

Abstract

Introduction

Anabolic-androgenic steroids (AAS), synthetic derivatives of testosterone, are misused by athletes to enhance performance despite known cardiovascular risks including dyslipidemia, hypertension, and acute myocardial infarction.

Case Summary

A 30-year-old male with a history of AAS abuse presented with acute chest pain and was diagnosed with non-ST elevation myocardial infarction. Coronary angiography revealed intimal hyperplasia, plaque erosion, and thrombus formation in the proximal left anterior descending artery, confirmed by optical coherence tomography. He was managed with glycoprotein IIb/IIIa inhibitors, anticoagulation, and triple therapy (aspirin, clopidogrel, apixaban) and was shifted to dual therapy post discharge.

Discussion

Literature links AAS abuse to atherogenic, thrombogenic, and vasospastic mechanisms, increasing coronary artery disease risks. This case highlights AAS-induced coronary pathology in a young patient, emphasizing the need for awareness among athletes and clinicians to prevent life-threatening outcomes.

Take-Home Message

AAS abuse can cause severe coronary artery disease. Education is critical to mitigate cardiovascular risks in young athletes.

Graphical Abstract

Anabolic-androgenic steroids (AAS) are synthetic compounds derived from testosterone, primarily used to promote muscle growth and enhance athletic performance. While they have legal medical applications, their illicit use among athletes and bodybuilders is widespread.¹ AAS cause an increase in muscle size as a consequence of a dose-dependent hypertrophy resulting in an increase of the cross-sectional areas of both type I and type II muscle fibers and myonuclear domains. Moreover, it has been reported that AAS can increase tolerance to exercise by making the muscles more capable of overload, therefore shielding them from muscle fiber damage and improving the level of protein synthesis during recovery.²

Take-Home Messages

• •Anabolic-androgenic steroids abuse can cause severe coronary artery disease.
• •Education is critical to mitigate cardiovascular risks in young athletes.

AAS abuse has been linked to numerous adverse effects, including dyslipidemia, hypertension, and left ventricular hypertrophy.¹ Acute myocardial infarction, although less commonly reported, remains one of the most severe complications associated with AAS abuse.³

The mechanisms underlying AAS-induced cardiovascular complications are multifaceted. Proposed models include atherogenic effects due to altered lipid profiles, increased thrombogenicity, vasospasm mediated by nitric oxide release, and direct myocardial injury leading to fibrosis and necrosis. These mechanisms collectively increase the risk of sudden cardiac death (SCD) in AAS abusers, particularly when combined with intense physical activity.²

History of Presentation

A 30-year-old male bodybuilder on 2 types of AAS (metenolone 150-mg tablet once daily, and trenbolone 100 mg intramuscular every other day) presented to emergency department with acute-onset typical chest pain radiating to the left shoulder and back, persisting for 4 hours. He has negative for medical and family history of similar condition. His electrocardiogram (ECG) revealed sinus rhythm with incomplete right bundle branch block with no significant ST-T changes (Figure 1). His clinical examination was unremarkable, with a heart rate of 90 beats per minute, blood pressure of 140/80 mm Hg, oxygen saturation of 99% on room air. His initial troponin I was negative. He was admitted to a cardiac care unit for further management as per acute coronary syndrome pathway.

Figure 1.

The 12-Lead ECG Shows Sinus Rhythm With Incomplete Right Bundle Branch Block

Investigations

On follow-up in cardiac care unit, high-sensitivity troponin I came back elevated and rising. His lipid profile indicated low high-density-lipoprotein cholesterol and high low-density-lipoprotein cholesterol, while liver function tests were abnormal (Table 1). A diagnosis of acute non-ST elevation myocardial infarction was established. His echocardiography revealed an upper normal septal wall thickness but was otherwise unremarkable. We decided to proceed for coronary angiography (CAG) and intervention if needed.

Table 1.

Laboratory Investigations

Test	Result	Normal Reference
High-sensitivity troponin I	First set: <1 Second: 357.4 Third set: 1,174	0-11 ng/L
LDL cholesterol	136	65-130 mg/dL
HDL	34	35-86 mg/dL
SGPT	75	5-50 u/L
SGOT	89	17-59 u/L

HDL = high-density lipoprotein; LDL = low-density lipoprotein; SGOT = serum glutamic oxaloacetic transaminase; SGPT = serum glutamic pyruvic transaminase.

Management

CAG identified a large filling defect in the proximal left anterior descending artery (LAD) with TIMI flow grade 3 and no obstruction in mid and distal LAD or diagonal branch. The left main trunk, left circumflex artery, and right coronary artery were normal (Figure 2). The decision was to treat with infusion of glycoprotein IIb/IIIa inhibitors for 48 hours, followed by therapeutic anticoagulation, and bring him back to a catheterization lab after 3 days for control CAG with optical coherence tomography (OCT) interrogation.

Figure 2.

Coronary Angiography Showing Proximal LAD Occlusion and Normal Other Coronary Vessels

Coronary angiography showed that there is a large filling defect in the proximal left anterior descending artery (LAD). The mid and distal LAD are unobstructed. The diagonal branch is unobstructed. The LAD has TIMI flow grade 3. The left main trunk, left circumflex artery (LCX), and right coronary artery (RCA) were normal.

Control CAG and OCT interrogation revealed proximal plaque erosion (Figure 3A), likely organized thrombus (Figure 3B), and intimal hyperplasia (Figure 3C), and distally, there was normal intima (Figure 3D, Video 1). There was no luminal obstruction. Therefore, the patient was managed conservatively with triple therapy (aspirin 100 mg; clopidogrel 75 mg; apixaban 5 mg) for 1 week, followed by a dual therapy (clopidogrel 75 mg; apixaban 5 mg) for 1 to 3 months. The plan was to convert him to dual antiplatelet therapy (aspirin 100 mg; clopidogrel 75 mg) later.

Figure 3.

OCT Imaging of LAD Pathology

Optical coherence tomography (OCT) interrogation showed proximal plaque erosion (A) with a proximal mobile thrombus (B), followed by a segment of intimal hyperplasia (C), and distally there was normal intima (D). There was no luminal obstruction.

Outcome and Follow-Up

Up to 2 months post hospitalization, the patient remained pain-free, with no ECG changes observed. His medical treatment was adjusted to dual therapy as planned upon discharge.

Discussion

AAS are synthetic analogs of testosterone, utilized safely in certain medical conditions. However, they are widely misused by bodybuilders as performance-enhancing drugs.¹ The Middle East exhibits the highest prevalence rate, accounting for 21.7% of global users, followed by South America (4.8%), Europe (3.8%), North America (3.0%), Oceania (2.6%), Africa (2.4%), and Asia (0.2%).⁴

While AAS use can lead to positive effects such as increased muscle mass, strength, energy, concentration, and reduced fat mass, it also poses numerous negative health impacts. These adverse effects range from mild and transient (fluid retention, acne, agitation, gynecomastia, aggressiveness) to severe, affecting multiple organ systems including cardiovascular, reproductive, musculoskeletal, endocrine, renal, immunologic, and neuropsychiatric functions.^5,6

The cardiovascular system is particularly vulnerable to AAS side effects. AAS use can enhance vascular resistance and blood pressure, alter serum lipoproteins, and produce direct myocardial toxicity. Reported adverse cardiovascular events include impaired left ventricular function, arterial thrombosis, pulmonary embolism, and left ventricular hypertrophy associated with myocytolysis and fibrosis.⁷ AAS abuse can promote cardiac tissue growth, leading to hypertrophic cardiomyopathy and subsequent apoptotic cell death. This phenomenon is linked to ventricular remodeling, cardiomyopathy, myocardial infarction, and SCD, even in the absence of coronary thrombosis or atherosclerosis.²

Previous literature proposes 4 mechanisms responsible for cardiac complications in AAS abusers: the atherogenic mechanism in which there is alterations in serum lipoprotein levels with a subsequent increase in atherosclerosis risk, the thrombosis mechanism in which there is enhanced platelet aggregation and polycythemia increasing thrombus formation risk, the vasospasm mechanism where there is anabolic agent-induced nitric oxide release inducing arterial vasospasm, and the direct myocardial injury mechanism where direct myocardial toxicity causes apoptosis, increased collagen deposition, fibrosis, and altered microcirculation leading to chronic ischemic damage. These mechanisms collectively associate AAS use with a high risk of SCD.²

Previous literature has confirmed increased arterial thickening, although it was not associated with any significant abnormalities in arterial structure or function. Another study identified carotid intima-media hyperplasia in similar patients, suggesting that this condition is part of the premature atherosclerosis progression process.⁸

In a young patient with no traditional cardiovascular risk factors, chest pain may be related to exercise-induced muscular strain, tear, costochondritis, rib fracture, and delayed-onset muscle soreness or could have a cardiac origin. Despite being categorized as low risk based on his age, risk factors, and family history, CAG revealed evidence of coronary artery disease. Findings included intimal hyperplasia, plaque erosion, and subsequent thrombus formation, resulting in acute non-ST-segment elevation myocardial infarction.

The management plan was based on recent studies and expert consensus that support conservative management in selected cases of plaque erosion, especially in young patients with preserved flow, to avoid unnecessary stent implantation and its long-term complications. In the EROSION trial, 60 acute coronary syndrome patients with plaque erosion diagnosed by OCT (96.7% with ST-segment elevation myocardial infarction), residual diameter stenosis <70%, and TIMI flow grade on angiography were treated with antithrombotic therapy alone without stent implantation.⁹

In addition, Prior studies suggest that thrombin activate multiple protease-activated receptors (PARs), contributing to inflammation and atherosclerosis. Thrombin-mediated activation of PAR-1 induce vascular smooth muscle cell proliferation and migration, a pivotal mechanism in atherosclerosis development. Similarly, factor Xa activate PARs, contributing to highlighting inflammation, fibrosis, and vascular endothelial dysfunction. Recent evidence demonstrate that factor Xa directly stimulate PAR-1, enhancing platelet activation and thrombus formation.¹⁰ Based on these findings and the observed thrombus in LAD, the patient was discharged on oral anticoagulant therapy to reduce thrombus burden and inhibit platelet activation, with a plan to transition to dual antiplatelet therapy (aspirin and clopidogrel) after 1 to 3 months.

Had this patient been treated as low risk and discharged home, he might have experienced serious complications, including acute ST-elevation myocardial infarction and potentially sudden cardiac arrest. This case underscores the necessity of specific assessment criteria for bodybuilders, particularly those using AAS, such as ECG, stress treadmill test screening of lipid profile, and liver function test with a view to other noninvasive or invasive tests if the initial screening is abnormal.

Conclusions

AAS abuse can induce pathological changes in the coronary intima, such as intimal hyperplasia, plaque erosion, and thrombus formation, potentially linking it to SCD. It is imperative to educate young athletes and bodybuilders about the serious health risks and long-term consequences of AAS abuse. Clinicians should pay close attention to complaints from bodybuilders, even if they appear healthy. Further investigations are necessary to fully understand the impact of AAS abuse on health and to have screening protocols or guideline for AAS users.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose. The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors' institutions and food and drug administration guidelines, including patient consent where appropriate.

Appendix

Video 1

Optical Coherence Tomography of the Left Anterior Descending Artery During Coronary Angiography

This video demonstrates optical coherence tomography (OCT) interrogation of the proximal left anterior descending artery, revealing plaque erosion, mobile thrombus, intimal hyperplasia, and normal distal intima, illustrating anabolic-androgenic steroid-induced coronary pathology.