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From Muscle Gains to Cardiac Losses: A 40-YearOld Male with Heart Failure with Reduced Ejection Fraction and Erectile Dysfunction Secondary to Chronic Anabolic-Androgenic Steroid Use

Charlie Vidal*, MD, MPH, MBA1, Milay Valentin Sosa, MD1, Jose Martinez Barroso, MD2

¹Department of Cardiology, Manati Medical Center, Manati, Puerto Rico
²Head of Cardiology Department of MMC, Manati, Puerto Rico

*Corresponding author

Charlie Vidal, Department of Cardiology, Manati Medical Center, Manati, Puerto Rico
Email: dr.vidal@doctor.com
orcid.org/0000-0001-7631-6018

Abstract

Background: Anabolic-androgenic steroids (AAS) misuse is an emerging cause of nonischemic cardiomyopathy. Chronic exposure can lead to left ventricular hypertrophy, myocardial fibrosis, and apoptosis. The concomitant use of illicit erectile dysfunction agents may further compound cardiovascular risk.

Case Presentation: A 40-year-old male with long-standing testosterone enanthate use presented with progressive dyspnea, fatigue, and dry cough over 3 weeks. History revealed use of unregulated erectile dysfunction pills and creams. Examination showed bibasilar crackles and hypertension. Echocardiogram revealed concentric LV hypertrophy, global hypokinesia, pseudonormal diastolic pattern, and ejection fraction (EF) 25–30%. MUGA scan confirmed EF 15.9%. Labs showed elevated troponin, NT-proBNP, proteinuria, and positive ANA (1:80). No evidence of coronary ischemia was found. Also found with renal function impairment.

Investigations: Comprehensive cardiac imaging, renal ultrasound, CT chest, and autoimmune panel.

Treatment: Core therapy with an ARNI (Sacubitril/Valsartan), Beta-Blocker (Metoprolol Succinate), SGLT2 (Jardiance), IV diuretics, and discharged with a wearable cardioverter-defibrillator (WCD) for 3 months pending EF reassessment. Reassessment of LVEF at 3-6 months recommended to guide device decisions and continued optimization.

Outcome: Discharged in stable condition with outpatient follow-up for possible recovery of cardiac function. Education on permanent AAS cessation.

Discussion: AAS-induced cardiomyopathy is mediated via androgen receptor–driven hypertrophy, oxidative stress, and apoptosis. WCD provides interim sudden cardiac death protection in newly diagnosed severe LV dysfunction.

Background

Chronic AAS misuse is associated with structural and functional myocardial changes, often underrecognized in young or middle-aged men without traditional cardiovascular risk factors (1,4). Pathophysiologic mechanisms include myocardial hypertrophy, interstitial fibrosis, and apoptosis through androgen receptor activation, oxidative injury, and calcium handling abnormalities (4). This case highlights the role of WCD in potentially reversible toxin-induced cardiomyopathy (3).

Case Presentation

Age/Sex: 40-year-old male

Symptoms: Fatigue, dyspnea, dry cough for 3 weeks

History: Long-term testosterone enanthate injections; illicit erectile dysfunction pills

Exam: Bibasilar crackles, hypertension, no edema

Hospital Course: Admitted for acute decompensated HFrEF and AKI vs CKD stage 3. Treated with GDMT, evaluated by cardiology, pulmonology, nephrology. Discharged with WCD.

Supplementary

Table 1: Clinical Timeline

table 1

Investigations

Table 1: Selected Laboratory Data

table 2

Table 2 : Cardiac Imaging Summary

table 3

Differential Diagnosis

  • Ischemic cardiomyopathy – excluded by normal perfusion SPECT
  • Autoimmune myocarditis – unlikely, normal complements
  • Viral myocarditis – possible but less likely given chronic AAS use

Treatment

  • Sacubitril/valsartan
  • Metoprolol Succinate
  • Jardiance
  • IV diuretics
  • WCD for 3 months pending EF reassessment

Outcome and Follow-up

  • Discharged stable, WCD in place
  • Outpatient cardiology and nephrology follow-up
  • Plan for repeat echocardiogram in 3 months

Table 3:Evidence Summary: WCD in Newly Diagnosed NICM

table 4

Table 4: Evidence Summary: AAS-Induced Cardiomyopathy Mechanisms

table 5
fig 1

Figure 1: Echocardiogram (apical 4-chamber) – concentric LVH, reduced EF.

fig 2
fig 3

Figure 2: CT chest (axial) – cardiomegaly, septal thickening.

Ethics Statement Patient consent obtained for publication of this case report.

References

  1. McDonagh T. A; Metra M; Adamo M; (2021). 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. European Heart Journal, 42(36), 3599–3726.
  2. Heidenreich P. A; Bozkurt B; Aguilar D; (2022). 2022 AHA/ACC/HFSA guideline for the management of heart failure. Journal of the American College of Cardiology, 79(17), e263–e421.
  3. Kovacs B; Reek S; Krasniqi N; (2018). Extended use of the wearable cardioverter-defibrillator: Which patients are most likely to benefit? Cardiology Research and Practice, 2018, 7373610.
  4. Zaugg M; Schaub M. C; (2001). Anabolic-androgenic steroids induce apoptotic cell death in adult rat ventricular myocytes. Journal of Cellular Physiology, 187(1), 90–95.
  5. Grennan K. N; Thota-Kammili S; McKenna A L; (2024). Supplement misadventures: Acute heart failure and hormonal dysregulation from surreptitious use of multiple hormonal supplements. Journal of the Endocrine Society, 8(Suppl 1), A158.

Journal of Clinical Case Reports, Medical Images and Health Sciences (ISSN 2832-1286) is a peer-reviewed journal dedicated to publishing clinical images from all sectors of medicine. The goal of this magazine is to disseminate information about new discoveries and treatments in science and medicine.

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