Steroid‐Induced Cardiomyopathy: Insights From a Systematic Literature Review and a Case Report

ABSTRACT

Anabolic‐androgenic steroids (AAS) abuse is associated with severe cardiovascular risks, particularly AAS‐induced cardiomyopathy. This systematic review highlights that most cases show left ventricular dilation and reduced ejection fraction. AAS, synthetic testosterone derivatives, are widely used to enhance athletic performance and muscle mass. However, misuse of AAS is associated with severe cardiovascular complications, including AAS‐induced cardiomyopathy. This study presents a case of AAS‐induced cardiomyopathy and systematically reviews the existing literature on the condition. A systematic search was conducted across PubMed, Web of Science, Cochrane, and Google Scholar using relevant terms related to AAS and cardiomyopathy. Studies were reviewed to assess clinical presentations, patient demographics, AAS regimens, diagnostic methods, and treatment strategies. The JBI critical appraisal tool was used to evaluate risk of bias. The review included 32 cases of AAS‐induced cardiomyopathy, predominantly in males (97%), with a mean age of 38.3 years. Most patients exhibited left ventricular dilation, reduced ejection fraction, and mitral regurgitation. Most cases showed improvement in heart function after discontinuation of AAS and heart failure treatment. AAS misuse poses significant cardiovascular risks, particularly cardiomyopathy. AAS effect on cardiac remodeling may lead to sudden cardiac death. While some patients recover after cessation, others may require lifelong management. Greater awareness and research are needed to betterunderstand and manage AAS‐induced cardiomyopathy.

1. Introduction

Anabolic‐androgenic steroids (AAS), synthetic derivatives of testosterone, are widely used to enhance muscle mass and athletic performance. However, AAS misuse has been linked to numerous serious health complications, impacting various organ systems, including cardiovascular complications. One condition is AAS‐induced cardiac myopathy, a form of heart disease characterized by diminished cardiac function resulting from prolonged AAS exposure. The use of AAS has increased substantially over the past few decades, not only among athletes but also within the general population [1]. This growing trend in non‐medical use is a significant public health concern due to the associated risks of cardiac dysfunction, myocardial hypertrophy, and fibrosis [2, 3]. Despite the clear evidence linking AAS to adverse cardiovascular outcomes, the exact prevalence of AAS‐induced cardiomyopathy remains uncertain. This report will introduce a new case study of AAS‐induced cardiomyopathy and perform a comprehensive systematic review to assess the current literature on AAS‐induced cardiac myopathy. The review will focus on the clinical manifestations, patients' demographics, AAS regime, diagnostic methods, and potential interventions for reversing this condition.

2. Methods

A comprehensive electronic search was conducted up until June 2024 across four major databases: PubMed, Web of Science, Cochrane, and Google Scholar. The primary search terms employed were ((cardiomyopathy) AND (Anabolic androgenic steroids OR anabolic steroids OR anabolic–androgenic steroids)). For Google Scholar, the search terms were refined to (all in the title: cardiomyopathy androgenic OR steroids). In addition, a further manual search in the reference list of relevant reports was performed. All studies reporting an association between the use of AAS and the incidence of cardiomyopathy were included. Of note, no restrictions were imposed on study design, language, and year of research. The risk of bias among included studies was assessed using the JBI critical appraisal tool for case studies [4]. Two assessors independently conducted data extraction and assessed the risk of bias, followed by a comparison of the data to ensure accuracy.

3. Results

3.1. Case Presentation/Examination

A 40‐year‐old white male bodybuilder with no prior medical history presented to the emergency department after experiencing waxing and waning left‐sided headaches for approximately 2 months. These headaches were associated with lacrimation and a runny nose, each episode lasting 1–2 h. The patient also reported reduced exercise tolerance but denied any persistent dyspnea, palpitations, or chest pain. He has a history of regular anabolic‐androgenic steroid (AAS) injections (nandrolone decanoate, trenbolone acetate, oxymetholone, sustanon, testosterone enanthate, testosterone cypionate, testosterone propionate, and drostanolone propionate) for approximately 25 years, following a pattern of 3 months on and 3 months off; he had apparently stopped this regimen 2 months prior to his hospital presentation.

Clinical examination did not reveal any signs of heart failure or focal neurological deficits. Kidney function tests indicated a creatinine level of 117 μmol/L, while liver function tests, lipid profile, BNP (187 ng/L), full blood count, thyroid function tests, and cardiac markers returned unremarkable results. Initial investigations in the emergency department included a computed tomography (CT) scan of the brain and a CT venogram to exclude the possibility of venous sinus thrombosis; however, both results were negative. A routine chest X‐ray revealed an enlarged heart (Figure 1). An ECG showed ST depression in the inferior leads and T wave inversion in the inferolateral leads. Subsequently, a transthoracic echocardiogram demonstrated mild dilation of the left ventricle, an ejection fraction (EF) of 35%, grade one diastolic dysfunction, and mild mitral valve regurgitation (Figure 2).

FIGURE 1.

CXR of reported case report.

FIGURE 2.

Echocardiography of reported case study.

The patient was started on Sacubitril‐Valsartan, spironolactone, Bisoprolol, and dapagliflozin. He showed improvement in his symptoms and was planned for outpatient follow‐up with the cardiology team.

3.2. A Systematic Review of the Literature

3.2.1. Systematic Review and Critical Appraisal of Included Studies

Initially, 342 articles were identified from four different databases. After removing duplicates using EndNote and screening articles based on title and abstract, 39 articles were selected for full‐text reading. Of them, 28 articles were deemed relevant, along with one additional case study provided by the authors, leading to a total of 29 case reports (Figure 3). The majority of the studies (n = 26) have clearly described patient's demographic characteristics. The intervention applied was mentioned in 22 studies. All reports provided take‐home messages. The overall quality of reporting was robust, with most case reports fulfilling the key criteria outlined by the tool (Appendix A).

FIGURE 3.

PRISMA flow‐diagram of study selection and screening.

3.2.2. Patients' Demographic/Clinical Characteristics and Their Anabolic Steroid Regimes

A total of 29 studies entailing 32 cases involving AAS use were reviewed (Table 1). The cohort predominantly consisted of males (n = 31). The patients' ages ranged from 22 to 73 years, with a mean age of 38.3 years. Most patients (65.6%) had no significant medical history prior to presentation, while others had conditions such as asthma (n = 3), hypogonadism (n = 2), and obesity (n = 2).

TABLE 1.

Baselines demographic and clinical characteristics of included case studies.

Author/Year	Gender	Age	Past Hx	HOPC	Relevant clinical/vital signs	Name of AAS	AAS duration of use	AAS last use before admission
Adhikari/2022/[5]	M	54	Asthma, Polycythaemia	SOB, LL oedema, haemoptysis	Bibasilar crackles and decreased breath sounds, Tachycardia	Testosterone cypionate	18 years	1 month
Shah/2023/[6]	M	50	Hyperlipidaemia, Obesity, Asthma, Hypogonadism	SOB, LL oedema	Tachycardia	Testosterone and anastrozole	N/A	N/A
Andhale/2020/[7]	M	36	Nil	Decreased ET, SOB	Tachycardia, Raised JVP, Mild pitting ankle oedema, B/L fine crackles	Enanthate injections, Oxandrolone tablets	2 years	Current
Angelini/2019/[8]	M	31	Nil	SOB, Orthopnoea	Tachypnea, Raised JVP	Stanozolol, Boldenonem, Trenbolone, Testosterone propionate, Enanthate	12 years	1 year
Bhattad/2022/[9]	M	29	Nil	Decreased ET, SOB	Unremarkable	AAS	8 months	Current
Bispo/2009/[10]	M	40	Nil	Fatigue, Decreased ET, Anorexia, Vomiting, RUQ pain, Jaundice.	Hypotension, Tachycardia, Tachypnea, Jaundice, Hepatomegaly	Methandrostenolone, Stanozolol and Oxymetholone (oral); and Nandrolone decanoate, Testosterone enanthate and Trenbolone enanthate (IM)	10 years	1 month
Clark/2005/[11]	M	40	Depression, Acne	SOB, Orthopnoea, Fatigue, Productive cough, 10‐lb weight gain, dark urine, Acholic stools, Insomnia, Irritability, Anorexia, N&V	Tachycardia, Tachypnea, Raised JVP, A 2/6 holosystolic murmur at the apex, Bibasilar crackles and decreased breath sounds, Tender hepatomegaly	Methandrostenolone, Nandrolone decanoate	3 months	2 weeks
Doleeb/2019/[12]	M	53	Nil	SOB, Palpitations, Headache, and an episode of syncope	Hypertensive, Holosystolic murmur, third heart sound present	AAS	3 years	Current
Ferenchick/2016/[13]	M	41	Nil	Orthopnoea and Paroxysmal nocturnal dyspnoea	Peripheral cyanosis of the extremities, Tachypnea, Raised JVP with +ve hepatojugular reflux	AAS	3 years	7 months
Ferrera/1997/[14]	M	24	Varicocele	SOB, Chest pain	Soft ejection systolic murmur	Testosterone propionate, Sustanon	6 months, then resumed after 3 months.	3 days
Garner/2018/[15]	M	60	Hypogonadism	Acute hypoxic RF	Tachycardia, Tachypnea, Hypotension, Desaturation, Audible S3 & S4, Decreased urine output	Testosterone cypionate	N/A	Current
Ge/2017/[16]	M	25	Liver Cysts	SOB, Epigastric discomfort, N&V, Diaphoresis	Hypertension, Tachycardia, Raised JVP	Testosterone enanthate	N/A	Current
Gul/2022/[17]	F	47	Non‐Hodgkin lymphoma	SOB, Productive cough	Raised JVP, Bilateral crackles, Peripheral oedema	Testosterone	Several months	Current
Ha/2018/[18]	M	73	Nil	Light‐headedness, Palpitations, Generalized weakness	Ventricular tachycardia (210 bpm)	AAS with clenbuterol	20 years	30 years
Han/2015/[19]	M	30	Nil	SOB, Palpitations, Epigastric discomfort	Tachycardia, Raised JVP, Gallop rhythm, Apical pan‐systolic murmur	Testosterone, Trenbolone, Methandrostenolone, Anastrozole	7 years	6 weeks
Ilonze/2022/[20]	M	31	Nil	SOB, Haemoptysis, Chest pressure, Palpitation	Tachycardia, Hypotension, Raised JVP, Systolic murmur	Testosterone enanthate	6 months	Current
Jamal/2022/[21]	M	30	Nil	SOB, Anxiousness, Hair loss, Excessive anger	Hypertension, Audible S3, Displaced apex beat	Equipoise, Nandrolone	4 years	Current
Joseph/2017/[22]	M	33	Asthma	SOB, Orthopnoea, LL oedema	Tachycardia, Tachypnea, Desaturation, Diffuse rales	AAS	1 year	Current
Kalmanovich/2014/[23]	M	34	Nil	SOB, Haemoptysis	Hypoxia (Required mechanical ventilation)	Boldenone	N/A	N/A
Li/2018/[24]	M	22	Nil	SOB, Paroxysmal nocturnal dyspnoea, Haemoptysis, LL oedema	Tachycardia, Muffled heart sounds, Gallop rhythm, Ejection systolic murmur, Icteric sclera	Stanozolol	10 days	12 days
Luc/2018/[25]	M	26	Nil	SOB, Haemoptysis		Testosterone, Trenbolone, Primobolan	3 years	Current
Milevski/2022/[26]	M	46	Obesity	SOB, Palpitations	Plethora	Testosterone isocaproate, Testosterone cypionate, Testosterone propionate, Testosterone enanthate	10 years	10 days
Nieminen/1996/[27]	M	33	Nil	Referred to cardiac assessment because of long use of steroids	Bradycardia	Methandienone, Mesterolone, Oxymetholone, Stanozolol, Methyltestosterone, Oxandrolone, Fluoxymesterone, Testosterone undecanoate, Testosterone proprionate	Sporadic over the years 1985–1993	Current
	M	29	Nil	At routine exercise test at 250 W work level, had monomorphic VT then polymorphic VT then VF	Ventricular tachycardia	Methandiennone, Methyltestosterone, Oxandrolone, Testosterone undecanoate, Stanozolol, Testosterone proprionate	Sporadic over the previous 8 years	Current
	M	31	Nil	CHF symptoms	Unremarkable	Methandienone, Stanozolol, Testosterone	2 years	Current
M	27	Cardiac dilatation of unknown etiology	Arterial thrombus in the left leg	Unremarkable	Testosterone	Many years	N/A
Placci/2015/[28]	M	25	Basedow syndrome, Total thyroidectomy	Chest pain, Sweating, N&V	N/A	Nandrolone, Stanozolol	3 weeks	Current
Shamloul/2014/[29]	M	37	Nil	Tonic‐colonic seizure followed by acute confusional state with right‐sided weakness	Lethargy, Peripheral oedema, Tender hepatomegaly	Methandienone, Methenolone acetate	2 years	Current
Sodhi/2020/[30]	M	30	Nil	SOB, Orthopnoea, paroxysmal nocturnal dyspnoea, Fatigue	Raised JVP, Bi‐basal crackles	Testosterone cypionate, Trenbolone acetate.	11 years	Current
Youssef/2011/[31]	M	39	Nil	Dizziness, Recent aphasia	Right facial palsy, Upper motor neuron lesion	Nandrolone	3 years	Current
White/2018/[32]	M	39	T2DM	SOB	Tachypnea, Raised JVP, Diffuse rales	Boldenone, Testosterone	3 months	Current
Current report	M	40	Nil	Headache, reduced ET	Unremarkable	Nandrolone decanoate, Trenbolone acetate, Oxymetholone, Sustanon, Testosterone enanthate, Testosterone cypionate, Testosterone propionate, Drostanolone propionate	25 years	2 months

Abbreviations: AAS, anabolic‐androgenic steroids; CHF, chronic heart failure; ET, exercise tolerance; F, female; HOPC, history of presenting complaint; JVP, jugular venous pressure; LL, lower limbs; M, male; N and V, nausea and vomiting; N/A, not available; Nil, none; SOB, shortness of breath; VF, ventricular fibrillation; VT, ventricular tachycardia.

The most common presenting symptom was shortness of breath, reported by 25 patients (78.1%). Other frequent symptoms included lower limb edema (n = 9), orthopnea (n = 5), and palpitations (n = 6). Tachycardia was the most common physical finding (n = 18, 56.3%), while other common findings included raised jugular venous pressure (n = 9, 28.1%) and bibasilar crackles (n = 6, 18.8%).

The type and duration of AAS use varied considerably. Testosterone (cypionate, propionate, enanthate) was the most frequently used steroid (n = 19), either alone or in combination with agents such as trenbolone, stanozolol, and nandrolone. The duration of use ranged from 10 days to 25 years, with an average of 6.9 years. At the time of admission, 19 patients (59.4%) were still using AAS, while 13 had discontinued use, with a cessation period ranging from 3 days to 1 month (Table 1).

3.2.3. Cardiac Diagnostic Modalities Among Included Studies

Electrocardiographic (ECG) abnormalities were frequently observed, sinus tachycardia was the most common ECG finding (n = 9), while atrial fibrillation with a fast ventricular rate was reported in four cases. (n = 4). Some patients exhibited sinus rhythm with/without left bundle branch block (n = 5). Chest X‐rays (CXR) revealed cardiomegaly in 15 cases, and congested lungs with bilateral pleural effusions were noted in 8 patients. Echocardiography demonstrated global hypokinesis and dilated left ventricles in most cases, with left ventricular ejection fraction (LVEF) ranging from < 10% to 45%. Severe mitral regurgitation was identified in six patients, while tricuspid regurgitation was noted in two cases. Cardiac catheterization was performed in some cases and revealed normal coronary arteries (n = 11). Additional imaging, including cardiac magnetic resonance imaging (n = 5) and CT (n = 6), corroborated the findings of cardiac dilatation and impaired systolic function (Table 2).

TABLE 2.

Cardiac diagnostic modalities and management of included patients.

Author/Year	ECG finding	CXR finding	Echo finding	Cardiac catheterization	Other imaging	Treatment received	Clinical outcome and follow‐up
Adhikari/2022/[5]	AF with FVR	Congested lungs, b/l pleural effusion	Increased LV size with normal thickness, global hypokinesis, LVEF: 15%–20%	Normal coronaries	CT Chest: Pulmonary oedema and pleural effusion	Furosemide, Diltiazem and Heparin, Lisinopril, Spironolactone, Metoprolol, Apixaban, amiodarone	Symptoms improved, rhythm returned to SR. At 12 months, LVEF improved to 44%
Shah/2023/[6]	NSR	Cardiomegaly	Increased LV size, global hypokinesis, LVEF: 20%	Normal coronaries	Severely dilated LV and RV in MRI	Guideline‐directed medical therapy	Symptoms significantly improved. At 7 months, LVEF reached 45% with nondilated LV
Andhale/2020/[7]	ST	Cardiomegaly	Increased LV size, global hypokinesis, LVEF: 30%	Normal coronaries	N/A	Diuretics, ACEIs, Digoxin	Symptoms improved
Angelini/2019/[8]	LAD, inverted T‐waves on I, aVL and V4–V6	Pulmonary oedema	Dilated ventricles, LVEF: 23%	Normal coronaries	Significant cardiac dilatation in MRI	Diuretics, Guideline‐directed medical therapy	At 40 days, no functional improvement in echo; thus, S‐ICD placed
Bhattad/2022/[9]	SR, left anterior fascicular block, inverted T wave in II, III, AvF, V5‐V6. Borderline ST elevation in V1‐V3	N/A	Increased LV size, global hypokinesis, LVEF: 21.7%, grade 3 diastolic dysfunction	N/A	N/A	ACEIs, beta blockers	N/A
Bispo/2009/[10]	N/A	Cardiomegaly	Dilated cardiomyopathy, LVEF: 15%, large thrombus in both ventricles	Normal coronaries	Abdominal US: hepatomegaly with patent flow of the IVC and hepatic veins	Dopamine, Dobutamine, Diuretics, DOAC	Serial Echo: disappearance of the intraventricular thrombus, improved LVEF up to 25%
Clark/2005/[11]	ST, occasional PVCs, poor R‐wave progression	Congested lungs with B/L pleural effusion, Cardiomegaly	Moderate‐to‐severe cardiomegaly, global hypokinesis, severe MR/TR, LVEF: 10%–15%	Normal coronaries	CTAP: B/L pleural effusions, cardiomegaly, hepatomegaly, ascites	Diuretics, ACEIs, Inotropes, Sodium nitroprusside Digoxin	Symptoms improved. At 18 months, normal‐sized LV, LVEF of 50%–55%, mild MR/TR
Doleeb/2019/[12]	N/A	Cardiomegaly	Increased LV size, global hypokinesis, severe MR, LVEF: 15%	N/A	N/A	Carvedilol, Lisinopril, Spironolactone	Symptoms improved. At 6 months, normal LV size, improved LVEF: 53%, resolution of MR
Ferenchick/2016/[13]	Atrial tachycardia, and Non‐specific ST‐segment and T‐wave changes	Congested lungs, cardiomegaly	Four chambers cardiomegaly, LVEF of 17%	Normal coronaries	N/A	Oxygen, Diuretics, Digoxin, Warfarin	Symptoms controlled, but Patient deceased after 6 weeks of discharge
Ferrera/1997/[14]	Inverted T‐wave in II, III, AvF, V4‐6	Unremarkable	LVEF 39%	Moderate pulmonary HTN	N/A	Metoprolol, Aspirin, Lisinopril	Symptoms improved. At 1 month, LVEF of 69%, mild LV hypertrophy
Garner/2018/[15]	ST, Inverted T‐wave V4‐V6	Congested lungs, Cardiomegaly	LVEF: 25%–30%	Normal coronaries	CT chest: Pulmonary oedema with B/L pleural effusions, cardiomegaly	IABP, Dopamine infusion, Carvedilol, Aspirin, Valsartan, Furosemide, Digoxin	At 6 months, recovery of LV function, LVEF 50%–55%
Ge/2017/[16]	ST, LV hypertrophy, ST segment and T wave changes inferior/lateral leads	Globular cardiac silhouette	Increased LV size, global hypokinesis, LVEF 29%	N/A	N/A	ACEIs, BBs	Discharged against medical advice, and lost follow‐up.
Gul/2022/[17]	SR with LBBB	Congested lungs	Increased LV thickness, global hypokinesia, LVEF: 34%	Normal coronaries	N/A	BBs, ACEIs, Aldosterone antagonist	At 5 months, cardiac MRI normal sized, non‐hypertrophied LV with LVEF 57%. At 9 months, symptoms improved.
Ha/2018/[18]	VT	Congested lungs	LVEF: 40%–45%	Mild atherosclerotic disease	N/A	Amiodarone, ICD inserted Diuretics, control of ectopy	At 2 weeks, returned with congestive HF, treated by diuretics
Han/2015/[19]	AF with FVR	N/A	Severe global biventricular dysfunction, biatrial enlargement, MR, LVEF: < 15%	N/A	N/A	Electrical cardioversion, Metoprolol, LMWH, Amiodarone, Carvedilol, Ramipril, Dobutamine infusion, Diuretics	Symptoms improved. At 15 months, improvement in LV structure and function, LVEF: 63%
Ilonze/2022/[20]	AF with FVR	N/A	Biatrial enlargement, MR, LVEF: 15%	N/A	CT chest: B/L congested lungs with pleural effusions Cardiac MRI: Global LV hypokinesis with LVEF of 22%	Adenosine, Diltiazem, Cardioversion, Amiodarone, Mechanical intubation after ARDS, Lisinopril, metoprolol, Spironolactone, Empagliflozin, DOAC	At 6 months, symptoms improved. Moderate LV dysfunction, LVEF: 35%
Jamal/2022/[21]	N/A	Enlarged cardiac silhouette	Dilated LA and aortic root, Enlarged LV cavity, global hypokinesia, LVEF: 20%	N/A	N/A	BBs, ACEIs, Aldosterone antagonist	At 1 year, symptoms improved. LVEF: 55%
Joseph/2017/[22]	ST	Congested lungs, cardiomegaly	Moderate four‐chamber cardiomegaly, global hypokinesis, moderate MR, LVEF: 25%	Elevated pulmonary capillary wedge pressure, reduced cardiac index	Cardiac MRI showed no infiltrative diseases	Mechanical intubation, metoprolol and enalapril	At 9 months, symptoms improved. LVEF: 45%
Kalmanovich/2014/[23]	SR, P pulmonale, inverted T wave in anterior leads	Congested lungs	Increased LV size, global hypokinesis, minimal MR/TR, LVEF: 20%	Normal coronaries	N/A	Beta‐blockers, ACEIs, Aldosterone antagonist	At 1 year, no further admissions. LVEF: 40%, improved left ventricular size, no hypertrophy
Li/2018/[24]	ST, LVH	N/A	Global hypokinesis, Severe TR, Moderate MR, LVEF: 20%	N/A	CT Chest: B/L pneumonia, pleural effusion, pericardial effusion	Symptomatic and supportive medical therapy	Improved cardiac markers and LFTs
JGY Luc/2018/[25]	N/A	Congested lungs, cardiomegaly	LVEF: < 10%	N/A	Cardiac MRI: A severely dilated and impaired LV and mildly dilated RV	Mechanical intubation for respiratory failure, vasopressors and inotropes for cardiogenic shock, BBs, ACEIs, ARBs, Aldosterone antagonists. HeartMate II LVAD implanted	At 18 months, Heart function remained excellent postLVAD discontinuation (LVEF > 60%) and patient discharged heart failure management
Milevski/2022/[26]	AF with FVR	Unremarkable	Moderate dilated RV, moderate MR, LVEF: 12%	Normal coronaries	Cardiac MRI: mildly increased myocardial mass and wall thickness	Bisoprolol, Perindopril, Spironolactone, Rivaroxaban Direct cardioversion to revert to SR	Recovered clinically. At 6 months, normal LV size and systolic function, LVEF: 61%
Nieminen/1996/[27]	SR	N/A	Dilated LV with increased thickness	N/A	N/A	N/A	N/A
	VT then VF (Cardioverted with 300J) then returned to NSR	N/A	Dilated LV with increased thickness, LVEF: 30%	Open epicardial coronaries with slow flow	N/A	Cardioversion with 300, Isoprenaline infusion	No symptoms of angina, no more VT attacks. At 5 months, normal LV dimensions, hypertrophy slightly reduced, LVEF: 33%
	LVH	N/A	Dilated LV with increased thickness, LVEF: 14%	Right heart catheterization showed low stroke volume in relation to left ventricular size	Thallium scintigraphy showed scar formation of the anterior and posterior walls of LV myocardium	N/A	Symptoms improved. At 5 months, reduced LV thickness, LVEF: 27%
	SR, RBBB	N/A	Large lobular intra‐ventricular thrombus, dilated LV with increased thickness	N/A	N/A	Embolectomy	Lost follow‐up
Placci/2015/[28]	ST elevation in inferior leads	N/A	Hypokinesia, LVEF 40%	Apical ballooning	N/A	N/A	At 1 week, cardiac MR showed normalization of systolic function with normal perfusion
Shamloul/2014/[29]	ST	Augmented cardiothoracic index	Dilated cardiomyopathy, multiple thrombi in LV, LVEF: 13%	N/A	CT brain: chronic infarction in left frontal lobe and a sub‐acute left temporoparietal infarction	Inotropes, Diuretics LMWH followed by oral anticoagulant	At 2 weeks, disappearance of one of intra‐ventricular thrombi and improved LV function, LVEF: 20%. Few weeks later, patient deteriorated and died with inferior MI
Sodhi/2020/[30]	ST, LVH	Prominent interstitial opacifications	Increased LV size, global hypokinesis, grade II diastolic dysfunction, LVEF: 15%	N/A	CT chest: B/L pleural effusion, congested lungs, enlarged heart with dilated LV	ACEIs, Hydralazine, Isosorbide dinitrate, BBs	Symptoms improved
Youssef/2011/[31]	SR, Q waves in leads II, III and AVF, poor R waves in V1–V3	Cardiomegaly	Increased LV size with global hypokinesia, left mobile apical thrombus, LVEF: 35%	N/A	CT and MRI brain showed left frontal infarction	IV unfractionated heparin, Statins, ACEIs, BBs, Aspirin, Warfarin	At 3 months, resolution of thrombus, LVEF: 40%–45%. At 6 months, symptoms improved
White/2018/[32]	ST, LVH	Pulmonary oedema	Severe global biventricular failure, LVEF: 15%	N/A	Cardiac MRI showed dilated LV with global hypokinesis	Trial of NIV, Diuretics and Nitro‐glycerine was unsuccessful. Patient was intubated and transferred to CCU	Symptoms improved. At 6 months: partial recovery of systolic function, LVEF: 39%
Current report	ST depression in inferior leads, inverted T wave in inferolateral leads	Cardiomegaly	Increased LV size, grade one diastolic dysfunction, mild MR, LVEF: 35%	NA	CT brain and CT venogram: unremarkable	Sacubitril‐Valsartan, Spironolactone, Bisoprolol, Dapagliflozin	Symptoms improved on discharge

Abbreviations: ACEIs, angiotensin‐converting enzyme inhibitors; BBs, beta blockers; CCU, coronary care unite; CT, computed tomography; FVR, fast ventricular response; LBBB, left bundle branch block; LVEF, Left ventricular ejection fraction; LVH, left ventricular hypertrophy; MR, mitral regurgitation; MRI, magnetic resonance imaging; N/A, not available; RBBB, right bundle branch block; SR, sinus rhythm; ST, sinus tachycardia; TR, tricuspid regurgitation.

3.2.4. Therapeutic Interventions and Outcome

Most patients (90%) were treated with guideline‐directed medical therapy for heart failure, which included beta‐blockers, diuretics, angiotensin‐converting enzyme inhibitors (ACEIs), and aldosterone antagonists. In several cases, advanced therapies were employed; mechanical ventilation with or without inotropic support was necessary for some patients (n = 4). One patient underwent left ventricular assist device implantation due to cardiogenic shock [25], and another received an implantable cardioverter‐defibrillator following recurrent ventricular tachycardia [8]. For those with rhythm disturbances, electrical cardioversion was used to restore sinus rhythm (n = 4).

During a follow‐up period ranging from 2 weeks to 18 months, most patients (n = 26) showed symptom resolution, with LVEF improving to over 60% following heart failure treatment and cessation of AAS. Despite these overall positive outcomes, there was one mortality case; this patient presented with dilated cardiomyopathy and multiple intraventricular thrombi and deteriorated after suffering an inferior myocardial infarction [13]. Two patients were lost to follow‐up (Table 2) [16, 27].

4. Discussion

AAS‐induced cardiomyopathy is a condition marked by structural and functional alterations in the heart, commonly manifesting as left ventricular hypertrophy, impaired diastolic function, and, in severe cases, heart failure [2, 3]. The growing literature on AAS use and cardiomyopathy is raising significant public health concerns, especially as more athletes and individuals use these substances for non‐medical reasons [33]. Findings from our case study and systematic review highlight the cardiac complications linked to AAS misuse, including left ventricular hypertrophy, heart failure, and arrhythmias.

The presenting symptoms of AAS‐induced cardiomyopathy are often non‐specific, ranging from shortness of breath to serious cardiac events such as ventricular tachycardia and cardiogenic shock. This variation underscores the complexity of diagnosing AAS‐induced cardiomyopathy as it may not hold a distinct presentation. However, a notable feature of AAS‐induced cardiomyopathy is left ventricular dysfunction. Most cases reviewed revealed marked left ventricular dilation, reduced ejection fraction (LVEF), and significant mitral or tricuspid regurgitation [34]. The patient discussed in this case report had AAS‐induced cardiomyopathy presenting with initial symptoms unrelated to cardiac distress, making early detection challenging. This patient's left ventricular dysfunction (LVEF of 35%) and subsequent treatment with sacubitril‐valsartan, spironolactone, bisoprolol, and dapagliflozin has led to symptoms resolution, reflecting a typical therapeutic approach to heart failure. However, the long‐term outcomes in such cases remain variable. While some patients in the review experienced partial or full recovery of LVEF with guideline‐directed medical therapy, some cases have demonstrated persistent cardiac dysfunction or required advanced therapies such as left ventricular assist devices (LVADs) [25].

The cardiotoxic effects of AAS misuse on the heart are multifactorial, involving direct myocardial injury, fibrosis, and endothelial dysfunction. These mechanisms contribute to the structural changes seen in imaging, such as global hypokinesis and cardiomegaly [35]. The current study emphasizes the reversibility of some cardiac damage following cessation of AAS use, although this is not universal. The HAARLEM study, as reported in the literature, proposed that left ventricular hypertrophy and other cardiac abnormalities may reverse after cessation of AAS, but the extent and timeline of recovery remain unpredictable, with some users experiencing irreversible damage despite cessation [36].

A gap in knowledge regarding AAS‐induced cardiomyopathy is still present. Most existing studies focus on athletes or bodybuilders, creating a potential bias that may underestimate the true prevalence of AAS‐related cardiac dysfunction in the broader population. Furthermore, the precise mechanisms through which AAS induces heart failure are not understood, necessitating further research into the underlying pathophysiological processes [35]. In the study published by Piatkowski et al., the authors provided valuable insights into the prevalence of non‐medical AAS use such as body image and physical appearance, psychological influences, and enhancement of fitness performance. This study underscores the need to address AAS use as a widespread societal issue that extends beyond athletic communities [37].

The potential reversibility of AAS‐induced cardiomyopathy remains uncertain. While some studies have reported improvements in heart function after discontinuing AAS use, others had permanent cardiac damage [18]. In the current study, the majority of the included patients have shown some reversibility to their cardiomyopathy. This highlights the importance of long‐term studies to accurately predict outcomes and guide treatment strategies. Healthcare providers should remain vigilant when managing patients with a history of AAS use, even if their symptoms are mild or nonspecific.

The stigma associated with AAS use may deter users from seeking medical advice; thus, integrating an underground environment that facilitates healthcare access is crucial. In another study conducted by Piatkowski et al. the authors highlighted the key role community pharmacies can play in reducing the harms associated with AAS use [38, 39]. They could provide a safe and accessible space to address public health concerns linked to AAS use. With growing trust and support system, their roles may move beyond education to address AAS use's social and cultural factors [38, 39].

5. Conclusion

AAS misuse poses serious cardiovascular risks, with cardiomyopathy being among the most severe consequences. This review indicates that while some patients may recover after cessation of AAS, others may experience persistent cardiac dysfunction that requires lifelong care. Clinicians need to be more aware of the potential heart‐related effects of AAS, particularly in patients who do not fit the typical steroid‐user profile. Literature findings highlight the serious health risks of AAS abuse, especially among young male athletes who may underestimate these dangers. The significant heart changes observed in our study, alongside the absence of prior heart issues, emphasize the hidden risks of AAS. Future research should prioritize understanding the long‐term impacts of AAS‐induced cardiomyopathy and focus on developing targeted treatments to improve patient outcomes.

Author Contributions

Zaydoun Alhusban: conceptualization, data curation, formal analysis, funding acquisition, investigation, methodology, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Mustafa Mohammad Alaaraj: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Abdul Rahman Saimeh: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Waleed Nassar: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Ahmed Awad: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Kamar Ghanima: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Moustafa Abouelkheir: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – original draft, writing – review and editing. Ahmed Mohamed Hamed: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, supervision, validation, visualization, writing – original draft, writing – review and editing. Ahmed Afsa: conceptualization, data curation, formal analysis, funding acquisition, investigation, project administration, resources, software, validation, visualization, writing – review and editing. Mostafa Ebraheem Morra: conceptualization, data curation, formal analysis, funding acquisition, investigation, methodology, project administration, resources, software, supervision, validation, visualization, writing – original draft, writing – review and editing.

Ethics Statement

As this manuscript contains no identifiable information, the need for ethics approval was waived. Written informed consent was obtained from the patient.

Consent

Written informed consent was obtained from the patient to publish this report with its associated images in accordance with the journal's patient consent policy.

Conflicts of Interest

The authors declare no conflicts of interest.

Appendix A.

Critical appraisal of included studies using JBI tool.

Author/Year	1. Were patient's demographic characteristics clearly described?	2. Was the patient's history clearly described and presented as a timeline?	3. Was the current clinical condition of the patient on presentation clearly described?	4. Were diagnostic tests or methods and the results clearly described?	5. Was the intervention (s) or treatment procedure(s) clearly described?	6. Was the post‐intervention clinical condition clearly described?	7. Were adverse events (harms) or unanticipated events identified and described?	8. Does the case report provide takeaway lessons?
G Adhikari/2022/[5]	Y	Y	Y	Y	Y	Y	N/A	Y
R Shah/2023/[6]	Y	Y	Y	Y	N	Y	N/A	Y
A Andhale/2020/[7]	N	Y	Y	Y	Y	N	N/A	Y
G Angelini/2019/[8]	Y	Y	Y	Y	Y	Y	N/A	Y
PB Bhattad/2022/[9]	Y	Y	Y	Y	Y	N	N/A	Y
M Bispo/2009/[10]	Y	Y	Y	Y	Y	Y	N/A	Y
BM Clark/2005/[11]	Y	Y	Y	Y	Y	Y	N/A	Y
S Doleeb/2019/[12]	Y	Y	Y	Y	Y	Y	N/A	Y
Ferenchick, G. S./2016/[13]	Y	Y	Y	Y	Y	Y	Y	Y
PC Ferrera/1997/[14]	Y	Y	Y	Y	Y	Y	N/A	Y
O Garner/2018/[15]	Y	Y	Y	Y	Y	Y	N/A	Y
Y Ge/2017/[16]	N	Y	Y	Y	N	N	N/A	Y
U Gul/2022/[17]	Y	Y	Y	Y	Y	Y	N/A	Y
ET Ha/2018/[18]	Y	N	Y	Y	Y	Y	N/A	Y
HC Han/2015/[19]	Y	Y	Y	Y	Y	Y	N/A	Y
OJ Ilonze/2022/[20]	Y	Y	Y	Y	Y	Y	Y	Y
M Jamal/2022/[21]	Y	Y	Y	Y	Y	Y	N/A	Y
J Joseph/2017/[22]	Y	y	y	y	N	y	NA	Y
E Kalmanovich/2014/[23]	Y	Y	Y	Y	Y	N	N/A	Y
C Li/2018/[24]	Y	Y	Y	Y	N	N	N/A	Y
JGY Luc/2018/[25]	Y	Y	Y	Y	Y	Y	NA	Y
SV Milevski/2022/[26]	Y	Y	Y	Y	Y	Y	N/A	Y
MS Nieminen/1996/[27]	N	N	N	N	N	N	N/A	Y
A Placci/2015/[28]	Y	Y	Y	Y	N	Y	N/A	Y
R.Shamloul /2014/[29]	Y	Y	Y	N	Y	Y	Y	Y
P.Sodhi /2020/[30]	Y	Y	Y	Y	N	Y	N/A	Y
MYZ Youssef/2011/[31]	Y	Y	Y	N	N	Y	N/A	Y
M.White/2018/[32]	Y	Y	Y	N	N	Y	N/A	Y

Data Availability Statement

The data that support the findings of this study are openly available in study tables and figures.