Treatment‐seeking behavior and cardiovascular morbidity among men with anabolic‐androgenic steroid use: A cross‐sectional study

To determine associations between anabolic‐androgenic steroid (AAS) use‐related morbidity including cardiovascular disease (CVD) and engagement to health services.

Anabolic-androgenic steroids (AAS) are testosterone and its synthetic derivatives, which have been used for decades, to increase physical strength and to build muscles more easily. 11][12] Our research group has recently described biventricular cardiomyopathy with severely affected left myocardial function among current and former long-term AAS users. 13A longitudinal study also revealed that individuals who tested positive for AAS in urine had twice the risk of developing CV morbidity and mortality, compared with those that tested negative. 14Another study showed a threefold risk of developing cardiomyopathy and atrial fibrillation among AAS users compared with healthy controls as well a fivefold higher risk of thromboembolic events. 150][21] In addition, long-term use of AAS in supraphysiological doses disrupts endogenous testosterone production through negative feedback of the hypothalamic-pituitary-gonadal (HPG) axis, and may result in anabolic steroid-induced hypogonadism (ASIH). 17SIH symptoms include fatigue, reduced libido, sexual dysfunction, and depression that typically manifest after discontinued AAS use. 21The AAS prevalence together with its negative health consequences, make AAS use a public health problem.The adverse effects associated with long-term supraphysiological AAS levels, would suggest frequent visits to health services among AAS users.3][24] This is concerning as underlying and potentially serious AAS risks may go undetected without targeted medical examinations.It remains unclear whether it is the individuals who actively seek health services who also experience the most complications from AAS use.In a recent study from our research group, we found that treatment-seeking behavior among AAS users was associated with younger age, greater health concerns and more self-reported side effects from AAS use. 24However, there is a significant knowledge gap on whether individuals who seek health services for AAS-related issues differ in terms of objective measures of physical health including CVD.
In this study, we investigated the associations between treatment-seeking behavior and objective measures on physical health including CVD, in a sample of men with current or former AAS use.Specifically, we aimed to determine differences between AAS users who actively seek treatment facilities for AAS-related health issues and those who do not, in regards to demographics, objective (n = 21), 44% (11) and 43% (9) respectively, had never engaged health services due to AAS-related adverse effects.Deviant liver-and kidney parameters were frequently observed in the total sample but without between-group differences.

Conclusions:
Treatment-seeking behavior among current AAS users may be associated with increased levels of dyspnoea and established CVD.Despite objective signs of severe CVD among a substantial amount of study participants, it is of great concern that the majority had never sought treatment for AAS-related concerns.

K E Y W O R D S
anabolic androgenic steroids, acute kidney injury, androgens, cardiovascular disease, chemical and drug induced liver injury, health care seeking behavior measures including CV pathology, endogenous hormone levels, and potential harms to the liver or kidneys.Notably, we particularly aimed to bring attention to the potential underlying and undetected pathology exhibited by the group that had never sought health services for AAS-related effects.

| Setting
In Norway, inhabitants are entitled to a publicly funded general practitioner (GP) where they can receive treatment or be referred to specialized somatic health services, typically involving a cardiologist or an endocrinologist.Additionally, patients may contact a fully private GP or a private specialist directly without a referral, but at their own expense.In 2013, use and possession of AAS became illegal when the Norwegian Drug Act was amended, and people with AAS-related health problems received patient rights to outpatient substance use disorder (SUD) treatment. 25

| Study design and population
This study is based on cross-sectional data from a longitudinal research project that investigates long-term effects of AAS use on cognition, brain, and cardiovascular health at Oslo University Hospital, Norway. 7,13,18,26ata collection was conducted in 2017-2019.Study participants were recruited through social media and other relevant online forums that targeted people engaged in heavy weight and resistance strength training and bodybuilding.In addition, posters and flyers were distributed at selected gyms in Oslo.The participants were males >18 years of age, capable of giving consent, with either a current or former cumulative AAS use of at least 1 year.A self-report web questionnaire was used to collect data on socioeconomic demographics, consumption of tobacco or alcohol, history and nature of AAS use, and treatment-seeking behavior for AAS-related issues.The estimated lifetime AAS dose was determined by calculating the average weekly dose reported over lifetime and multiplying it by the number of weeks they had been exposed to AAS, consistent with previous research. 18,19In this specific study, the primary focus was on the lifetime patterns of seeking treatment, with categorization into current or former AAS use considered secondary.The participants were categorized into a treatment-seeking group (TSG) and a non-treatmentseeking group (non-TSG) based on their responses to the self-report web questionnaire.Participants were classified as treatment seekers if they reported to have been in contact with any healthcare provider at least once during or after AAS use due to one or several AASrelated side effects or health concerns (organ health, hypogonadism, sexual health, mental health, changes to hair or skin, cognitive function, gynecomastia, musculoskeletal harm, or other effects).Healthcare providers included their public assigned GP, a public specialist in SUD treatment or somatic health care through a referral from their GP, and/or private health care.Private health care could encompass either a private GP or a private specialist in various somatic health disciplines.Current AAS use was classified based on participants' response to the question "Do you still use AAS?" with the subsequent inquiry about the duration since AAS discontinuation.Former use was defined as at least 1 year since AAS cessation.A follow-up question prompting participants to specify their use phase, allowed for responses such as "I am on-cycle," "I'm off (between cycles)," "I am continuously on," "I have quit using AAS," or "I use TRT prescribed by a doctor."It is important to highlight that the majority of participants that reported to receive prescribed TRT, also exhibited non-medical AAS use alongside their prescribed TRT.Note that the sample is largely overlapping with the sample described in recent studies. 13,24

| Clinical measurements
Health professionals at the outpatient clinic of Department of Cardiology, Oslo University Hospital (OUH), conducted both the clinical interview and the physical examination.The participants were systematically asked about symptoms that could indicate CVD such as dyspnoea, chest pain, palpitations, dizziness, and syncope.Blood pressure measurements were obtained using an automatic sphygmomanometer equipped with a standard bladder cuff for most patients, and larger cuffs were utilized for those participants with larger arm circumference.Sign of hypertension was defined as a systolic blood pressure of ≥140 and/ or or a diastolic pressure ≥90 mm Hg, while sign of prehypertension, also known as high normal blood pressure or borderline hypertensive, was defined as a systolic blood pressure of ≥130 and ≤139 and/or or a diastolic pressure ≥80 and ≤89 mm Hg. 27

| Echocardiographic measurements
Transthoracic echocardiographic examinations were performed at Department of Cardiology at OUH. 13 Echocardiographic measurements were obtained by one investigator using Vivid E95 (GE Vingmed Ultrasound, Horten, Norway).The data were then analyzed offline by another investigator, blinded to AAS use status, using the software, EchoPAC v203 (GE, Horten, Norway).Left ventricular mass was estimated from parasternal views using the formula provided by Devereux et al. 28 and adjusted for body surface area using the Du Bois' formula. 29Left ventricular hypertrophy (LVH) was defined as LV mass/BSA >115 g/m 2 in accordance with recent EAPC and EACVI recommendations on evaluation of the athlete's heart. 30LV mass index (LVMI) was not calculated in cases with poor image quality or inadequate image alignment.LVEF was calculated by modified Simpson's biplane method and categorized into three groups: ≥50% (normal), 41%-49% (reduced), and ≤40% (severely reduced). 31

| Laboratory analyses
All reference ranges are according to laboratory standards of OUH (Table S1) where all blood samples were obtained.Laboratory measures of hematocrit, hemoglobin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, estimated glomerular filtration rate (eGFR), total cholesterol, low-density lipoprotein (LDL), and high-density lipoprotein (HDL) were analyzed at the routine laboratory (all with Roche Diagnostics) at the Department of Medical Biochemistry, OUH.The eGFR was calculated using the CKD-EPI formula and reported in units of mL/min/1.73m 2 .An eGFR of less than 30 mL/min/1.73m 2 was defined as severely reduced kidney function. 32All hormones were analyzed at the Hormone Laboratory, Oslo University Hospital: folliclestimulating hormone (FSH), luteinizing hormone (LH), sex hormone binding globulin (SHBG) (all with Simens, Immulite), total testosterone (TT) (Hormone Laboratory, LC-MSMS), free androgen index (FAI was calculated automatically by the following formula: testosterone (nmol/L) × 10/SHBG (nmol/L)), oestradiol (Diasorin, Liason), and thyroid-stimulating hormone (TSH) and free thyroxine (fT4) with Perkin-Elmer, DELFIA.The analyses at the Department of Medical Biochemistry and the Hormone Laboratory were all accredited according to ISO 15189 and ISO 17025, respectively.
As the majority of the objective measures included in the study is affected by current AAS use, 33 we distinguished between current and former users, and assessed the groups separately for all objective measures.Blood analyses among men with former AAS use (i.e., at least 1 year since AAS cessation) was included as Supplementary material.

| Statistical analyses
Normality was visually assessed with histograms.Numerical variables following a normal distribution were presented as mean ± standard deviation (SD) and two sample t-tests were used to compare differences between the TSG and the non-TSG.Numerical data that were not normally distributed were presented as medians (25th-75th percentiles) and nonparametric tests such as the Wilcoxon rank sum tests (Mann-Whitney) were used for betweengroup comparisons.The chi-square tests were employed for comparison of categorical and/or dichotomous variables, and Fischer's exact test was used when the expected number were based upon less than five cases.A two-sided p-value of <0.05 was considered statistically significant.To correct for multiple testing, the Benjamini-Hochberg procedure was implemented to adjust p-values where appropriate (i.e., in tables that included p-values <0.05) to control for the false discovery rate (FDR).All statistical calculations and analyses were performed using STATA (version 17.0, StataCorp LLC, Texas, USA).

| Ethics
The study was approved by the Regional Committees for Medical and Health Research Ethics South East Norway (REC) (2013/601).All research was carried out in accordance with the Declaration of Helsinki.Prior to participation, all participants received oral and written information about the study and written informed consent was collected from all subjects.Participants were compensated with NOK 500 (≈$50) for participating in the study.All participants could refrain from the study at any point.All pathological findings were evaluated by a physician and investigated further when indicated.

| RESULTS
Of note, as objective measures may vary considerably among those who currently use AAS compared to those who have quit, the total sample is assessed separately for current and former AAS users on cardiovascular examinations including echocardiography, and on blood measures (Tables 2-6; Figures 1 and 2; Table S2).

| Demographics and characteristics of AAS use
Demographic data and AAS use characteristics are presented in Table 1.In the total sample of 90 participants, mean AAS debut age was 23 years with a mean accumulated AAS use of 12 years.The TSG consisted of 41 (46%) participants whereas the non-TSG comprised 49 (54%).The two groups were similar on demographics and background characteristics with the exception of age, where AAS users in the TSG were found to be approximately 5 years younger than those in the non-TSG (p = 0.03).However, this age difference was not significant after correction for FDR (pFDR = 0.36).At time of study inclusion, 59 (66%) men in the total sample reported current use of AAS, with no differences between the two subgroups.Participants with former AAS use had a median time of 2 years (25th-75th percentiles 1-4.5 years) since last AAS use.

| Clinical measurements
Potential cardiac-related symptoms and blood pressure measurements among current and former users are listed in Tables 2 and 3, respectively.Fifty-eight percent of the sample with current AAS use reported one or more cardiac-related symptom, with no differences between the TSG and non-TSG.The proportion of current AAS users that reported dyspnoea was significantly higher in the TSG compared to the non-TSG (p = 0.000, p-FDR = 0).No differences were seen between the TSG and non-TSG among those with former use.As shown in Figure 1, 48% (n = 16) of current AAS users with sign of hypertension and 70% (7) with sign of prehypertension had not engaged health services.Among those with former AAS use, 42% (5) with sign of hypertension and 50% (4) with sign of prehypertension had not sought prior treatment (Figure 2).There were 14 missing from the total sample on cardiac-related symptoms and four missing on blood pressure measurements.

| Echocardiography and other vascular measures
CVD, including LV systolic dysfunction and LVH, was observed in both the TSG and non-TSG, with seven missing from the total sample on LVEFcategories and four missing on LVMI.A higher proportion of treatment seekers were found among current AAS users with combined LVEF <50, LVH and hypertension, as well as those with combined LVEF <50 and hypertension or combined LVEF <50 and LVH (see Table 4).The same differences were not found among those with former AAS use, see Table 5. Notably, among current AAS-using participants with reduced LVEF (n = 25) and LVH (n = 21), 44% (11) and 43% (9), respectively, had never sought treatment for AAS-related adverse effects (Figure 1).At the same time, among men with former AAS use and reduced LVEF (12) or present LVH (4), 42% (5), and 50% (2) had never engaged health services, respectively (Figure 2).

| Hormone parameters
Table 6 presents hormone levels in participants with current AAS use (missing 8-10 in the TSG and 5-7 in non-TSG group).No significant differences were observed between the TSG and non-TSG in hormone measurements reflecting endogenous testosterone production.Overall, the

T A B L E 5 Comparisons of echocardiographic findings and sign of hypertension between the TSG and non-
TSG with former AAS use.
current use had low gonadotropin levels and LH) and high testosterone levels, indicative of active AAS use.Table S2 presents the hormone levels, as well as liver, kidney, and metabolic parameters, for participants with former AAS use, with no between-group differences (1-5 missing in the TSG and 4-8 in the non-TSG).

| Liver, kidney, and metabolic parameters
There were no significant differences on liver, kidney or metabolic parameters between the TSG and non-TSG with current or former AAS use (8-13 missing in the TSG and 5-11 in the non-TSG), see Table 6 and Table S2, respectively.However, deviant results were observed in both groups with current use (n = 42): Common observations included elevated levels of hematocrit (16, 38%), hemoglobin (18, 43%), AST (18, 43%), and creatinine (17, 40%).It is worth noticing that these blood parameters were largely within the physiologic range among men with former AAS use (see Table S2).Notably, among those with current AAS use, two men with long-term use exceeding 20 years showed signs of severely reduced kidney function, indicated by an eGFR of <30 mL/min/1.73m 2 .Both men had concurrent signs of myocardial disease, but only one had sought healthcare for AAS-related adverse effects.

| DISCUSSION
This is the largest study to date exploring treatmentseeking behavior in relation to objective health measures such as CVD in long-term AAS users.Our findings demonstrated how the majority of treatment seekers with current AAS use, exhibited potential cardiac-related symptoms and simultaneous heightened prevalence of impaired LVEF.In addition, experienced shortness of breath, and reduced LVEF in combination with LVH and/or hypertension, were more common in the TSG compared to the non-TSG.Although the average cumulative AAS use was 12 years among our participants, 54% of the men had never engaged health services for any AAS-related side effects.Our findings showed that a substantial proportion of both current and former users in the non-TSG had potential symptoms and signs of CVD.In fact, among the  in the non-TSG AAS use, 47% had one or more symptom could be cardiac-related, 34% had reduced LV systolic function, 28% LVH, and 48% possibly undiagnosed hypertension.Among the men with former use, as much as 77% had one or more symptom that could be cardiac-related, 38% had reduced LVEF, 15% had signs of LVH, and 36% possibly undiagnosed hypertension.
Not seeking treatment despite experiencing userelated symptoms is not a new phenomenon among AAS users. 22,23,34Many AAS users do not consider related side effects significant enough to seek professional help, 24,34 while others fear stigmatization from healthcare professionals or perceive physicians to be too uninformed on AAS. 22,35,36In fact, adequate AAS knowledge among health personnel has previously shown to be a contributing factor to treatmentseeking among AAS users. 25However, while some do seek health services as a preventive measure, 15,24 use is not necessarily disclosed in meetings with physicians. 22Consequently, serious side effects from AAS use may be overlooked on regular check-ups, leading to false beliefs of good health and ultimately continued AAS use with further morbidity risk.Indeed, in a sample of 100 men who used AAS in a cyclic pattern including 21 men who initiated their first cycle during the study, the observed physical effects from AAS use were reversed after (temporary) AAS cessation. 33However, AAS may still lead to substantial risk of CVD in long-term users and also be detectable among those with former use. 13otably, despite being a common finding on echocardiography, LVH is often not detected in AAS users with screening tools like ECG. 4,6,8,13 As a result, the effectiveness of preventive health examinations such as ECG by visits to the GP or private health services remains a subject of question and should be addressed in future research.Furthermore, to predict the magnitude of adverse effects associated with AAS use proves challenging when relying solely on self-reported weekly or cumulative doses. 33This difficulty arises from substantial variation in cycles, including the length and dosages, differences with respect to type of AAS used, and the fact that illegally obtained AAS often do not correspond to the specifications on the label. 37n our study, we included CV measures and blood panels to investigate whether any underlying pathology was associated with treatment-seeking behavior.Remarkably, CV findings were highly frequent in the non-TSG among both former and current users.This shows that many AAS users do not engage health services, despite experiencing potential severe adverse effects from use.For instance, hypertension is a known important risk factor for heart failure, heart valve diseases and coronary heart disease, 11,27 and both reduced LV systolic function and hypertension are associated with higher risk of sudden cardiac death. 12,27Fifty-nine percent of the men with current use and 40% of the men with former use were identified as having sign of hypertension, and nearly half of these had never sought health services for AAS-related morbidity.Additionally, 18% of current users and 27% of former users exhibited sign of prehypertension.According to the 2023 ESH Guidelines for the management of arterial hypertension, 27 lifestyle advice and opportunistic screening for hypertension, are recommended for patients with prehypertension, given their heightened long-term risk of CV events and mortality.The AAS users that had sought life-time treatment due to AAS-related side effects and reported current use, there were also more reports of dyspnoea and a higher prevalence of reduced LV systolic function in combination with LVH and/or high blood pressure, when compared to the non-TSG.This suggests that the presence of some cardiac-related symptoms and established CVD may increase the likelihood of pursuing medical intervention.However, drawing associations between symptoms categorized as "cardiac-related" in our study and confirmed cardiac pathology proves challenging, as these symptoms are nonspecific for CVD and may not be directly connected.Despite this, 50% of the TSG with current AAS use reported dyspnoea, 63% exhibited LVEF <50 and 18% had LVEF <40, suggesting that the experienced dyspnoea could potentially be cardiac-related in some of these individuals.
While the CV adverse effects from AAS use are well documented, [3][4][5]9,14 potential renal toxicity lacks comparable research attention. 1 Inour study, several men exhibited abnormal creatinine and eGFR levels, and two participants with current long-term AAS use displayed signs of severely reduced kidney function. Hwever, whether AAS holds true nephrotoxic effects with potential clinical significance has been disputed.33,38 The underlying cause of renal impairment associated with AAS use might be multifactorial, involving damage to the glomeruli by increased lean body mass and muscle breakdown, as well as overconsumptions of proteins in diet.20 Furthermore, renal biopsies of AAS users have revealed structural changes in kidney tissue, 39 indicating a potential direct toxic effect of AAS on cells involved in GFR.20 According to laboratory standards at OUH at time of blood collection, we used serum creatinine levels to measure the eGFR with the CKD-EPI equation.32 While eGFR is typically deemed a reliable predictor of decreased kidney function in the general population, 32 it may be not be as attributable among AAS users.This could be explained by the increased daily production of creatinine in muscle-building AAS users due to elevated skeletal muscle mass, the enhancing impact of AAS on endogenous creatine production, and the frequent simultaneous use of dietary supplements aimed to boost muscle creatine stores.38 Regardless of whether AAS are detrimental to kidney function, it is crucial to note that AAS usage could lead increased aortic stiffness and hypertension which ultimately might sult in renal damage if left untreated.5 Thus, the clinical significance of AAS-related kidney damage should not be underestimated, as even a slight decrease of GFR is associated with increased risk of chronic kidney disease, which in turn is associated with overall mortality and higher risk of CVD events.40 On the other hand, liver toxicity from AAS use is primarily linked to oral androgens, causing elevated bilirubin levels and jaundice.41 While most participants in our study had ALT levels within normal range, median AST was pathologically high in the TSG and in the upper normal range in the non-TSG with current use.However, AST was considerably lower among those with former use, indicating a gradual normalization after AAS cessation. In fat, higher levels of liver aminotransferases among current AAS users have previously been attributed to intense workout-sessions and muscle building, and could therefore be of less clinical relevance.33 Notably, a higher AST than ALT, in co-occurrence with high creatinine kinase (CK) levels may be of more clinical use when assessing liver function in recreational strength athletes who use AAS, as it may be indicative of muscle damage rather than liver pathology.42 While no differences were observed between the TSG and non-TSG in relation to endogenous testosterone production, the sex hormone panel confirmed ongoing AAS use among current users.In both the TSG and non-TSG groups, low levels of gonadotropins (FSH and LH) due to the suppression of the HPG axis 43 were found, as well as high levels of TT and FAI due to excessive consumption of exogenous androgens.In contrast, individuals that had ceased AAS use ≥1 year prior to study inclusion, had to a greater extent normal levels of gonadotropins and testosterone, supporting previous findings that ASIH usually lasts 3-12 months following cessation.43 Although ASIH is a commonly observed and feared side effect among AAS users due to its distressing withdrawal symptoms, 17 it does not necessarily lead to an increase in the rate of treatment seeking.24 This could partly be explained by the absence of clinical guidelines on how to treat ASIH, 44 and the fact that users often self-medicate with non-prescribed post-cycle therapy and testosterone replacement therapy to prevent ASIH symptoms following AAS cessation.17,44 Despite minimal differences between the TSG and the non-TSG, we consider the potential high morbidity level in the non-TSG to be one of the key findings of our study.From previous observations of the same sample of AAS-using men engaging health services, 24 we know that treatment-seeking behavior among AAS users is associated with more health concerns and a higher symptom-burden.Hence, our primary focus for this paper was on individuals who have not sought contact with the healthcare system and who have underlying health conditions, as opposed to exploring what attracted the other group to health services. Ithas previously been questioned whether harms related to AAS use have been overestimated, with many individuals reporting only mild side effects from use.33 However, our findings suggest otherwise and stress the importance of further education of both people who use AAS and health professionals on the use and risks of AAS.Our study provides insights into the reluctance among AAS users to contact health services, despite experiencing symptoms and signs of underlying AAS-related disease.Although further research is needed to understand the reasons behind the lack of health service engagement, our study should be considered an addition to the existing body of research on treatment-seeking behavior among AAS users.

| Limitations
Our study has important limitations worth noting.It is possible that AAS-related physical side effects might be exaggerated in our sample, since those who experience symptoms could be more prone to become part of a research project investigating health, and study population might therefore not be fully representative of the target population.Life-time treatment seeking for AASrelated symptoms was measured, but further details on the exact time of health service engagement and AAS use status were not explored.Some of the answers given in the questionnaires, especially those involving a precise length of accumulated AAS use, might be subject to recall and reporting bias if use ended years ago.It is worth noting that AAS users often engage healthcare for preventive purposes, and the motivation for seeking treatment may therefore not necessarily stem from concerns from having dyspnoea or other "cardiac-related" symptoms.Furthermore, the cause of these symptoms and its potential association with CVD remains difficult to determine without a full clinical history, an adequate physical examination and additional investigations.Moreover, objective data collection was incomplete on some measures, especially on blood panels, due to a neglect of participant attendance or the incorrect completion of requisition forms.As previously discussed, eGFRs based on creatinine levels might not be as attributable in this particular population due to several confounding factors among AAS users.Lastly, CK was not measured and could therefore not be used to distinguish between liver and muscle damage among participants with higher AST than ALT.

Perspective
AAS use is recreational athletes and visitors of fitness centers.study examined the link between long-term AAS use, physical health problems and treatment seeking.Although deviant liver-and kidney function tests were highly present among participants in our study, the associations with AAS and its clinical significance remain unclear.Signs and symptoms indicative of CVD were prevalent in the majority of current AAS users, and some of these were more present among AAS users who had sought health services compared to those who did not.Our findings suggests that the presence of CVD in this particular group of AAS users may result in symptoms such as dyspnoea, thereby prompting these individuals to seek medical attention.However, despite notable health issues, most of the study participants had never sought medical help for AAS-related issues.Symptoms and signs indicative of potential severe cardiovascular disease were present in a significant number of AAS users in our study that refrained from health service engagement.Our findings may indicate a lack of knowledge among AAS users regarding the potential severity of cardiovascular adverse effects.It emphasizes the importance of increased awareness of AASrelated health risks and of seeking timely medical care to minimize further cardiovascular harm.Both users and clinicians need to acknowledge that underlying CV pathology associated with AAS use may be asymptomatic and even undetectable on certain screening tools.Therefore, blood pressure monitoring and echocardiography are important tools to diagnose AAS-related CVD at an early stage, particularly among AAS users with long-term use.

F I G U R E 1
Distribution of observed cardiovascular conditions in the two subgroups among men with current AAS use.The chart displays the percentage of treatment seekers versus non-treatment seekers within the total population (100%) who exhibited established cardiovascular condition following echocardiographic and blood pressure measurements.LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy.F I G U R E 2 Distribution of observed cardiovascular conditions in the two subgroups among men with former AAS use.The chart displays the percentage of treatment seekers versus non-treatment seekers within the total population (100%) who exhibited established cardiovascular condition following echocardiographic and blood pressure measurements.LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy.

T A B L E 6
Comparisons of blood parameters between the TSG and the non-TSG with current long-term AAS use.
Comparisons of demographics and characteristics between the TSG and the non-TSG.Comparisons of potential cardiac-related symptoms and blood pressure measurements between the TSG and non-TSG with current use.Comparisons of potential cardiac-related symptoms and blood pressure measurements between the TSG and non-TSG with former use.Fisher's exact test was used when the expected number were based upon less than five cases.Significant difference between the groups (p < 0.05).Comparisons of echocardiographic findings and sign of hypertension between the TSG and non-TSG with current AAS use.
T A B L E 1*Significant difference between the groups (p < 0.05).T A B L E 2 All (N = 52) TSG (n = 22)Non-TSG (n = 30) t or χ 2 p-value p-FDR Note: Fisher's exact test was used when the expected number were based upon less than five cases.Abbreviations: AAS, anabolic-androgenic steroids; BMI, body mass index; FDR, false discovery rate (Benjamini-Hochberg) corrected p-values, non-TSG, nontreatment-seeking group; TSG, treatment-seeking group.*Significantdifferencebetween the groups (p < 0.05).T L E 3Note:Abbreviations: AAS, anabolic-androgenic steroids; BMI, body mass index; non-TSG, non-treatment-seeking group; TSG, treatment-seeking group.T A B L E 4Note: ↑BP defined as a systolic blood pressure of ≥140 and/or a diastolic pressure ≥90 mmHg.Fisher's exact test was used when the expected number were based upon less than five cases.Abbreviation: BP, blood pressure; FDR, false discovery rate (Benjamini-Hochberg) corrected p-values; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; non-TSG, non-treatment-seeking group; TSG, treatment-seeking group.*Significantdifferencebetween the groups (p < 0.05).Note: Fischer's exact test was used when the expected number were based upon less than five cases.↑BPdefined as a systolic blood pressure of ≥140 and/or a diastolic pressure ≥90 mmHg.Significant difference between the groups (p < 0.05).Abbreviations: BP, blood pressure; LVEF, left ventricular ejection fraction; LVH, left ventricular hypertrophy; non-TSG, non-treatment-seeking group; TSG, treatment-seeking group.