REVIEW ARTICLE

Sports Med 2012; 42 (2): 119-134

0112-1642/12/0002-0119/$49.95/0

2012 Adis Data Information BV. All rights reserved.

Anabolic Steroids and Cardiovascular Risk

Peter Angell,1 Neil Chester,1 Danny Green,1,2 John Somauroo,3 Greg Whyte1 and Keith George1
1 Research Institute for Sport and Exercise Sciences, Liverpool John Moores University, Liverpool, UK
2 School of Sport Science, Exercise and Health, The University of Western Australia, Nedlands,
WA, Australia
3 Cardiology Department, Countess of Chester Hospital NHS Foundation Trust, Countess of Chester Health
Park, Chester, Cheshire, UK

Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
2. Search Strategies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
3. Anabolic Steroid (AS) Use and the Presence of Cardiovascular Disease (CVD) . . . . . . . . . . . . . . . . . .
4. AS Use and CVD Risk Factors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5. AS Use and Cardiac Electrical Activity, Structure and Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.1 Cardiac Electrical Activity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.2 Cardiac Structure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.3 Systolic Function. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
5.4 Diastolic Function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
6. AS and Vascular Health. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
7. Future Directions. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
8. Limitations to Research in AS Users. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
9. Conclusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Abstract

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Recent reports from needle exchange programmes and other public health
initiatives have suggested growing use of anabolic steroids (AS) in the UK
and other countries. Data indicate that AS use is not confined to bodybuilders or high-level sportsmen. Use has spread to professionals working in
emergency services, casual fitness enthusiasts and subelite sportsmen and
women. Although the precise health consequences of AS use is largely undefined, AS use represents a growing public health concern. Data regarding
the consequences of AS use on cardiovascular health are limited to case
studies and a modest number of small cohort studies. Numerous case studies
have linked AS use with a variety of cardiovascular disease (CVD) events or
endpoints, including myocardial infarction, stroke and death. Large-scale
epidemiological studies to support these links are absent. Consequently, the
impact of AS use upon known CVD risk factors has been studied in relatively
small, case-series studies. Data relating AS use to elevated blood pressure,
altered lipid profiles and ECG abnormalities have been reported, but are
often limited in scope, and other studies have often produced equivocal
outcomes. The use of AS has been linked to the appearance of concentric left
ventricular hypertrophy as well as endothelial dysfunction but the data again

Angell et al.

120

remains controversial. The mechanisms responsible for the negative effect of

AS on cardiovascular health are poorly understood, especially in humans.
Possibilities include direct effects on myocytes and endothelial cells, reduced
intracellular Ca2+ levels, increased release of apoptogenic factors, as well as
increased collagen crosslinks between myocytes. New data relating AS use to
cardiovascular health risks are emerging, as novel technologies are developed
(especially in non-invasive imaging) that can assess physiological structure
and function. Continued efforts to fully document the cardiovascular health
consequences of AS use is important to provide a clear, accurate, public
health message to the many groups now using AS for performance and image
enhancement.

1. Introduction
The use and abuse of anabolic steroids (AS)
gains popular and media attention when elite
athletes fail doping tests. Although significant,
in some respects, these cases underplay the pervasive nature of AS use in Western societies. Whilst
official figures suggest a decrease in AS use, reports from needle exchange programmes and
other public health initiatives have pointed towards a growing use of AS in the UK.[1] The
clandestine nature of AS use makes an accurate
assessment of the prevalence of use difficult. Despite this, some studies have attempted to quantify the level of use in specific groups. Yesalis and
Bahrke[2] found that between 4 and 6% of highschool males and 12% of high-school females
had tried AS. Bahrke and Yesalis[3] remarked that
studies from countries including Canada, Sweden,
England, Australia and South Africa suggest
13% of high-school students had tried AS at some
time. The widespread use of AS has been documented in professionals working in emergency
services, casual fitness enthusiasts, as well as sportsmen and women from a wide variety of different
sports.[4] Although the exact health consequences
of AS use are largely undefined, AS use represents
a growing public health concern.
The therapeutic use of testosterone is somewhat controversial with conflicting data, although
some studies have indicated limited positive effects on isolated cardiovascular risk factors.[5]
The use of AS outside of therapeutic prescription
has raised significant concerns about negative cardiovascular health consequences.[6] Despite the
2012 Adis Data Information BV. All rights reserved.

commonly held belief that AS are detrimental to

cardiovascular health, scientific data detailing cardiovascular disease (CVD) prevalence, morbidity
and mortality are limited and controversial.[4]
This review considers the current evidence base
regarding AS use in humans and the presence
of CVD or elevated risk of developing CVD.
We seek to present the latest data, as well as
limitations and future directions for work in this
area. For the purposes of this review, data has
been delimited to available human studies. Whilst
much can be learned from animal models,[7] and
recent data suggests a direct link between AS use
and coronary lesion formation,[8] such studies rarely reflect the reality of human AS use for
performance or image enhancement. Throughout the review we will seek to critique available
evidence and discuss potential mechanism(s)
where relevant human and/or animal data provide insight.
2. Search Strategies
In order to locate relevant studies for this review, a literature search was performed through
the Liverpool John Moores University electronic
library, which covers a number of databases including SPORTDiscus, Web of Science, ScienceDirect, Emerald, CINAHL Plus, PubMed and
Academic Search. The search terms used were
anabolic steroids, anabolic androgenic steroids,
with additional operators of cardiovascular effects, cardiac and vascular with the search
period being set between 1970 and 2010. Inclusion
of studies was delimited to human and cellular
Sports Med 2012; 42 (2)

Steroids and Cardiac Health

studies, with animal studies only being used to

infer possible mechanisms of action.
3. Anabolic Steroid (AS) Use and
the Presence of Cardiovascular
Disease (CVD)
Assessment of the presence of CVD in any
population can be made in a number of ways.
Epidemiological approaches, which follow large
cohorts over prolonged follow-up periods, assess
specific endpoints including cardiac-related death,
acute myocardial infarction, cardiac failure and
presence of coronary disease on coronary angiography. Such studies have been performed to assess the impact of various risk factors on CVD
presentation (e.g. physical [in]activity[9,10]). In
many sporting subcultures AS use is banned,
partially because of concerns over adverse health
effects as well as the fact that it constitutes cheating
and a breakdown of the Olympic ideal.[11] These
issues would make many users, some of whom are
involved in competitive sport, reluctant to admit
their use.
Alternative ways to determine the presence of
CVD include the assessment of the presence and
nature of any atherosclerotic load or burden within
an individual. Assessments can be made before a
significant cardiovascular event occurs, providing another option in the assessment of the effects
of AS on cardiovascular health. The National Institute for Health and Clinical Excellence (NICE)
guidelines for assessment of chest pain use an algorithm starting with the assessment of the presence of cardiovascular risk factors (smoking,
diabetes mellitus, hyperlipidaemia) coupled with
sex and age. This is then followed by non-invasive
and invasive testing as required, depending on the
perceived degree of risk. Of the tools available,
invasive coronary angiography remains the gold
standard for assessment of coronary atherosclerosis.
However, the use of an invasive test in AS users
without a history of chest pain, coupled with the
use of radiation, cost and complexity, in addition
to the semi-invasive nature of angiography, are
why this is not routinely performed outside of a
clinical setting and why there appears to be no controlled human trials of AS use using these tech 2012 Adis Data Information BV. All rights reserved.

121

niques. Non-invasive computerized tomography

(CT) coronary angiography is an alternative technique, but again cost, radiation and limited resolution available until recently, has lead to its use
being limited. Other assessments exist including
CT coronary calcium scores, which indicate the
overall atherosclerotic burden without indicating
the degree of stenosis in the coronary arteries but,
again, we are unaware of any such data in AS
users. This would be a useful technique given the
rapid acquisition time, but also requires low-dose
radiation. Another option is the assessment of the
carotid artery intima-media thickness (cIMT)
that measures the width or depth of the wall of a
conduit artery, most often the carotid artery. The
subintimal space is where plaque formation typically occurs in arterial disease, and assessment of
cIMT is easily and accurately performed using
ultrasound technology, which thus provides a
non-invasive assessment of atherosclerotic burden.[12] Despite being assessed in a peripheral
artery, the measurement of cIMT has been shown
to reflect atherosclerotic burden in the coronary
arteries.[13] Sader et al.[14] reported no difference
in the cIMT of AS-using and non-AS-using subjects, despite a greater cIMT observed in both
bodybuilding groups compared with the sedentary control cohort.
The only substantial and growing database
related to the association between AS use and
the presence of CVD is provided by case study
reports[15] (see table I). Case studies can present
cardiovascular events or disease endpoints (e.g.
sudden cardiac death, acute myocardial infarction, etc.), as well as autopsy data that directly
determine atherosclerotic burden. The developing
list of case studies provides compelling evidence of the significant, and often fatal, association between AS and CVD.[59,60] Although not
completely exhaustive, table I documents the occurrence of a number of significant CVD endpoints, such as strokes, myocardial infarctions
and thromboembolism. Often these events are
fatal and, even if not, can lead to significant disability and functional impairment. The physical,
psychological and sociological ramifications are
likely significant in those who survive an initial
event.
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Angell et al.

122

Table I. Case study events in anabolic steroid users and reported presence of risk factorsa
Event

Case studies [cardiovascular disease risk factors present]b

Stroke

Frankle et al.[16] [ HDL, liver enzymes]; Mochizuki et al.,[17] Kennedy et al.,[18] Akhter et al.,[19] Sahraian et al.,[20]
Santamarina et al.[21] [ Apo B]

Myocardial infarction

McNutt et al.[22] [ LDL, HDL]; Bowman[23] [ TC, HDL]; Ferenchick and Adelman[24] [family history];
Kennedy[25] [ TC, HDL, smoker]; Appleby et al.[26] [smoker, BP]; Huie[27] [family history, ALT, ASP, CK];
Fisher et al.,[28] Goldstein et al.,[29] Fineschi et al. (pt 1),[30] Gunes et al.[31] [ HDL]; Angelilli et al.[32] [ Trig, history
of hypertension]; Wysozcanski et al.[33] [ BP, CK, HDL]; Lunghetti et al.[34]

Sudden death

Luke et al.,[35] Campbell et al.,[36] Hausmann et al.,[37] Madea and Grellner[38] [ BP, TC and LDL, HDL Trig];
Fineschi et al., (pts 3 and 4)[39]

Thromboembolism

Laroche[40] [smoker]; Gaede and Montine,[41] Jaillard et al.,[42] Mewis et al.[43] [ LDL]; Nieminen et al., (pt 4)[44];
Palfi et al.,[45]; Falkenberg et al.,[46] [pt 2: smoker]; Hourigan et al.,[47] McCarthy et al.,[48] Ment and Ludman[49]
[smoker, TC]; Alhadad et al.[50] [protein C deficiency]; Liljeqvist et al.,[51] Frogel et al.[52]

Cardiac hypertrophy

Nieminen et al., (pt 2)[44] Mark et al.[53]

Cardiomyopathy

Ahlgrim and Guglin[54] [ ALT and AST]; Bispo et al.[55]

Endocarditis

Nieminen et al.[44] [pt 1: HDL] ; Fineschi et al.[39] (pts 1 and 2), Frogel et al.[52]

Atrial fibrillation

Sullivan et al.[56] [Tachycardia, CK].

Heart failure

Clark and Schofield[57] [Sinus Tachycardia, ALT, AST]

Subdural haematoma

Alaraj et al.,[58] Alhadad et al.[50] [protein C deficiency].

Case studies where no cause of death is reported or ascertained are grouped under sudden death whereas those case studies where
death is attributed to a myocardial infarction are grouped accordingly.

Where there are no risk factors cited after a study, no observations of negative results of CV risk factors were reported.

ALT = alanine transaminase; Apo B = apolipoprotein B; AST = aspartate transaminase; BP = blood pressure; CK = creatine kinase;
HDL = high-density lipoprotein; LDL = low-density lipoprotein; pt(s) = patient(s); TC = total cholesterol; Trig = triglycerides; indicates
increase; indicates decrease.

Few common themes emerge from consideration of the case studies presented in table I.
A broad spectrum of specific events is observed in
a range of individuals. A noticeable pattern of
disease presence and/or risk is hard to deduce. It
is also difficult to be sure of accurate reporting of
a broad spectrum of physiological or behavioural
risk factors for CVD for each subject.
Whilst case studies provide a useful initial insight into the effects of AS that may help drive
case-series or case-control studies, they are by no
means conclusive and cannot be considered strong
evidence of causal relationships. Case studies are
also reliant on self-reporting of substance use,
which can often be unreliable, with a lack of independent confirmation of what the person believes they are taking.
4. AS Use and CVD Risk Factors
Independent risk factors for CVD include hypertension, hyperlipidaemia, diabetes, obesity and a
2012 Adis Data Information BV. All rights reserved.

family history of premature coronary disease.

High levels of homocysteine and high-sensitivity
C-reactive protein (CRP) have also been used as
surrogate markers for the development of CVD.[61]
In the absence of data from epidemiological or
coronary imaging studies assessing CVD presence or prevalence in AS users, studies have assessed the prevalence of known risk factors, with
or without comparison to matched controls. The
link between each of these factors and the development/progression of atherosclerosis, combined
with case reports of the presence of risk factors in
AS users who have had significant cardiovascular
events (see table I), has prompted their assessment as a potential measure of future CVD risk.
Not surprisingly, these data are somewhat contradictory and thus inconclusive (see table II).
Hypertension has been identified as an important CVD risk factor.[73] Freed et al.[62] and Riebe
et al.[64] reported significantly higher systolic blood
pressure in bodybuilders using AS compared with
non-AS-using bodybuilding controls. Conversely,
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Steroids and Cardiac Health

Sader et al.[14] and Lane et al.[65] reported no

elevation of blood pressures in AS users. The
disparity between studies may reflect significant
variance in the inclusion of smokers and the lack
of control of diet across the groups. Of interest, is
that only Riebe et al.[64] assessed blood pressure
during exercise and this was elevated in AS users.
The importance of an exaggerated blood pressure
response to exercise for cardiovascular risk has
been postulated[74] but not fully assessed in AS
users. Another factor associated with elevated
arterial blood pressure is aortic stiffness (lowered
aortic compliance). Stiffer arteries tend to augment pulse pressure and alter systolic and/or
diastolic blood pressure. Interestingly, large artery stiffness may be increased with resistance

123

training.[75] The impact of AS use on central or

large artery stiffness has received some attention
recently. For example Kasikcioglu et al.[76] found
that AS use could be associated with a reduction
in aortic elastic properties (increased stiffness),
which could directly increase the risk of a
cardiovascular event. The authors suggested that
AS directly affect nitric oxide (NO)-mediated relaxation through the inhibition of guanylate cyclase, a second messenger that carries the signal
for smooth muscle to relax.
Elevated total cholesterol (TC), low- and highdensity lipoproteins (LDL and HDL) cholesterol
have been shown to increase cardiovascular
risk.[77] Studies of TC, LDL and HDL levels in
AS users have produced contradictory outcomes.

Table II. AS and associated risk factors

Study

Groups vs controls [n]

Findings

ASU vs P [13]

ASU SBP*

Kuipers et al.

ASU vs P [14]

ASU DBP

Riebe et al.[64]

ASU [10] vs BC [10]

ASU SBP at rest and exercise; ASU DBP during

exercise

Sader et al.[14]

ASU [10] vs BC [10]

No significant difference between groups

Lane et al.[65]

ASU [10] vs off AS [8] vs BC [10]

No significant difference

ASU [14] vs BC [17] and AS on vs off [10] treatment

ASU TC**; ASU HDL***; on HDL***

T vs TL vs T and TL (3 wk administration) [14]

T HDL* ; T and TL HDL* ;

no significant change in LDL in all groups

Sader et al.[14]

ASU [10] vs BC [10]

TC no significant difference; ASU HDL***

Hartgens et al.[68]

ASU [19] vs BC [16]

TC no significant difference; ASU LDL; ASU HDL

Lane et al.[65]

ASU [10] vs off AS [8] vs BC [10] vs SC [10]

TC no significant difference; ASU LDL*; ASU HDL***

ASU [10] vs BC [10] vs SC [8]

ASU CRP* vs BC and SC

Blood pressure
Freed et al.[62]
[63]

Cholesterol
Baldo-Enzi et al.[66]
Zmuda et al.

[67]

High-sensitivity CRP
Grace and Davies[69]
HCY
Zmuda et al.[70]

T vs TL vs T and TL (3 wk administration) [14]

No change in all groups

Graham et al.[71]

ASU [10] vs off AS [10] vs BC [10] and SC [10]

ASU** and off AS* HCY vs BC and SC

Study 1: ASU [19] vs BC [16]

Study 2: AS [19] (200 mg/wk of nandrolone
decanoate) vs P [16]

ASU APO (A-1 and B)***; no significant difference

between groups

ASU [5] vs BC [6]

Tendency for Hb to be higher in ASU group

APO
Hartgens et al.[68]

Hb
Alen[72]

APO = apolipoproteins; AS = anabolic steroids; ASU = AS users; BC = bodybuilding controls; CRP = C-reactive protein; DBP = diastolic blood
pressure; Hb = haemoglobin; HCY = homocysteine; HDL = high-density lipoprotein; LDL = low-density lipoprotein; off AS = abstinent from AS
for 3 mo; P = placebo; SBP = systolic blood pressure; SC = sedentary controls; T = testosterone; TC = total cholesterol; TL = testolactone;
indicates increase; indicates decrease; * p < 0.05, ** p < 0.01, *** p < 0.001.

2012 Adis Data Information BV. All rights reserved.

Sports Med 2012; 42 (2)

124

Although most studies report little difference in

TC, most demonstrate a decrease in HDL with
some observing an increase in LDL.[14,65,68] Lane
et al.,[65] observed little difference in total cholesterol
levels between AS users, (4.0 0.83 mmol/L), and
non-users, (3.8 0.38 mmol/L), whilst LDL (2.9
0.7 vs 2.1 0.3 mmol/L), was significantly elevated
and HDL (0.7 0.4 vs 1.3 0.3 mmol/L) significantly decreased in the AS group. A rise in LDL
cholesterol often leads to increased arterial fat
deposition and this change in lipoprotein profile
is therefore associated with an increased atherosclerotic risk.[77] Apolipoprotein, a component of
HDL cholesterol, has also been studied in AS
users. Studies, by Hartgens et al.[68] and Hartgens
and Kuipers[15] reported conflicting data, possibly due to issues of drug dosage and comparisons
of single- to poly-drug regimens. Whilst the exact
mechanisms for the effect of AS on lipid profiles
is yet to be fully established, some mechanisms
have been postulated. Applebaum-Bowden et al.[78]
suggested that after administration of stanozolol
for 7 days, there was a decrease in HDL levels
with a concomitant increase in hepatic triglyceride lipase (HTGL). HTGL is partly responsible
for the production of LDL but these results would
also suggest a possible catabolic effect of HTGL
on HDL, thereby leading to negatively affected
lipid profiles.
High-sensitivity CRP is a marker of inflammation and has been associated with cardiovascular events, including myocardial infarctions
and stroke.[61] Measurement of high-sensitivity
CRP is not routinely performed by doctors in the
evaluation of cardiovascular risk in the general
population. As such, limited attention has been
paid to high-sensitivity CRP in AS users. Grace
and Davies[69] reported that high-sensitivity CRP
was elevated in AS-using bodybuilders compared
with both non-AS-using bodybuilders and sedentary controls. Although the mechanism(s) for
this observation is not known, and such findings
require replication, the data highlights the possibility that AS use could result in local or systemic
inflammation that has the potential to damage
cardiomyocytes and/or the vascular endothelium.
Elevated levels of the amino acid homocysteine
have also been associated with increased CVD
2012 Adis Data Information BV. All rights reserved.

Angell et al.

risk[79] as a consequence of endothelial damage.[80]

As with many CVD risk factors, the data regarding homocysteine and AS use are conflicting.
Zmuda et al.[70] reported no change in homocysteine in AS users, whereas Graham et al.[71]
observed high homocysteine levels even in those
subjects who had abstained from AS use for
3 months. The disparity in outcomes is difficult to
explain but maybe related to subject-specific issues such as diet. A possible explanation for an
increase in homocysteine in AS users is that the
AS could affect the absorption of certain B vitamins (in particular B6 and B12), a deficiency that
can lead to an increase in homocysteine levels.
Other medical conditions which cause elevated
haemoglobin levels (polycythaemia) are associated with increased cardiovascular risk, and this
therefore may be an additional cause in AS users.
Finally, Alen[72] and Lane et al.[65] reported
significantly elevated haematocrit/haemoglobin
levels in AS users. In addition, Lane et al.[65] observed that haemoglobin levels were not different
to controls after a 3-month abstinence from AS.
In contrast, Hartgens et al.[81] reported that haematocrit and haemoglobin remained unaffected.
In summary, whilst it has become quite apparent
that AS use can have a significantly negative
effect on HDL levels,[65,68,78] and can therefore
increase cardiovascular risk,[77] much of the research that has assessed the association of AS use
with alterations in CVD risk factors is limited,
contradictory and may be multifactorial. It is,
therefore, worthwhile reflecting on the case-study
data in table I, where there are no clear patterns
of measurable CVD disease risk in cases with
hard CV-event endpoints. Scope for ongoing
work reflecting long-term poly-drug users with
attention paid to variations with cycle phase is
apparent. Further, when available data for CVD
risk factors in AS users are combined with case
study reports, one could surmise that factors additional to traditional CVD risk factors may be
responsible for any association between AS use
and CVD occurrence. It is for this reason that
other research groups have assessed the link between AS use and cardiac electrical, structural
and functional parameters as well as any impact
of AS use on vascular health.
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Steroids and Cardiac Health

125

5. AS Use and Cardiac Electrical Activity,

Structure and Function
The assessment of cardiac electrical activity,
structure and function are commonly used in the
determination of the presence or risk of CVD.
An example is the association of increasing left
ventricular (LV) mass and prognostic CVD
relevance.[82,83]
5.1 Cardiac Electrical Activity

Case reports have shown a possible effect of

AS use on cardiac electrical activity, with some
finding an association between AS use and atrial
fibrillation, and cardiac failure precipitated by
sinus tachycardia.[56,57] Human (and animal)
studies have shown an association between testosterone and an increase in the rate of cardiac
repolarization.[84,85] Consequently, the potential
for AS use to alter cardiac electrical activity
would seem a valuable line of enquiry. However,
there is limited research on the effect of AS abuse

on cardiac de/repolarization or any other aspect

of the ECG in humans. Whilst previous findings
have suggested prolonged QT interval may be
present in some athletes as a result of training,[86]
one study has suggested that AS use may be associated with a shortening of the QT interval.[87] It has
been suggested that the androgenic component of
AS impacts on cardiac electrical activity via facilitation of the expression of two potassium channel
proteins, Kir 2.1 and Kir 4.3, which are responsible
for mediation of the background inward rectifier
K+ current (Ik1) and the transient outward K+ current (Ito), respectively.[85] The relevance of the effect
on Ik1 becomes clear as it has been cited as an important current involved in ventricular repolarization, which may cause the shortening of the QT interval.[88] To further understand the role that AS
may have on cardiac electrical activity, as well as the
mechanism through which they act, it is clear more
research is necessary.
A number of measures of cardiac structure and
function have been investigated in order to ascertain
the effects of AS use on the heart (tables IIIV).

Table III. Studies showing affects of anabolic steroids on cardiac structure

Study

Groups vs controls [n]

Parameters measured

Findings

Urhausen et al.[89]

ASU [14] vs BC [7]

Total heart volume, LVM,

LVD, LVPW, IVS, LVWT : D,
LVM : LVV

Total heart volume and LVM: no difference

LVD: ASU ** vs BC
LVPW, IVS, LVWT : D and LVM : LVV:
ASU ** vs BC

Sachtleben et al.[90]

ASU (on and off cycle) [11] vs

BC [13]

LVM, LV and IVS wall

thicknesses, LVD (s and d)

LVM and IVS thickness: ASU (on) * vs ASU (off)

LVM, IVS and LV posterior wall thickness: ASU
(on) * vs BC

Dickerman et al.[91]

ASU [8] vs BC [8]

LV wall thickness

LV wall thickness: 6/6 ASU >11 mm

3/7 BC > 11 mm

Hartgens et al.[92]

ASU [17] vs BC [15]

LVD, LVM, LVMI, IVS, RVD,

LVPW

No significant differences observed.

Nottin et al.[93]

ASU [6] vs BC [9] vs SC [16]

LVD (s and d), LVM,

LVV(s and d), LV wall
thicknesses

LVM and LVD: SU * vs BC and SC

LVV (s and d): ASU ** vs SC
LV wall thicknesses: no significant difference
between groups

DAndrea et al.[94]

ASU [20] vs BC [25] vs SC [25]

LVM, LVD

LVM and LVD: no significant difference between

groups

Kasikcioglu et al.[95]

ASU [12] vs BC [14]

LV and RV

LVM: ASU * vs BC
RVD: ASU * vs BC

Baggish et al.[96]

ASU [12] vs BC [7]

IVS, LVPW, LVD, LVM

No significant differences observed

ASU = anabolic steroid user; BC = bodybuilding control; IVS = inter-ventricular septum; LV = left ventricle; LVD = LV diameter; LVD = left
ventricular diameter; LVM = left ventricular mass; LVPW = left ventricular posterior wall; LVV = left ventricular volume; LVWT = left ventricular
wall thickening; RV = right ventricle; RVD = RV diameter; s = end systole; d = end diastole; SC = sedentary control; indicates increase;
indicates decrease; * p < 0.05, ** p < 0.01.

2012 Adis Data Information BV. All rights reserved.

Sports Med 2012; 42 (2)

Angell et al.

126

Table IV. Studies showing affects of anabolic steroids on systolic cardiac function
Study

Groups vs controls [n]

Parameters
measured

Findings

Hartgens et al.[92]

ASU [17] vs BC [15]

EF

No significant differences observed

Nottin et al.[93]

ASU [6] vs BC [9] vs SC [16]

No significant differences observed

DAndrea et al.[94]

ASU [20] vs BC [25] vs SC [25]

e and SR at LV lateral
wall and IVS, S

S: no significant differences observed

Peak systolic LV strain rate and e: IVS = ASU * vs BC and
SC; LV lateral wall = ASU ** vs BC and SC

Kasikcioglu et al.[95]

ASU [12] vs BC [14] vs SC [15]

LV and RV

LV: S = no significant differences observed; RV = S:

no significant differences observed

Baggish et al.[96]

ASU [12] vs BC [7]

EF, longitudinal e,
radial e

EF: ASU vs BC
Longitudinal e: ASU vs BC
Radial e: ASU vs BC

ASU = anabolic steroid user; BC = bodybuilding control; EF = ejection fraction; IVS = inter-ventricular septum; LV = left ventricle; RV = right
ventricle; SC = sedentary control; S = peak systolic myocardial velocity; SR = peak strain rate; e = peak strain; indicates decrease;
*
p < 0.001, ** p < 0.01.

However, it is clear that the deployment of novel

non-invasive imaging techniques in the study
of AS users is limited to only a few recent studies. New imaging tools provide both global and
regional assessments of cardiac structure and
function[98] that may provide extra insight in
regard to the impact of AS upon myocardial
tissue.

5.2 Cardiac Structure

A number of morphological adaptations of

the heart have been observed in AS users. In a
group of top-level bodybuilders, Urhausen et al.[89]
reported that AS users had an increased LV
posterior and septal wall thickness. This resulted
in an increased LV wall thickness : diameter ratio

Table V. Studies showing affects of anabolic steroids on diastolic cardiac function

Study

Groups vs controls [n]

Parameters measured

Findings

Dickerman et al.[91]

ASU [8] vs BC [8]

E, A, E : A ratio

No significant differences observed

Hartgens et al.[92]

ASU [17] vs BC [15]

E, A, E : A ratio

No significant differences observed

Nottin et al.

ASU [6] vs BC [9] vs SC [16]

E, A, E : A ratio

E: ASU * vs BC and SC
A: no significant difference observed
E : A ratio: ASU vs BC* vs SC**

DAndrea et al.[94]

ASU [20] vs BC [25] vs SC [25]

E : A ratio, strain rate and

strain at LV lateral wall and
IVS, S

E : A ratio: ASU * vs BC and SC

Krieg et al.[97]

ASU [14] vs BC [11] vs SC [15]

E : A, E : A ratios

E : A ratio: ASU vs BC and SC

E : A ratio: no significant differences
observed

Kasikcioglu et al.[95]

ASU [12] vs BC [14] vs SC

LV and RV

LV: E : A ratio, E, A, and E : A

ratio: ASU ** vs BC
RV: E = ASU ** vs BC

Baggish et al.[96]

ASU [12] vs BC [7]

E, A, E : A, E, A

E, E : A ratio and E: ASU vs BC

A: ASU ** vs BC
A: no significant differences observed.

[93]

A = late atrial diastolic filling velocities; A = atrial diastolic tissue velocity; ASU = anabolic steroid user; BC = bodybuilding control; E = early
diastolic filling velocities; E = early diastolic tissue velocity; IVS = inter-ventricular septum; LV = left ventricle; RV = right ventricle;
SC = sedentary control; indicates increase; indicates decrease; * p < 0.01, ** p < 0.05.

2012 Adis Data Information BV. All rights reserved.

Sports Med 2012; 42 (2)

Steroids and Cardiac Health

as well as an increased LV muscle mass : volume

ratio. These findings were supported by Sachtleben
et al.[90] who noted that AS users had greater LV
mass, interventricular septal wall thicknesses and
LV diameter in diastole compared with non-ASusing bodybuilding controls. It was also observed
that when the users were on cycle, they had a
greater LV mass, septal wall thickness and LV diameter compared to when off cycle. Some other
studies have reported differences in cardiac structure between AS-using and non-AS-using athletes.[91,94] Both DAndrea et al.[94] and Dickerman
et al.[91] reported cardiac dimensions in AS users
that were either greater than sedentary controls or
outside of normal ranges, despite no significant
difference to non-AS-using athletes. These studies
would suggest that training may be as potent a
stimulus for cardiac adaptation as for AS use. At
odds with most previous literature, Nottin et al.[93]
observed no differences in LV wall thickness but
significantly greater LV cavity size and mass in
AS-using bodybuilders compared with non-ASusing athletes. This supports an eccentric, as opposed to a concentric, LV remodelling in AS users.
The reason for this contradiction is unclear; however, significant differences in training between
groups could offer an explanation.
Marsh et al.[99] observed that AS can directly
alter cardiac muscle protein metabolism, following activation of cell surface androgen receptors,
through possible modulation of gene transcription
in animal and human cardiac tissue. This theory
offers an explanation for how AS use could cause
structural and functional changes to the cardiac
tissue of regular AS users.
5.3 Systolic Function

Whilst gross changes in cardiac structure provide one focus for studies of AS use, it is also
pertinent to assess if AS use has any impact upon
LV function. Both LV systolic (table IV) and
diastolic (table V) function have been assessed in
AS users and controls in cross-sectional studies.
Earlier studies, such as those by Nottin et al.[93]
and Hartgens et al.,[92] observed no difference in
ejection fraction between strength-trained athletes who did and did not use AS. The assessment
2012 Adis Data Information BV. All rights reserved.

127

of global LV systolic function may mask subtle or

regional changes in function. Consequently, most
recent research has adopted new imaging tools
that can assess tissue velocities or strain in localized segments of LV wall tissue. Nottin et al.[93]
observed no significant differences between AS
users and non-users in peak systolic myocardial
velocity (S) at the mitral annulus in the LV posterior wall, interventricular septum, inferior wall
or anterior wall, despite slightly elevated values
seen in the AS group. DAndrea et al.[94] found
reduced peak strain and strain rates at both the
mid and basal levels in the LV posterior wall and
interventricular septum in AS users versus nonAS users and a control group of sedentary men.
Kasikcioglu et al.[95] measured the LV septal and
right ventricular (RV) free wall S in AS users,
bodybuilding controls and sedentary controls.
No difference was observed in S between the two
bodybuilding groups and sedentary controls in
either the LV or RV. Conversely, in a recent study,
Baggish et al.[96] observed a reduced ejection fraction in an AS group compared with non-AS users
that was also clinically relevant in many individuals
(i.e. <55%). They[96] also reported significantly reduced longitudinal and radial strain in AS users
when compared with non-AS users. The reason
for the contradictions in the research mentioned
previously is not entirely clear. Baggish et al.[96]
has suggested that participant differences between studies, such as older AS users, as well as
the lower level of competitive individuals used in
their study, could have been the cause of the differences observed. This is because possible reductions in cardiac function with age, in addition
to previous studies using high-level competitors
that could have favoured healthier AS users. A
reduction in the ejection fraction could possibly
be caused by a reduction in myocardial elastance.
As LeGros et al.[7] have suggested, an increase in
collagen crosslinks within the myocardium through
upregulation of lysyl oxidase, an enzyme responsible for initiating crosslinks between adjacent
collagen molecules. Further in vitro studies of the
direct mechanistic pathway that may be responsible for this change are required to develop our
understanding of the direct effects of AS on
myocardial cells.
Sports Med 2012; 42 (2)

Angell et al.

128

5.4 Diastolic Function

There has, to some extent, been greater attention paid to whether AS use might alter LV diastolic
function, possibly because of a potential link to
AS-induced concentric hypertrophy. Dickerman
et al.[91] did not observe any differences in Dopplerderived early (E) and late atrial (A) diastolic
filling velocities as well as the E : A ratio in
bodybuilders who did or did not use AS. Krieg
et al.[100] found no significant difference in E : A
ratios of AS-using and non-AS-using strengthtrained athletes, although they did find a significant reduction in E to A diastolic (E/A) tissue
velocities in the AS group. Nottin et al.[93] reported a
greater isovolumic relaxation time and a smaller
peak E diastolic filling velocity in AS users, showing
a reduced contribution of early relaxation to LV
filling. This observation was supported by Baggish
et al.,[96] who also commented that the lower E : A
ratio in AS users was clinically significant in 10
of the 12 athletes assessed. Nottin et al.[93] also
recorded tissue Doppler measurements of E and
A diastolic myocardial wall (E/A) velocities
at the mitral annulus (in septal, lateral, inferior
and anterior wall segments) as an adjunct to
diastolic filling blood flow velocities. In the ASusing bodybuilders peak E and the peak E : A
ratio were significantly smaller than the bodybuilding and sedentary controls. DAndrea et al.[94]
and Kasikcioglu et al.[95] also reported significantly
lower E : A ratios in AS using bodybuilders
compared with non-AS-using bodybuilders and
sedentary controls. A recent study by Baggish
et al.[96] also found a significantly lower E in the
AS users but, interestingly, didnt report strain
rate measurements in diastole.
A reduction in early diastolic filling parameters (whether assessed regionally or globally)
suggests that AS use has a negative effect on early
relaxation and thus the suction that is exerted on
LV inflow by the rapid decline in LV pressure
compared with left atrial pressure. A reduction in
early relaxation in AS users could be explained by
a reduction in myocardial elastance[7] reflecting a
stiffer LV. Despite evidence of a direct effect of
AS use on cardiac structure and function being,
at times, contradictory, some effort has been di 2012 Adis Data Information BV. All rights reserved.

rected to try and ascertain potential mechanism(s) using animal models. The androgenic component of AS has received some attention with
research showing that AS can affect extracellular
calcium channels, as well as calcium mobilization
from the endoplasmic reticulum.[101] It has been
suggested that this effect on calcium channels
can, in turn, affect mitochondrial permeability
that may allow the release of apoptogenic factors.
This is supported by the findings of Zaugg et al.[102]
that found dose-dependent apoptotic cell death in
rat myocytes.
6. AS and Vascular Health
Limited positive effects of therapeutic doses of
testosterone on vascular function have been described.[5] The impact upon vascular health of AS
use at higher concentrations has received less attention. This is somewhat surprising given the
potential negative cardiovascular consequences
of AS use reported in the literature.[15,26,66,69,96]
The progression from endothelial dysfunction to
significant clinical atherosclerosis in coronary
arteries is important for underpinning and predicting cardiovascular events.
The assessment of peripheral conduit arteries,
using a number of techniques, facilitates the assessment of the cardiovascular risk and atherosclerotic burden of the circulatory system.[103,104]
As atherosclerosis is a progressive disease in
which endothelial dysfunction is an early and integral feature, assessment of the function of endothelium may provide an early window on the
negative effects of AS use. In a case study by
Green et al.,[105] an individual taking part in a
study assessing forearm blood flow in response to
methacholine and sodium nitroprusside, potent
NO-mediated vasodilators, had values that were
dramatically decreased on the second testing session. The investigators ascertained that the participant had been self-administering AS for 4 months.
He agreed to abstain from AS before the final
testing session. Values had returned to the level of
the first testing session following the period of abstinence. This suggests that AS have an acute effect
on the NO dilator system that is somewhat reversible following a short period of abstinence.
Sports Med 2012; 42 (2)

Steroids and Cardiac Health

Flow-mediated dilation (FMD) is a noninvasive method used to assess conduit artery

function, and abnormal FMD values can predict
future cardiovascular event rates.[106] Ebenbichler
et al.[107] and Sader et al.[14] reported that FMD
and glyceryl trinitrate-induced vasodilation of the
brachial artery was reduced in AS users compared with healthy controls, indicating that some
effect of AS on vascular smooth muscle function
may be evident. In support of this contention,
Lane et al.[65] reported that endothelial-independent
dilatation was impaired in those currently using
AS, compared with those who had abstained
from AS use for 3 months and a group of bodybuilding controls. Interestingly, Sader et al.[14]
reported a similar reduction in FMD in both ASusing and non-AS-using bodybuilders, suggesting that prolonged and intense resistance training
alone may be responsible for negative impacts
on vascular health. This conclusion is endorsed by
studies of the effect of resistance training on vascular function in otherwise healthy subjects.[108,109]
Whilst not investigating the effects of AS use in
strength-trained athletes, McCredie et al.[110]
examined the effect of testosterone implants on
vascular reactivity in a group of female-to-male
transsexuals against a group of female controls.
They found that glyceryl trinitrate values were significantly reduced in the transsexual group, whilst
there was a mean difference of 1.8% in FMD scores
between groups, with the transsexual group having
a lower mean FMD score. Whilst the authors did
state that the high number of smokers within both
groups is a likely confounding factor, the results
imply a lack of relaxation capability within the
vasculature due to high androgen exposure.
A number of mechanisms for an AS-mediated
reduction in vascular function, as a consequence
of AS use have been proposed. These include
suggestions that AS may have a direct, negative
effect on the NO dilator system. Kasikcioglu
et al.[76] proposed that downregulation of the NO
dilator system could underpin an AS-related increase in arterial stiffness and a reduction in FMD.
AS use has been shown to have a negative effect
on endothelial growth.[111] It is also possible that
AS have a detrimental effect of endothelial cell
turnover and renewal, implying that AS could
2012 Adis Data Information BV. All rights reserved.

129

cause stiffening within the heart and vasculature

through affecting endothelial proliferation and
propagation. However, no direct studies of endothelial progenitor cells currently exist. In addition, it has also been suggested that AS do not only
attenuate the effect of vasodilators, but also enhance the effects of vasoconstrictors.[112] McCrohon
et al.[113] investigated the effect of AS on monocyte
adhesion to endothelial cell in vitro and found that
androgens caused a dose-related increase in monocyte adhesion to endothelial cells. This increase in
cell adhesion was mediated by an upregulation in
vascular cell adhesion molecule-1. Whilst this study
was performed in vitro, it does give an indication of
another possible mechanism through which AS
might negatively impact atherosclerotic risk.
The effects of AS use on vascular health is inconclusive, yet significant negative effects of AS
on endothelial and vascular smooth muscle function have been demonstrated.[14,107] Whilst resistance training alone could cause a reduction in
endothelial function, AS could further confound
this effect by significantly impairing vascular
smooth muscle relaxation.[14] Despite conflicting
evidence with regards to the effect of endothelial
dependent relaxation as a result of AS, it is noteworthy to show that a mechanism for endothelial
vascular relaxation impairment has been demonstrated that could help to explain the propensity
of cardiovascular events in AS users.[111]
7. Future Directions
Whilst a slightly clearer picture is beginning
to emerge regarding the use/abuse of AS in an
otherwise healthy population, the specific cardiovascular health effects still require greater attention.
In the first instance, the small subject numbers in
most cross-sectional studies are a limiting factor
to this area of research alongside the inter- and
intraindividual drug dosages. More longitudinal
studies of real-life AS use, from as early in the
AS-use history as is reasonably possible, would
naturally factor in on/off cycles, along with the
differing cycles that are used for bulking or
cutting. Indeed, reversibility of any effects of AS
is also an issue that requires attention. This would
involve making assessments when users were
Sports Med 2012; 42 (2)

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130

both on and off cycle, as well as assessing longterm users who have ceased use. The inclusion of
the testing of AS products used by participants,
as well as testing of their urine, although costly,
would also increase the robustness of the data.
Integral to future studies, alongside longitudinal
designs (etc), is the need to utilize state-of-the-art
techniques to assess cardiovascular health, and
generate new data and insights. For example,
with a greater spatial resolution and the ability to
tissue track, as well as assess fibrosis and perfusion, using cardiac MRI would allow for a much
more comprehensive assessment of cardiac structure and function, as well as determine if perfusion defects, inflammation and/or fibrosis existed
within the cardiac muscle of AS users.
The cellular mechanisms responsible for any
negative cardiovascular changes that occur from
AS use/abuse also require further attention. Whilst
previous research has examined the effects of
AS on hepatic[114] and endothelial cells,[115] work
on myocardial cells has been limited to animal
studies.[102] Future animal in vitro work should
aim to replicate doses to that which occurs in human
users, with a particular focus on proteomics and
the area of subcellular enquiry.
8. Limitations to Research in AS Users
OSullivan et al.[116] stated that limitations
of, and barriers to, research in the field of AS
use are substantial. Because of issues of legality
and the consequent clandestine use of AS, large
population-based epidemiological data detailing
CVD presence in AS users are unavailable, with
open self-reporting on a large scale over a long
time period being hard to obtain. Simply gaining
access to this group is a difficult task. Many users
are suspicious of outsiders asking questions and
this can lead to a failure to reach the many that
are imbedded in the culture. That being said,
different methods have been employed to achieve
greater access to users. By employing a crossdepartmental/profession between those working
in public health or needle-exchange settings, the
access to data can be can greatly improved. The
immersion of a researcher into the culture in
order to gain the trust of AS users is still likely to
2012 Adis Data Information BV. All rights reserved.

be the most effective way to get open and honest

accounts of AS use. Randomized controlled
(placebo) trials of AS use are few and far between and are limited by ethical concerns in respect of the AS dose used. In real life, the dose of
AS is often large and complex. Multiple steroids
(stacking) are taken together, often with other
substances, in increasing and decreasing dosage
profiles. Use of AS may be suspended (off cycle)
for short periods before resumption (on cycle),
but all of these practices differ significantly between individuals. Another consideration is that
the true dose of AS is also difficult to verify, even
in honest self-reported cases, because of the blackmarket system of purchase and the widespread
distribution of counterfeit drugs.[117] Limitations
to the direct impact of AS use on CVD presence
or endpoint are apparent. As a consequence of
these limitations, the direct cardiovascular health
impacts of AS use are still to be fully determined.
What data exists in humans has largely been derived from case studies or case-series/case-control
studies.[118] Case studies, whilst useful in defining
and prompting hypothesis-driven research, are
limited in their ability to identify cause and effect.
Case-series or case-control studies suffer from a
number of limitations related to recruitment bias
and interindividual differences between subjects.
Specific issues include (i) the use of diverse subject groups, ranging from highly trained athletes
combining AS use with a high protein diet and a
large training load to relatively sedentary university
students, including failure to match for training
status, body mass and a true assessment of AS use/
non-use through urine assessment; (ii) the wide
spectrum of AS dosage (quantitatively), drug
type or source (e.g. veterinary), drug quality (e.g.
potency and homemade AS), and stacking or
poly-drug regimens that are often associated with
the use of AS; and (iii) the limitations of accuracy
in self-reported AS use.
9. Conclusion
The current data regarding the effects of AS
use/abuse on cardiovascular health is largely
contradictory and inconclusive. Whilst causal
relationships for negative cardiovascular effects
Sports Med 2012; 42 (2)

Steroids and Cardiac Health

have been suggested from case-study data, crosssectional studies have been less definitive and
there is an absence of longitudinal studies detailing effects within individuals. To date, the most
consistent data reflects a significant negative effect of AS use on lipid profiles and, in particular,
a reduction in HDL levels.[65,66] A common theme
appearing in recent data is the suggestion that a
decrease occurs in the relaxation properties of
both the myocardium and the vascular wall. An
increased stiffness within the ventricles of the heart
and vasculature could mean a reduced ability of AS
users to cope with physiological stressors.
Despite this, the data reviewed, mainly in the
form of a burgeoning body of case-study reports
of cardiovascular events and disease endpoints,
raises significant concerns about the cardiovascular
health consequences of AS use. This may be particularly relevant in specific individuals, but predicting those at greater risk among the AS-using
community is beyond our capacity at present.
Current evidence, allied to an appreciation of many
technical and design limitations when studying
AS use, should prompt ongoing research into
numerous aspects of cardiovascular health, risk
factors as well as cardiovascular structure and
function in those who choose to use AS for promoting performance and/or image enhancement.
Acknowledgements
The authors would like to thank Michael Evans-Brown
from Liverpool John Moores University Institute of Health
Research for his assistance in compiling the case-study data
for this review. No funding was used to assist in the preparation of this review. The authors are aware of no conflicts of
interest that are relevant to the content of this review.

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Correspondence: Mr Peter Angell, Research Institute for

Sport and Exercise Sciences, Liverpool John Moores
University, Tom Reilly Building, Byrom Street, Liverpool,
L3 3AF, UK.
E-mail: P.Angell@2004.ljmu.ac.uk

Sports Med 2012; 42 (2)