Ventricular structure, function, and focal fibrosis in

anabolic steroid users: a CMR study

Peter J. Angell, 1* Tevfik F. Ismail,2* Andrew Jabbour,2 Gillian Smith,2

Annette Dahl,2 Ricardo Wage,2 Greg Whyte,3 Daniel J. Green,3,4 Sanjay

Prasad,2* & Keith George. 3*

1 Health Sciences Department, Liverpool Hope University, Hope Park, Liverpool, UK. 2

CMR Unit, National Heart and Lung Institute, Royal Brompton Hospital, London, UK. 3 Research Institute for Sport and Exercise Sciences, Liverpool John Moore’s

University, Liverpool, UK.4 School of Sport Science, Exercise and Health, The

University of Western Australia, Nedlands, Australia.

*The first two and last two authors have contributed equally to this work.

Word Count: 2874

Address for Correspondence:

Peter Angell, Health Sciences Department, Liverpool Hope University, Hope Park, Liverpool, L16 9JD.

Tel: 0151 291 3287

Fax: 0151 291 3287

E-mail: angellp@hope.ac.uk

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ABSTRACT

Purpose: Anabolic steroid (AS) misuse is widespread amongst recreational bodybuilders, however, their effects

on the cardiovascular system are uncertain. Our aim was to document the impact of AS use on cardiac structure,

function and the presence of focal fibrosis using the gold standard cardiovascular magnetic resonance imaging

(CMR). Methods: A cross-sectional cohort design was utilised with twenty-one strength-trained participants

who underwent CMR imaging of the heart and speckle-tracking echocardiography. Thirteen participants (30 ± 5

yrs) taking AS for at least 2 years and were currently on a “using”-cycle were compared with age and training-

matched controls (n=8; 29 ± 6 yrs) who self-reported never having taken AS (NAS). Results: AS users had

higher absolute left ventricular (LV) mass (220±45 g) compared to NAS (163±27 g; p<0.05) but this difference

was removed when indexed to fat free mass. AS had a reduced right ventricular (RV) ejection fraction (AS:

51±4% vs. NAS: 59±5%; p<0.05) and a significantly lower left ventricular E:A myocardial tissue velocity ratio

(AS: 0.99[0.54] vs. NAS: 1.78[0.46] p<0.05) predominantly due to greater tissue velocities with atrial

contraction. Peak LV longitudinal strain was lower in AS users (AS:-14.2±2.7% vs. NAS:-16.6±1.9%; p<0.05).

There was no evidence of focal fibrosis in any participant. Conclusions: AS use was associated with significant

LV hypertrophy, albeit in line with greater fat free mass, reduced LV strain, diastolic function, and reduced RV

ejection fraction in male bodybuilders. There was, however, no evidence of focal fibrosis in any AS user.

Key Words: Left Ventricular Hypertrophy, Fibrosis, Echocardiography, Diastolic Function

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Introduction

The use of anabolic steroids (AS) has been associated with significant adverse cardiac events including acute

myocardial infarction (Lunghetti et al. 2009; Wysoczanski et al. 2008) and sudden cardiac death (Luke et al.

1990; Fineschi et al. 2007). Much of the association between AS use and cardiovascular events has been

garnered from case study reports and consequently cause and effect has yet to be conclusively established.

Increased cardiovascular risk is assumed with the use of AS, but the potential mechanism(s) remain

controversial (Angell et al. 2012a). Whether alterations in left (LV) or right (RV) ventricular structure and

function, including the presence of focal fibrosis, occur as a consequence of AS use and mediate an increased

cardiovascular risk is unclear.

There is echocardiographic evidence of greater LV muscle mass in AS users (Baggish et al. 2010; Angell et al.

2012b), but this is not consistent (Urhausen et al. 1989; D'Andrea et al. 2007) and there is a paucity of data on

the effects of AS use on RV structure. Recent tissue Doppler and speckle tracking analyses have revealed

reduced LV longitudinal (D'Andrea et al. 2007; Baggish et al. 2010) and radial ε (Baggish et al. 2010) as well

altered diastolic strain rates (Angell et al. 2012b) in AS users, however, there is limited data describing RV

function in AS users.

Significant limitations exist with echocardiography including: operator variability; restricted acoustic windows;

low spatial resolution and the use of mathematical models to predict 3D structures or function (Kühl et al.

2003). Cardiovascular magnetic resonance (CMR) is considered the gold standard for non-invasive assessment

of global cardiac structure and function due to its high spatial resolution and its lack of reliance on geometric

assumptions (Pennell et al. 2004; Hundley et al. 2010). Unlike echocardiography, CMR is not limited by poor

acoustic windows and enables complete tomographic assessment of RV structure and function. In addition,

CMR allows tissue characterisation and the detection of focal fibrosis by late gadolinium enhancement (LGE)

imaging (Jellis et al. 2010). Focal fibrosis is thought to underlie abnormalities in cardiac function associated

with other causes of LV hypertrophy (Weber et al. 1993). CMR has not previously been employed in a

comprehensive assessment of cardiac structure, function and focal fibrosis in AS using strength trained athletes.

The aim of the current study was to assess cardiac morphology and function as well as the presence of focal

fibrosis in AS users, compared to age- and strength-trained matched participants with no previous history of AS

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use, using CMR and echocardiography. We hypothesised that AS use would result in greater LV and RV

dimensions, reduced LV and RV function, and that these changes would be associated with focal fibrosis.

Methods

Subjects

Strength-trained male participants (n=21) were recruited through local gyms, and personal contacts. Participants

were aged between 18 and 50 years of age with a minimum of 3 years continuous resistance training with at

least 3-4 training sessions per week. Exclusion criteria for the study were the presence of known respiratory,

cardiovascular, musculoskeletal or auto-immune disease. Inclusion criteria for the AS using group (AS: n=13,

age 30±5 years) included a documented self-reported history of AS use for at least 2 years and that all users

were in an “on-cycle” at the point of testing. The non-AS (NAS) group (n=8, age 29±6 years) inclusion criteria

was a self-report history of never taking AS. Groups were matched for age and training history.

Design

A cross-sectional cohort design was utilised with participants required to make a single visit to the CMR

laboratory. Initially, subjects completed questionnaires relating to general health, training status and history as

well as detailed accounts of AS use. This was followed by assessment of body composition and a

comprehensive cardiovascular evaluation including non-invasive brachial artery blood pressure, an

echocardiogram and CMR. All tests were conducted on the participants following an overnight fast and 24

hours abstention from resistance training.

Protocols: Participant History and AS use

Training history data recorded included: years of resistance/strength training; the average number and length of

sessions per week: and self-reported one repetition maximums (1RM: the maximum weight that can be lifted for

a single repetition) for the bench press and squat. Participants in the AS group provided a detailed history of AS

use including names, dosage and cycling information.

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Body-Composition

Height and body mass were recorded using standard scales allowing the calculation of BMI. Estimation of fat

mass and fat free mass was completed using bio-electrical impedance (InBody 230 Body Composition Analyser,

Biospace Co Ltd, Los Angeles, CA, USA).

Blood Pressure

At the end of a 10 minute resting supine period, repeated resting non-invasive brachial artery blood pressures

were recorded in duplicate from the left arm via an automated blood pressure monitor (V100 Dinamap, GE

Medical Systems, Chalfont St. Giles, Bucks, UK).

CMR Image Acquisition Protocol

All images were acquired using a dedicated 1.5T scanner (Siemens Avanto, Siemens Healthcare, Erlangen,

Germany) with a sixteen-element phased-array receiver coil. Using scout images for planning, expiratory

breath-hold, ECG-gated, balanced steady-state free precession cine images were acquired in the vertical long

axis (VLA), horizontal long axis (HLA) and left ventricular outflow tract (LVOT) planes. Using the VLA and

HLA images for planning ensured imaging was parallel to the atrioventricular groove and perpendicular to the

long axis of the ventricle. A contiguous short-axis stack was obtained from base to apex ensuring full LV and

RV ventricular myocardial coverage (Assomull et al. 2006).

After acquisition of cine images, gadolinium contrast (Gadovist, Bayer-Schering, Berlin, Germany, 0.1

mmol.kg-1) was injected at a rate of 3.5 ml.s-1 followed by a 15 ml saline bolus at 7 ml.s-1 via an 18G cannula in

the right antecubital fossa using a power injector (Medrad UK, Ely, Cambridgeshire, UK). After ten minutes,

LGE images were obtained using an ECG-gated expiratory breath-hold segmented turbo Fast Low Angle Shot

(FLASH) gradient echo sequence (Simonetti et al. 2001). Images were obtained in all long-axis planes and in

the same short-axis stack as for cine images with the inversion time optimised to null the normal myocardium.

This was then repeated in an orthogonal phase encoding direction to exclude artifact.

CMR Image Analysis

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All data were analysed by single experienced blinded observer. Global left and right ventricular parameters

(end-diastolic volume, end-systolic volume, stroke volume, and ejection fraction) and LV mass were determined

using a semi-automated threshold-based algorithm after manual tracing of epicardial and endocardial borders

using commercially available software (CMRtools, Cardiovascular Imaging Solutions, London, UK).

Ventricular volumes and mass were recorded as absolute data and normalised for individual differences in fat-

free mass (Batterham et al. 1999). LV remodelling was assessed through unadjusted LV mass to volume ratio

(M:C). Late gadolinium enhancement (LGE) was assessed qualitatively to determine the presence or absence of

focal fibrosis.

Echocardiography

A single experienced echocardiographer performed all imaging with the subject in the left lateral decubitus

position using a commercially available system (Vivid Q, GE Healthcare, Chalfont St. Giles, Bucks, UK). In

the apical 4-chamber view Doppler flow analysis of LV filling was used to assess early (E) and atrial (A) peak

diastolic filling velocities (and E:A ratio). Tissue-Doppler imaging (TDI) was performed to determine peak

systolic (S’) as well as early (E’) and atrial (A’) diastolic tissue velocities in the basal septum. The ratios E’:A’

and E:E’ were calculated. 2D cine loops of an apical 4-chamber view were stored determination of segmental

(6) and global (mean) longitudinal strain (ε) and SR data in systole (SSR) as well as early (ESR) and atrial

diastole (ASR). All measurements were made off-line (Echopac, GE Healthcare, Chalfont St. Giles, Bucks, UK)

by a single experienced technician and reflected the average of 3 to 5 continuous cardiac cycles.

Data Analysis

Statistical analysis of data was performed using SPSS Version 17 (IBM Inc., New York, USA). All continuous

data were subjected to tests of normality and are presented as mean±standard deviation (SD) for normally

distributed variables or as medians with inter-quartile ranges for non-normally distributed data. Differences

between AS and NAS participants were analysed using independent t-tests and ANCOVA (with years of

training and number of sessions per week as covariates) if normally distributed or the Mann-Whitney U test if

not. In AS users only, we performed Pearson’s bivariate correlation analyses to examine the relationship

between the number of years of AS use or the amount/dose of AS currently being taken and measurements of

structure and function in the LV and RV. Two-tailed values of p<0.05 were considered statistically significant.

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Results

AS Use and Training

A broad range of AS were reported to be used in multiple stacking procedures with varied periods of abstinence

or “off-cycles”. There were large individual variations in AS dose reported. The median daily testosterone

equivalent dose of AS was 228 mg (range 35–685 mg). When the average weekly AS dose when using was

averaged across the whole year for each user, the median testosterone equivalent dose of AS was 154 mg (range

96-1480 mg). The number of different AS used in a cycle also varied between individuals with a median of 3

(range 1-7). There was no self-report evidence of social or other performance enhancing drug use in any

participant. Training history did not differ between groups (See Table 1). The AS group had significantly greater

1RM for both bench press and squat (Table 1).

Anthropometry and Physical Examination Findings

There was no significant difference in height, fat mass or body fat percentage between the groups. The AS

group were, however, significantly heavier and had significantly greater fat free mass and BMI. Blood pressure

did not differ significantly between groups but resting heart rate was significantly greater in the AS group (Table

2).

CMR

Absolute data for maximum end-diastolic wall thickness, LV end-diastolic volume and LV mass were greater in

AS users even after covariate analysis. These differences were eliminated when the data were indexed for fat-

free mass (Table 3). A similar pattern was observed for RV end-diastolic volume. A significantly greater LV

mass:volume ratio was observed in the AS group. LV stroke volume (SV) and ejection fraction (EF) were

similar between groups but RV EF was significantly reduced in AS users, mainly because of a significantly

elevated RV end-systolic volume. None of the scans exhibited any sign of focal fibrosis.

Echocardiography

There was no significant difference in early (E) diastolic filling velocities between groups (Table 4). Atrial (A)

diastolic filling velocity was significantly elevated in the AS group, leading to a significant reduction in E/A

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ratio. Peak E’ and E’/A’ were significantly lower and A’ significantly greater in the AS group and the

differences remained in covariate analysis. Longitudinal ε and systolic SR were significantly reduced in the AS

group. There was no significant difference in diastolic E SR whilst the AS group had a significantly higher A

SR (Table 4). No significant associations were observed between the number of years of AS use or the number

of weeks of use within the last year and cardiac structural and functional measures (Table 5).

Discussion

This CMR study offers novel insights into the effects of AS use on cardiac structure and function. We observed

a greater LV mass in AS users compared to an age and training history-matched non–using groups, although this

appears to be proportional to group differences in fat free mass. We also observed a smaller RV EF, LV

longitudinal ε as well as differences in indices of LV diastolic function in the AS users. Despite these changes

CMR did not detect any evidence of LGE in the AS group or controls.

The AS group were heavier and had a higher fat free mass and BMI in comparison to the non-users. This can be

explained by findings that show an up-regulation of skeletal muscle protein synthesis associated with AS use

when taken in conjunction with resistance training (Ferrando et al. 1998). This is despite little difference

between groups, in the amount of training per week and the length of time the participants had been training for.

Resting heart rates were significantly elevated in the AS group and confirms a previous study from our group

(Angell et al. 2012b). Whilst it has been suggested that AS use can interfere with cardiac electrical signalling

(Bigi and Aslani 2009; Maior et al. 2012), it is unclear if this extends to the regulation of heart rate and if it is a

direct effect of AS use. The lack of difference in BP between groups supports some past work (Sader et al.

2001) but contradicts others (Riebe et al. 1992). A large variation in individual BP between subjects may

highlight a lack of power with regard to this data.

AS use was associated with a greater mean LV wall thickness, LV end-diastolic volume and thus LV mass.

These data are in agreement with previous echocardiographic findings (Angell et al. 2012b). Of note, the

current LV mass data was somewhat lower than reported by another echocardiographic study (Baggish et al.

2010). Recent data has shown significant discrepancies between echocardiography and CMR, with

echocardiography significantly overestimating LV mass (Stewart et al. 1999). This overestimation may relate to

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the differing geometric assumptions and equations used in echocardiographic assessment of LV mass, which are

not applicable when using CMR (Pluim et al. 1997; Missouris et al. 1996). The increased spatial resolution and

full myocardial coverage offered by CMR provides clarification of conflicting echocardiographic data.

The between group difference in peak wall thickness and LV mass did not persist after indexing for individual

differences in fat free mass suggesting increases in LV size occur in-line with increases in skeletal muscle mass

in AS users. For the first time in AS users, CMR data for RV structure and function was provided. RV end-

systolic volume was significantly higher in the AS users. However, the difference was lost after scaling for fat-

free mass which suggests a similar adaptation to AS, and relationship with body size, in both the RV and LV.

The M:C ratio was higher in the AS users but were within the normal range in both groups.

The cardiac morphology in AS users was accompanied by significant differences in both LV and RV function

when compared with controls. Notably we observed a significantly lower longitudinal ε in the AS group even

though global EF and SV were not altered. The lower longitudinal ε in the AS group is in agreement with past

work (2010). Whilst the differences in longitudinal ε are statistically significant, the clinical implication is

difficult to interpret as there is limited normative athletic data on these parameters. A novel finding from the

present study was the negative effect of AS use on RV EF. Whilst reduced RV diastolic function has been

observed in AS users (Kasikcioglu et al. 2009), any AS impact on RV EF has not been previously reported. As

with the observed difference in longitudinal ε, the clinical significance of the smaller RV EF in AS users is

unclear. The data remain within normal limits but could be an initial sign indicative of more substantive cardiac

dysfunction should AS use continue. These issues require further study and evaluation.

The mechanism(s) responsible for the negative effects on cardiac structure and function are unclear (Fineschi et

al. 2007). Myocardial cells have been shown to have a high affinity for androgens (McGill et al. 1980) and an

increase in protein synthesis is likely the mediator of skeletal and cardiac muscle mass. The lower LV diastolic

functional data in AS users agrees with previous work (Missouris et al. 1996) and suggests a reduction in LV

early relaxation/compliance, an increase in LA contractility or a combination of these factors. An increase in

collagen cross-links as a result of AS use was observed by D’Ascenzo et al. (2007) which may offer an

explanation for the lower diastolic function observed in the AS group. This would imply that the myocardium

would become more rigid and have reduced contractility and compliance as a consequence of AS use. In

addition, work by Zaugg et al. (2001) noted that AS induced apoptosis in rat myocardial cells that could have

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structural and functional consequences. Although alterations in electrical conduction and repolarisation of

myocytes have been suggested as a possible mechanism for alterations in cardiac function, recent data has been

conflicting (Maior et al. 2010; Bigi and Aslani 2009). A plausible hypothesis that can be partially rejected in

the current study is a potential role for focal fibrosis. In contrast to other populations with cardiac hypertrophy,

such as hypertrophic cardiomyopathy, where two-thirds of patients exhibit LGE (O'Hanlon et al. 2010), we

observed no evidence of focal fibrosis in any participant, AS user or not. This was despite the fact that all AS

users were tested during an “on-cycle” and reported as a minimum 2 years of AS use alongside their training. In

specific cases no LGE was noted even in an AS user with a >20 year history of drug taking and intense training.

This would imply that long-term AS use does not cause focal fibrosis, although further studies are required to

confirm this. Whilst the absence of observable focal fibrosis is noted, we cannot completely rule out the

presence of diffuse myocardial fibrosis. Given recent data that has reported LGE in lifelong endurance athletes

(Wilson et al. 2011) it may be that longer term training with different patterns of different hemodynamic loading

and/or AS use maybe required to see LGE on CMR.

Limitations and Future Research

Whilst this study affords new data in relation to the cardiac effects of AS abuse due to the use of CMR, there are

some limitations. Firstly, methodological confounders are common in AS research (Angell et al. 2012a).

Variations in drug stacks, dosages and, cycle composition and lengths make a definitive statement regarding the

effect of any specific AS dose problematic. Secondly, although we assessed longitudinal myocardial ε and SR in

the LV we did not to assess ε and SR strain rate in the RV. We observed negative alterations in cardiac function

at rest in AS users and it might be pertinent to determine if exercise augments these data. Whilst we measured

focal fibrosis, we are aware that other forms of fibrosis may be responsible for reductions in cardiac function.

Diffuse fibrosis, characterised by extracellular matrix expansion, may be responsible for any negative changes

observed in the AS users and future work should use CMR techniques that focus on this form of adverse

remodelling. Further, on-going studies of the cardiac consequences of AS use should evaluate the impact of on-

and off-cycling commonly practiced by these athletes. Finally, whilst most of the correlations between current

AS dose, AS use history and cardiac function were small this area of interest requires more data collected in

bigger samples over longer periods of use.

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Conclusions

The current study demonstrates that CMR-determined LV and RV remodelling is present in AS users and is

associated with increases in whole body fat-free mass suggesting a global effect on muscle hypertrophy. AS use

was associated with a smaller longitudinal LV ε, a smaller RV EF and differences in indices of diastolic

function when compared to training matched non-AS using controls. These data suggest a possible reduction in

myocardial performance in those who use AS that requires further evaluation, although it would appear that

these changes are not mediated by focal fibrosis.

Acknowledgements

Dr Ismail is supported by the British Heart Foundation, Imperial College London and the National Institute for

Health Research Cardiovascular Biomedical Research Unit at the Royal Brompton Hospital. We would like to

thank the staff of the Royal Brompton CMR Unit, in particular, Ms Susan Clark, Ms Bethan Cowley and Ms

Claire McLeod for their contributions to data collection. The results from this work do not constitute

endorsement by ACSM.

Conflict of interest

There are no conflicts of interest for any of the authors.

Ethical Standards

The study was conducted in accordance with the principles set out by the declaration of Helsinki. All

participants provided written informed consent and local ethics approval was obtained.

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Abbreviations List

AS=Anabolic Steroids

ε=Myocardial Strain

CMR=Cardiovascular Magnetic Resonance

LV=Left Ventricle

RV=Right Ventricle

LGE=Late Gadolinium Enhancement

HLA=Horizontal Long Axis

BMI=Body Mass Index

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Table 1. Training and performance data for AS and NAS groups (data are mean ± SD).

AS Non-AS

Training (years) 9±4 10±6

Training (sessions/wk) 4±1 4±1

Session Duration (min) 74±27 69±8

1RM Bench (kg) 157±30 111±18*

1RM Squat (kg) 191±37 132±52*

1RM=one repetition maximum; *p<0.05

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Table 2. Anthropometric and blood pressure measures for AS and NAS groups (data are mean±SD).

AS Non-AS

Height (cm) 179±8 180±7

Weight (kg) 100.9±14.4 80.3±9.4*

BMI (kg/m2) 31.3±4.2 24.8±1.7*

Fat free mass (kg) 85.6±9.9 71.5±7.7*

Fat mass (kg) 15.1±9.1 8.8±3.1

Body fat %† 14.4±7.1 10.9±3.3

Systolic BP (mmHg) 132±16 125±7

Diastolic BP (mmHg) 71±10 66±10

Resting HR (beats/min) 74±8 60±7†

BMI=Body Mass Index, 1RM= 1 Repetition Maximum, BP= Blood Pressure, HR= Heart rate. * p<0.05,

†p<0.005

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Table 3. CMR structural and functional measures in AS and NAS groups (data are mean ± SD).

AS Non-AS

Peak WT(mm) 13.0±2.2 9.4±1.3†

LV EDV (ml) 204.7±25.4 187.5±28.4*

LV ESV (ml) 81.1±14.3 70.6±14.7

LVM (g) 220±45 163±27*

Peak WT/FFM (mm.g-0.33)‡ 0.46[0.11] 0.40[0.09]

LV EDV/FFM (ml.g-1)‡ 2.32[0.46] 2.51[0.28]

LV ESV/FFM (ml.g-1)‡ 0.97[0.30] 0.97[0.16]

LVM/FFM‡ 2.56[0.40] 2.43[0.48]

LV Mass/Volume‡ 1.10[0.26] 0.88[0.16]*

RV EDV (ml) 225.9±40.8 199.8±39.6

RV ESV (ml) 110.4±24.7 83.1±23.0*

RV EDV/FFM (ml.g-1)‡ 2.63[0.72] 2.78[0.62]

RV ESV/FFM (ml.g-1)‡ 1.27[0.37] 1.15[0.37]

LV SV(ml) 122±13 117±16

LV EF (%) 61±3 63±3

RV SV (ml) 115±19 117±18

RV EF (%) 51±4 59±5†

Fibrosis Negative Negative

LV=Left Ventricle, EDV=End-diastolic Volume, ESV=End-systolic volume, SV=Stroke Volume, EF=Ejection

Fraction, LVM= Left Ventricular Mass, RV=Right ventricle, WT= Wall thickness, FFM= Fat-free mass,

*p<0.05, †p<0.005 ‡Data given as median [interquartile range].

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Table 4. Echocardiographic data for AS and NAS groups (data are mean ± SD).

Measure AS Non-AS

E (m.s-1) 0.67±0.11 0.77±0.20

A (m.s-1) 0.54±0.10 0.38±0.61†

E:A‡ 1.31[0.50] 1.88[0.35]†

S’ (m.s-1) 0.10±0.01 0.10±0.02

E’ (m.s-1) 0.09±0.02 0.13±0.23†

A’ (m.s-1) 0.10±0.01 0.07±0.01†

E’:A’‡ 0.99[0.54] 1.78[0.46]†

E:E’‡ 7.19[1.45] 5.66[0.77]*

ε (%) -14.2±2.7 -16.6±1.9*

Peak S SR (s-1) -1.00±0.23 -1.14±0.11†

Peak E SR (s-1) 1.40±0.38 1.65±0.28

Peak A SR (s-1) 1.02±0.36 0.72±0.25*

E= Early Diastolic Filling, A= Late Diastolic Filling, E:A= Early:Late Diastolic Ratio

S’=Systolic tissue velocity, E’= Early Diastolic tissue velocity,

A’= Late Diastolic tissue velocity, E’:A’= Early:Late Diastolic tissue velocity ratio. ε = Strain, SR= Strain Rate,

*p<0.05, †p<0.005, ‡Data given as median [interquartile range].

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Table 5. Correlation coefficients of cardiac parameters with number of years of AS and mean weekly AS dose

when ‘On’ cycle.

Measure Years of AS Use Weeks AS use/year

LVM/FFM (g/ffm-1) -.290 (p=.361) .007 (p=.982)

LV-EF (%) -.076 (p=.813) -.224 (p=.484)

RV-EF (%) -.037 (p=.914) .369 (p=.265)

E:A -.481 (p=.114) -.147 (p=.648)

E’:A’ -.371 (p=.262) -.258 (p=0.443)

LV=Left Ventricle, RV=Right Ventricle, EF=Ejection, LVM= Left Ventricular Mass, E:A= Early:Late Diastolic Ratio, E’:A’= Early:Late Diastolic tissue velocity ratio

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