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HARTVERSAKING IN
LANGTERMYN
ANABOLIESE STEROIED
GEBRUIK
Dr. Gawie van
Jaarsveld
PASIENT GEVAL
45jr manlike pasient
Amateur Body builder
Kompetisie deelname ouderdom 30jr tot 35jr
Anaboliese
Geen verdere inligting ivm tiepe of hoeveelheid anaboliese
steroied in gesk
 Presenteer met klagte en simtome van CCF
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 Pulmunale edeem
 Puttende pedale edeem en veneuse ontoereikenheid
 Verhoode JVP, sagte en muffled hartklanke
PASIENT GEVAL
 Spesiale ondersoeke: Geen agv die inperking van mediese
fonds
 Begin op enalapril, furosemied en kort kursus van topikale
hidrokortizoon vir veneuse stase ekseem
INDEX
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Oorsig oor AAS
Cardiovascular ef fects of AAS
Take Home messages
Bronnelys
ANABOLIC STEROID
 Testicular hormone 1935
 Androgen and anabolic effect
 Molecule adjust for maximal anabolic effect
 Anabolic effect via increased protein synthesis
 Increased aggressive behavior
 Performance enhancing
 2 nd WW
 1954 weight lifting championships Russian national team
 1976 Olympic games declared banned substances
 Massive industry
ANABOLIC STEROID
 World anti-Doping Agency(WADA)
 Anabolic Agent
 Exogenous AAS
 Endogenous AAS
 Use
 PO, IM, Nasal spry, gels, bucale tablet
 10 to 100 times the normal therapeutic dose
 Cycling, Pyramid stacking
CARDIOVASCULAR
Ef fects of AAS on the CVS can be divided into:
 direct effects of the androgens
 Vasculature
 myocardium
 indirect effects via
 alteration in clotting profile
 Lipids
CARDIOVASCULAR
Direct effects
 Vasculature
 Blood pressure
 Endothelium
 Heart
 rhythm
 morphology
 function
Indirect effects
 thrombotic profile
 lipids
CARDIOVASCULAR
DIRECT EFFECTS
VASCULATURE
Hypertension
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AAS abuse and hyper tension is controversial
Systolic and diastolic increase
Transient
AAS renal retention of sodium
Blood pressure response to AAS abuse dose related
Additional studies are necessar y to definitively reveal a link
between AAS and blood pressure
CARDIOVASCULAR
DIRECT EFFECTS
VASCULATURE
Abnormal endothelial function
 impaired endothelial reactivity (vasodilatation and
vasoconstriction)
 bodybuilders currently using AAS vs previous users and non-users
 Reversible
CARDIOVASCULAR
DIRECT EFFECTS
CARDIAC
 Abnormal cardiac rhythm: cardiac arrhythmias
 atrial fibrillation; small risk; reversible
 ventricular fibrillation; small risk; reversible
 “ Alarming data have linked AAS with fatal events, although these
are mostly case-control studies and case reports of acute coronary
syndromes, MIs, and ventricular arrhythmias (Suraj Achar, 2010)”
CARDIOVASCULAR
DIRECT EFFECTS
 CARDIAC
 Abnormal cardiac function
 ventricular dysfunction
 echocardiographic study: systolic and diastolic dysfunction
related to dose and duration of AAS use
 compromised left ventricular contractile function
 Alterations ventricular relaxation
 ?Ventriculêre hypertrofie
CARDIOVASCULAR
DIRECT EFFECTS
 CARDIAC
 Abnormal cardiac morphology
 ventricular hypertrophy and dilatation
 septal and left ventricular hypertrophy (may persist)
 increase of heart chamber diameters
 LVH resistance training in the absence of AAS use
 AAS-use associated with
 larger ventricular volume and wall mass
 systolic dysfunction and impaired ventricular inflow
 Reverses after discontinuation
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persistent effects for a prolonged period
CARDIOVASCULAR
INDIRECT EFFECTS
PRO-THROMBOTIC STATE
AAS enhanced pro-thrombotic (hyper-coagulable) state:
 polycythaemia
 increase in platelet aggregability
 increase of thromboxane A2 and/or
 decrease of prostaglandin PgI2
 effects on the coagulation cascade
 17α-alkylated steroids (primarily from oral ingestion)
highest risk of thrombus formation
CARDIOVASCULAR
INDIRECT EFFECTS
ATHEROGENIC LIPID PROFILE
 Increases of LDL and decreases of HDL,
 increasing the risk of CAD
 increase hepatic lipase activity, contributing to dyslipidemia
 Increase LDL levels 20%, decrease HDL levels by 20% to 70%.
 Reversible
 normalize 5 months after discontinuation
 Longer effect than expected from half-lives of AAS agents
CARDIOVASCULAR
SUDDEN DEATH/MYOCARDIAL INFARCTION
2 major patterns found on autopsy:
 Normal coronary arteries and no thrombosis : non -thrombotic
 Normal coronary arteries and thrombosis : thrombosis
 MI secondary to ischaemia
 increased oxygen demand ? LVH
 decreased supply, e.g. coronary artery spasm, coronary embolism,
anaemia, arrhythmias, hypertension, or hypotension
CARDIOVASCULAR
SUDDEN DEATH/MYOCARDIAL INFARCTION
Normal coronary arteries and no thrombosis: non thrombotic
 Autopsy finding: hypercontracted, eosinophilic cardiac myocytes
with disruption of myofibrillar structure
 a hypercontracted myocardium
 manifestation of increased sympathetic activity
 androgens enhance the pressor response to catecholamines
CARDIOVASCULAR
SUDDEN DEATH/MYOCARDIAL INFARCTION
Normal coronary arteries and thrombosis:
 pro-thrombotic state
 abnormal endothelial reactivity
 Arrhythmias
TAKE HOME MESSAGE
 Persistent cardiovascular changes
 myocardial hypertrophy and ventricular dysfunction
 Atherosclerosis
 Lipied
 Increased risk for CVS disease and sudden death: MI and
stroke
 Tim Noakes preformance driven society
BRONNELYS
 Hageman, G(2012). “SIDE EFFECTS OF AAS”
 Brunker & Khan’s. Clinical Spor ts medicine 4 th ed
 Hamid Reza(2011) “Cardiac hypertrophy in deceased users of
anabolic androgenic steroids: an investigation of autopsy
finding”
 Tim Luijkx() “Anabolic androgenic steroid use is associated with
ventricular dysfunction on cardiac MRI in strength trained
athletes.”
 Suraj Achar, MD(2010) “Cardiac and Metabolic Ef fects of
Anabolic- Androgenic Steroid Abuse on Lipids, Blood Pressure,
Left Ventricular Dimensions, and Rhythm”