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Dr. Gawie van Jaarsveld
HARTVERSAKING IN LANGTERMYN ANABOLIESE
STEROIED GEBRUIK
45jr manlike pasientAmateur Body builderKompetisie deelname ouderdom 30jr tot 35jrAnaboliese Geen verdere inligting ivm tiepe of hoeveelheid anaboliese
steroied in geskPresenteer met klagte en simtome van CCF
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
PASIENT GEVAL
Oorsig oor AASCardiovascular effects of AASTake Home messagesBronnelys
INDEX
Testicular hormone 1935
Androgen and anabolic effect Molecule adjust for maximal anabolic effect Anabolic effect via increased protein synthesis Increased aggressive behavior
Performance enhancing 2nd 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
ANABOLIC STEROID
CARDIOVASCULAR
Effects 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 profilelipids
CARDIOVASCULARDIRECT EFFECTS
VASCULATURE
Hypertension
AAS abuse and hypertension is controversial Systolic and diastolic increase Transient AAS renal retention of sodium Blood pressure response to AAS abuse dose related Additional studies are necessary to definitively reveal a link between
AAS and blood pressure
VASCULATURE
Abnormal endothelial function
impaired endothelial reactivity (vasodilatation and vasoconstriction) bodybuilders currently using AAS vs previous users and non-users
Reversible
CARDIOVASCULARDIRECT EFFECTS
CARDIOVASCULARDIRECT 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)”
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
CARDIOVASCULARDIRECT 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 persistent effects for a prolonged period
CARDIOVASCULARDIRECT EFFECTS
CARDIOVASCULARINDIRECT 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
CARDIOVASCULARINDIRECT 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
CARDIOVASCULARSUDDEN DEATH/MYOCARDIAL INFARCTION
2 major patterns found on autopsy:Normal coronary arteries and no thrombosis : non-thromboticNormal 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
CARDIOVASCULARSUDDEN 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
CARDIOVASCULARSUDDEN DEATH/MYOCARDIAL INFARCTION
Normal coronary arteries and thrombosis:
pro-thrombotic stateabnormal endothelial reactivityArrhythmias
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
TAKE HOME MESSAGE
Hageman, G(2012). “SIDE EFFECTS OF AAS”
Brunker & Khan’s. Clinical Sports medicine 4th 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 Effects of Anabolic-Androgenic Steroid Abuse on Lipids, Blood Pressure, Left Ventricular Dimensions, and Rhythm”
BRONNELYS