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