Transcript AAS gvj
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 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 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 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 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”