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Some thoughts on AAS and Cardiovascular health

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There is much debate regarding AAS and cardiovascular health, and how that use may have negatively impacted major organs and tissue of the body.?


Several studies show that high doses of AAS such as nandrolone, may lead to growth-promoting effects on cardiac tissue, as seen in hypertrophic cardiomyopathy, followed by apoptotic cell death which is mediated by membrane-receptor second messenger cascades that increase intracellular Ca2+ influx..


AAS abuse associated with sudden cardiac death, myocardial infarction, ventricular remodelling and cardiomyopathy is related to apoptosis..


Several studies in isolated human myocytes have shown that AAS bind to androgen receptors and may directly cause hypertrophy, via tissue upregulation of the renin-angiotensin system..


AAS abuse causes decrease in high density lipoprotein cholesterol by 20% and increase in LDL cholesterol by 20% due to lipolytic degradation of lipoproteins and their removal by receptors through modification of apolipoprotein A-I and B synthesis. Apolipoprotein B has been experimentally linked to the development of atherosclerosis, mediating the interaction between LDL-C and the arterial wall...


These lipoprotein abnormalities increase the risk for coronary artery disease by three to sixfold and may occur within 9 weeks of AAS self-administration. Fortunately, lipid effects seem to be reversible after discontinuation..


AAS enhance platelet aggregation and thrombus formation by increasing platelet production of thromboxane A2, decreasing production of prostacyclin and increasing fibrinogen levels..


Ischaemic stroke can occur as a result of atherothrombosis or embolisation either in the carotids or the heart as AAS has been associated with changes in vascular reactivity, lipid profile, haemostasis and platelet aggregation. Accordingly, peripheral vascular disease can occur through the same mechanism..


I know I keep bringing up these cardiovascular issues on here periodically, but so few people consider them, and it really is worth having some awareness and an idea of how to ameliorate effects where possible...


However I think the take-home message is how all these vectors interact to cause serious health problems.


So, it's not just factors like lipids that cause clots - it's the platelet aggregation as the more acute factor. But furthermore, the AAS causing inflexibility of the vascular network (poor vasoreactivity) which promotes atherosclerotic plaque formation and makes the heart pump harder = the enlargement of the heart = inefficient pumping = reduced ejection fraction = relatively stagnant eddies of blood = increased risk of clotting.


And of course, is the likely increase in PCV (red blood cell concentration), which can be an equally important factor. It seems astonishing that most AAS users don't seem to be aware of the effect AAS have on RBCs and how that could aggravated their condition, but again that's part of the general lack of knowledge I keep referring to.


What can we do: fortunately, the lipid/thrombus issue is more of an acute concern that diminishes once the cycle is over, and for most people will pass unremarkably assuming they lead an otherwise healthy lifestyle and don't abuse high-dose AAS for prolonged periods..


Most guys on AAS should be using an angiotensin receptor blocker as standard in my opinion (eg Losartan, Olmesartan). Not only will it lower BP, it also prevents and reverses the accumulation of fibrotic tissue, both in the heart and across the cardiovascular system, which is the major concern from AAS use.


Cardio: The kind of adaptations we want in the heart are the kind that high intensity cardio bring. It can basically 'enlarge' the capacity of the heart (the chambers) and also improve the ejection fraction. So the heart becomes more efficient per beat, and hence the pulse rate tends to fall - very low in very fit athletes. It does cause a very mild form of hypertrophy, but it arranges the cardiac tissue structurally slightly differently to the type that forms from heavy weight lifting.


One of the other positives of HIIT is that it helps to stretch and (theoretically) break up the scarring/fibrotic tissue. We have to bear in mind that intense cardio pumps very large volumes of blood through the heart (unlike weights) which causes a nice eccentric stretch to the cardiac tissue, as opposed to more concentric-focus from weights...


Regular blood tests, and blood donation or venesection if hematocrit is too high..


[1] J. Payne, P.J. Kotwinski, H.E. Montgomery, Cardiac effects of anabolic steroids, Heart 90 (2004) 473?475.


[2] S. Nottin, L.-D. Nguyen, M. Terbah, P. Obert, Cardiovascular effects of androgenic anabolic steroids in male bodybuilders determined by tissue Doppler imaging, Am. J. Cardiol. (2006).


[3] L. Fanton, D. Belhani, F. Vaillant, A. Tabib, L. Gomez, J. Descotes, et al., Heart lesions associated with anabolic steroid abuse: comparison of post-mortem findings in ath- letes and norethandrolone-induced lesions in rabbits, Exp. Toxicol. Pathol. (2009).


[4] P.D. Thompson, A. Sadaniantz, E. Cullinane, K. Bodziony, D. Catlin, G. Torek-Both, et al., Left ventricular function is not impaired in weight-lifters who use anabolic steroids, J. Am. Coll. Cardiol. (1992) 19.


[5] N.A. Hassan, M.F. Salem, M.A.E.L. Sayed, Doping and effects of anabolic androgenic steroids on the heart: histological, ultrastructural, and echocardiographic assessment in strength athletes, Hum. Exp. Toxicol. (2009).


[6] J. Marsh, M.H. Lehmann, R.H. Ritchie, J.K. Gwathmey, G.E. Green, R.J. Schiebinger, An- drogen receptors mediate hypertrophy in cardiac myocytes, Circulation 98 (1998) 256?261.


[7] P. Liu, A.K. Death, D.J. Handelsman, Androgens and cardiovascular disease, Endocr. Rev. 24 (2003) 313?340.


[8] A.D'Andrea,P.Caso,G.Salerno,R.Scarafile,G.DeCorato ,C.Mita,et al.,Left Ventricular early myocardial dysfunction after chronic misuse of anabolic androgenic steroids: a Doppler myocardial and strain imaging analysis, Br. J. Sports Med. 41 (3) (2007) 149?155.


[9] S. Sharma, Athlete's heart?effect of age, sex, ethnicity and sporting discipline, Exp. Physiol. 88 (2003) 665?669.


[10] M. Galderisi, N. Cardim, A. D'Andrea, O. Bruder, B. Cosyns, L. Davin, et al., The multi- modality cardiac imaging approach to the Athlete's heart: an expert consensus of the European Association of Cardiovascular Imaging, Eur. Heart J. Cardiovasc. Imaging 16 (4) (2015) 353.


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Something I've been made aware of only this morning, AAS make pacemaker cells of the heart hypersensitive, leading to conditions such as SVT (supra ventricular tachycardia), which is a super fast abnormal rhythm 100-300bpm.. 

Obviously avoid stimulants..

Symptoms usually subside on their own, but consider lowering your dose or switching compounds if you start to present with SVT..





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