Attenuation/Reversal of AAS induced LVH

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    Attenuation/Reversal of AAS induced LVH


    Just had this question pop up after reading the thread here and my post here

    Was wondering what your thoughts on are BP meds by bodybuilders and AAS users for the prevention of LVH. It was hard to find research relating specifically to attenuation of LVH by AAS, but most studies stated there was no ventricular dysfunction and there was a degree of reversibility.

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    Quote Originally Posted by Steveoph View Post
    Just had this question pop up after reading the thread here and my post here

    Was wondering what your thoughts on are BP meds by bodybuilders and AAS users for the prevention of LVH. It was hard to find research relating specifically to attenuation of LVH by AAS, but most studies stated there was no ventricular dysfunction and there was a degree of reversibility.
    Admittedly, I have not read the thread in length yet,...however, in immediate response to your statement above...I gave a lecture on this very topic at 2010's ISSN meeting and I want to start by saying that cardiac remodeling OUTSIDE of hypertension is very prevelant with AAS use. But LVH secondary to hypertension (as such is seen most often with progestin-based and nandralone species) benefits most from a 2-week almost pre-cycle phase to adequately control BP...(and I see your physician accounts for it; although a setup that includes HCTZ which is only a 4-6 hour length of effective action I don't care for and atenolol would be my last choice for beta-blockade and is sometimes tricky in an athelete because of already existent relative bradycardia).


    From a histopathologic standpoint, it approximates that of dilated cardiomyopathy with overt cardiac hypertrophy. In fact, extended to autopsy report myocardial biopsy samples, this may progress to overt cardiac fibrosis.

    That all said...this appears to be VERY dose and length of cycle dependent.

    Now, there are several case reports that extend to ventricular arrhythmias and acute myocardial infarction, but you certainly won't get a study populace large enough to likely quench your thirst for obvious reasons. Some case studies you may be interested in:

    Sullivan ML, et al. Atrial Fibrillation and Anabolic Steroids. J Emerg Med. 17(5): 851-857, 1999.

    McNutt, et al. Acute myocardial infarction in a 22 year old world class weight lifter using anabolic steroids. Am J Cardiol. 62: 164, 1988.
    Ferrera PC, et al. Anabolic steroid use as the possible precipitant of dilated cardiomyopathy. Cardiology. 88: 218-220, 1997.

    I had those three citations from my presentation slides. There are some interesting leaps of faith we could imply from cross-over cardiomyopathy data and cardiac remodeling data with fish oil. Understand it is not AAS, but again...there is reason and you will likely never see it because it's a study that one - would never be funded, and two - is shrouded in secret due to AAS use, so power to a study would effectively be nil.

    Pharmacol Res. 2011 Apr;63(4):300-7. Epub 2010 Dec 28.
    Fish oil decreases inflammation and reduces cardiac remodeling in rosiglitazone treated aging mice.

    Halade GV, Williams PJ, Lindsey ML, Fernandes G.
    Source

    Division of Clinical Immunology and Rheumatology, Department of Medicine, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, TX 78229-3900, USA. halade@uthscsa.edu

    Abstract

    Clinical studies suggest that rosiglitazone (RSG) treatment may increase the incidence of heart failure in diabetic patients. In this study, we examined whether a high corn oil diet with RSG treatment in insulin resistant aging mice exerted metabolic and pro-inflammatory effects that stimulate cardiac dysfunction. We also evaluated whether fish oil attenuated these effects. Female C57BL/6J mice (13 months old) were divided into 5 groups: (1) lean control (LC), (2) corn oil, (3) fish oil, (4) corn oil+RSG and (5) fish oil+RSG. Mice fed a corn oil enriched diet and RSG developed hypertrophy of the left ventricle (LV) and decreased fractional shortening, despite a significant increase in total body lean mass. In contrast, LV hypertrophy was prevented in RSG treated mice fed a fish oil enriched diet. Importantly, hyperglycemia was controlled in both RSG groups. Further, fish oil+RSG decreased LV expression of atrial and brain natriuretic peptides, fibronectin and the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-α, concomitant with increased interleukin-10 and adiponectin levels compared to the corn oil+RSG group. Fish oil+RSG treatment suppressed inflammation, increased serum adiponectin, and improved fractional shortening, attenuating the cardiac remodeling seen in the corn oil+RSG diet fed C57BL/6J insulin resistant aging mice. Our results suggest that RSG treatment has context-dependent effects on cardiac remodeling and serves a negative cardiac role when given with a corn oil enriched diet.
    Copyright 2011. Published by Elsevier Ltd.

    PMID:21193042[PubMed - indexed for MEDLINE]

    Hypertension. 2009 Sep;54(3):605-11. Epub 2009 Jul 13.
    The cardioprotective effects of fish oil during pressure overload are blocked by high fat intake: role of cardiac phospholipid remodeling.

    Shah KB, Duda MK, O'Shea KM, Sparagna GC, Chess DJ, Khairallah RJ, Robillard-Frayne I, Xu W, Murphy RC, Des Rosiers C, Stanley WC.
    Source

    Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, 20 Penn Street, Baltimore, MD 21201, USA.

    Abstract

    Supplementation with eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) from fish oil may prevent development of heart failure through alterations in cardiac phospholipids that favorably impact inflammation and energy metabolism. A high-fat diet may block these effects in chronically stressed myocardium. Pathological left ventricle (LV) hypertrophy was generated by subjecting rats to pressure overload by constriction of the abdominal aorta. Animals were fed: (1) standard diet (10% of energy from fat), (2) standard diet with EPA+DHA (2.3% of energy intake as EPA+DHA), (3) high fat (60% fat); or (4) high fat with EPA+DHA. Pressure overload increased LV mass by approximately 40% in both standard and high-fat diets without fish oil. Supplementation with fish oil increased their incorporation into cardiac phospholipids, and decreased the proinflammatory fatty acid arachidonic acid and urine thromboxane B(2) with both the standard and high-fat diet. Linoleic acid and tetralinoloyl cardiolipin (an essential mitochondrial phospholipid) were decreased with pressure overload on standard diet, which was prevented by fish oil. Animals fed high-fat diet had decreased linoleic acid and tetralinoloyl cardiolipin regardless of fish oil supplementation. Fish oil limited LV hypertrophy on the standard diet, and prevented upregulation of fetal genes associated with heart failure (myosin heavy chain-beta and atrial natriuetic factor). These beneficial effects of fish oil were absent in animals on the high-fat diet. In conclusion, whereas treatment with EPA+DHA prevented tetralinoloyl cardiolipin depletion, LV hypertrophy, and abnormal genes expression with pressure overload, these effects were absent with a high-fat diet.

    PMID:19597033[PubMed - indexed for MEDLINE] PMCID: PMC3103889









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    Cardiovasc Res. 2009 Feb 1;81(2):319-27. Epub 2008 Nov 17.
    Fish oil, but not flaxseed oil, decreases inflammation and prevents pressure overload-induced cardiac dysfunction.

    Duda MK, O'Shea KM, Tintinu A, Xu W, Khairallah RJ, Barrows BR, Chess DJ, Azimzadeh AM, Harris WS, Sharov VG, Sabbah HN, Stanley WC.
    Source

    Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, 20 Penn Street, HSF2, Room S022, Baltimore, MD 21201, USA.

    Abstract

    AIMS:

    Clinical studies suggest that intake of omega-3 polyunsaturated fatty acids (omega-3 PUFA) may lower the incidence of heart failure. Dietary supplementation with omega-3 PUFA exerts metabolic and anti-inflammatory effects that could prevent left ventricle (LV) pathology; however, it is unclear whether these effects occur at clinically relevant doses and whether there are differences between omega-3 PUFA from fish [eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] and vegetable sources [alpha-linolenic acid (ALA)].
    METHODS AND RESULTS:

    We assessed the development of LV remodelling and pathology in rats subjected to aortic banding treated with omega-3 PUFA over a dose range that spanned the intake of humans taking omega-3 PUFA supplements. Rats were fed a standard food or diets supplemented with EPA+DHA or ALA at 0.7, 2.3, or 7% of energy intake. Without supplementation, aortic banding increased LV mass and end-systolic and -diastolic volumes. ALA supplementation had little effect on LV remodelling and dysfunction. In contrast, EPA+DHA dose-dependently increased EPA and DHA, decreased arachidonic acid in cardiac membrane phospholipids, and prevented the increase in LV end-diastolic and -systolic volumes. EPA+DHA resulted in a dose-dependent increase in the anti-inflammatory adipokine adiponectin, and there was a strong correlation between the prevention of LV chamber enlargement and plasma levels of adiponectin (r = -0.78). Supplementation with EPA+DHA had anti-aggregatory and anti-inflammatory effects as evidenced by decreases in urinary thromboxane B(2) and serum tumour necrosis factor-alpha.
    CONCLUSION:

    Dietary supplementation with omega-3 PUFA derived from fish, but not from vegetable sources, increased plasma adiponectin, suppressed inflammation, and prevented cardiac remodelling and dysfunction under pressure overload conditions.

    PMID:19015135[PubMed - indexed for MEDLINE] PMCID: PMC2721645
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    Lipids. 2001;36 Suppl:S111-4.
    Myocardial membrane fatty acids and the antiarrhythmic actions of dietary fish oil in animal models.

    McLennan PL.
    Source

    Smart Foods Centre, Department of Biomedical Science, University of Wollongong, NSW, Australia. petermcl@uow.edu.au

    Abstract

    Epidemiologic studies, animal studies, and more recently, clinical intervention trials all suggest a role for regular intake of dietary fish oil in reducing cardiovascular morbidity and mortality. Prevention of cardiac arrhythmias and sudden death is demonstrable at fish or fish oil intakes that have little or no effect on blood pressure or plasma lipids. In animals, dietary intake of fish oil [containing both eicosapentaenoic acid (EPA, 20:5n-3) and docosahexaenoic acid (DHA, 22:6n-3)] selectively increases myocardial membrane phospholipid content of DHA, whereas low dose consumption of purified fatty acids shows antiarrhythmic effects of DHA but not EPA. Ventricular fibrillation induced under many conditions, including ischemia, reperfusion, and electrical stimulation, and even arrhythmias induced in vitro with no circulating fatty acids are prevented by prior dietary consumption of fish oil. The preferential accumulation of DHA in myocardial cell membranes, its association with arrhythmia prevention, and the selective ability of pure DHA to prevent ventricular fibrillation all point to DHA as the active component of fish oil. The antiarrhythmic effect of dietary fish oil appears to depend on the accumulation of DHA in myocardial cell membranes.

    PMID:11837983[PubMed - indexed for MEDLINE]
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