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).
Originally Posted by Steveoph
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.Pharmacol Res. 2011 Apr;63(4):300-7. Epub 2010 Dec 28.
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.
Fish oil decreases inflammation and reduces cardiac remodeling in rosiglitazone treated aging mice.
Halade GV, Williams PJ, Lindsey ML, Fernandes G.
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. email@example.com
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.
Division of Cardiology, Department of Medicine, University of Maryland-Baltimore, 20 Penn Street, Baltimore, MD 21201, USA.
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