It is a proven medical fact that peeps who workout, e.g., weightlifting, running, sports, etc. will have the left ventricle of their hearts grow proportionally larger, due to the fact, the left ventricle is the part of the heart that works the most; it squishes the oxygenated blood out of the heart into the aorta then to the rest of the body. There hasn't been any definitive studies concerning heart growth and the use of steriods to date but logic dictates if your heart grows from all your athletic endeavor, it stands to reason that Anabolic Androgenic Steroids (AAS) will contribute also, just to what extent is unkown.
Also, growth hormone will cause all of your internal organs to grow, another a good reason to short cycle certain things.
Listen to StoneCold: he has the straight poop on heart enlargement (LVH or left ventricular hypertrophy).
Most common cause of LVH: hypertension, from any cause.
Another fairly common cause of hear muscle disease (cardiomyopathy): alcohol abuse!
Important to distinguish between cardiomyopathy ("heart-muscle-pathology"), and risk factors for coronary artery disease (inflammation, low HDL, high TG and LDL, smoking, etc). The blood vessel problems can LEAD to cardiomyopathy, but usually not direct causes.
Androgenic anabolic steroids and arterial structure and function in male bodybuilders*1
Mark A. Sader MBBS, FRACP*, , Kaye A. Griffiths, DMU*, Robyn J. McCredie BSc*, David J. Handelsman MBBS, PhD, FRACP, § and David S. Celermajer MBBS, PhD, FRACP
The study examined arterial and cardiac structure and function in bodybuilders using androgenic anabolic steroids (AAS), compared to non-steroid-using bodybuilder controls.
Adverse cardiovascular events have been reported in bodybuilders taking anabolic steroids. The cardiovascular effects of AAS, however, have not been investigated in detail.
We recruited 20 male bodybuilders (aged 35 ± 3 years), 10 actively using Anabolic Androgenic Steroids (AAS) and 10 who denied ever using steroids. Serum lipid and hormone levels, carotid intima-media thickness (IMT), arterial reactivity, and left ventricular (LV) dimensions were measured. Vessel diameter was measured by ultrasound at rest, during reactive hyperemia (an endothelium-dependent response, leading to flow-mediated dilation, FMD), and after sublingual nitroglycerin (GTN, an endothelium-independent dilator). Arterial reactivity was also measured in 10 age-matched non-bodybuilding sedentary controls.
Use of Anabolic Androgenic Steroids (AAS) was associated with significant decreases in high density lipoprotein cholesterol, sex hormone binding globulin, testosterone and gonadotrophin levels, and significant increases in LV mass and self-reported physical strength (p < 0.05). Carotid IMT (0.60 ± 0.04 mm vs. 0.63 ± 0.07 mm), arterial FMD (4.7 ± 1.4% vs. 4.1 ± 0.7%) and GTN responses (11.0 ± 1.9% vs. 14.4 ± 1.7%) were similar in both bodybuilding groups (p > 0.2). The GTN responses were significantly lower and carotid IMT significantly higher in both bodybuilding groups, however, compared with the non-bodybuilding sedentary controls (p = 0.01).
Although high-level bodybuilding is associated with impaired vascular reactivity and increased arterial thickening, the use of Anabolic Androgenic Steroids (AAS) per se is not associated with significant abnormalities of arterial structure or function.
Abbreviations: AAS, androgenic anabolic steroids; BP, blood pressure; FMD, flow-mediated dilation; FSH, follicle-stimulating hormone; GTN, sublingual nitroglycerin; HDL, high density lipoprotein; IMT, intima-media thickness; LH, luteinizing hormone; LV, left ventricle/left ventricular; SHBG, sex hormone binding globulin