Quote Originally Posted by Turkish Juicer View Post
There are no known properties of AAS themselves that would cause such process without bringing in the BP into the picture as a side effect.
That's not true, I wish it were but it's not.

Cardiac myocytes have androgen receptors that through upregulation from AAS use can directly cause thickening of the left ventricle wall.

It's not fully understood how hypertrophy can occur without the necessary resistance (high BP) but it is documented.




Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes
James D. Marsh, MD; Michael H. Lehmann, MD; Rebecca H. Ritchie, PhD; Judith K. Gwathmey, VMD, PhD; Glenn E. Green, MD; ; Rick J. Schiebinger, MD
From the Program in Molecular and Cellular Cardiology, Departments of Medicine and Otolaryngology, Harper Hospital, Detroit, Mich; the VA Medical Center, Boston University Medical Center, Boston, Mass (J.K.G.); and the Arrhythmia Center/Sinai Hospital (M.H.L.) and Wayne State University School of Medicine, Detroit, Mich (J.D.M.).
Correspondence to James D. Marsh, MD, Wayne State University School of Medicine, 421 E Canfield Ave, Detroit, MI 48201. E-mail [email protected]


Abstract
Background—The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain. Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response.

Methods and Results—We used reverse transcription–polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [3H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion.

Conclusions—Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.

Here's the full report. http://circ.ahajournals.org/content/98/3/256.full

And again here. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1768197/