Agreed. And I think this answers the spirit of the OPs question. But heart disease (of any type) is
secondary to everything you just mentioned.
For example, my father is 85 now. His cholesterol and triglycerides have been absolutely Polak horrendous for at least 40 years (probably all his life). So there is definitely a hereditary/genetic component here as well. My mother is 82. Hers is bad, too.
LVH isn't caused directly by steroids because LVH is found in non-bodybuilders as well. Same with hypertension and estrogen problems. Hypertension is the most common but it's not caused by the action of the heart either.
Need
@Type-IIx to maybe describe what steroids attach to heart muscle receptors because I'm not certain. That would be the key.
So what most of us do, is work to prevent high LDL, hypertension, etc which can lead to heart disease. Even doing so, is absolutely no guarantee.
But at this point, I'm not aware of any steroidal compound that directly affects the heart. Definitely cause health conditions that put the heart at risk, though.
True, besides increasing CV event/CVD risk by indirectly promoting atherosclerosis, dyslipidemia, & pressure-induced LVH, there are also other factors that include:
Endothelial cell dysfunction (effects on the vascular endothelium [including by action on the RAAS]): AR is expressed in both endothelial & vascular smooth muscle cells. Through its rapid nongenomic pathways (e.g., PKA, PKC, MAPK), AAS can stimulate rapid vasoconstriction via endothelium-dependent & -independent mechanisms. Testosterone increases renin levels & expression/activity of ACE & AT1R, while downregulating AT2R, thereby favoring a vasoconstrictor pathway & enhances vascular responsiveness to Ang II. AAS may modulate development & maintenance of Ang II-induced hypertension & increase vascular contractility to pressors...
Variously, direct harmful cardiac effects of AAS include myocyte apoptosis, effect on electrolyte channels and their associated proteins of the cardiac cells, shifts in the redox balance towards more oxidative stress, changes in the ionotropic response to adrenergic activity.
There are some particularized harms to AAS that antagonize the MR (e.g., Tren), inhibiting the aldosterone-induced absorption of Na⁺ in the kidneys. The principal consequences of MR antagonism are electrolyte disturbances and the development of hypertension and cardiovascular disease.
And similarly, AAS that inhibit 11β-HSD2 (mediating cortisol oxidation), e.g., Test, Halo, Anadrol, have particularized cardiac harms. 11β-HSD2 is an enzyme that controls the oxidation of cortisol. Its inhibition leads to glucocorticoid-mediated MR activation, potassium excretion, sodium and water retention, and increased blood pressure.
So generally, AAS with relative "flatness" or lacking "bulk," slide into the AR in a knife-like manner, but have broad homology for other nuclear receptors, including the MR; any effect on the MR by AAS is going to cause problems.
Generally, less potent, straightforwardly AR agonistic AAS (e.g., no effects on glucocorticoids, no effects on autocrine/paracrine IGF-I responsiveness) are relatively "heart healthy," i.e., those whose dose/response for increasing LBM are subject to a sigmoidal S-curve (e.g., Primo, Mast).