I’m 6 weeks into my cycle and until the 5th week I had thought that I was getting these very very slight heart flutters/fibrillations because of my lack of Estrogen control and after killing my estrogen levels with arimidex I realized I’m still getting them and now they’re worse. has anyone else experienced this? my blood pressure is normal and I’m getting no dizzyness or blurry vision. the dosage was 600mg for test and I’m knocking it down to 300mg from now on
You’re abnormal heart rhythm probably isn’t caused by oestrogen (or lack thereof…) though it could be as AI therapy is associated (when used for women with ER positive breast cancer) with an increased incidence of arrhythmia and pericarditis, but not myocardial infarction or all cause cardiovascular mortality… that being said when in conjunction with androgens being elevated aromatase inhibition tends to have a pronounced negative effect on lipids, thus the increase in MI risks over time would likely raise exponentially… furthermore, the beneficial effect of estrogen on endothelial functioning and AAS’s (when in very high concentrations) detrimental effect may further elict an increase in overall cardiovascular mortality rates when using AAS in conjunction with an AI…
However there are numerous mechanisms at play here. Anabolic steroids tend to induce autonomic dysfunction, sympathetic nervous system dominance. Aside from a potentially direct mechanism (very controversial, but direct AR binding in cardiac myocytes… results regarding changes in cardiac morphology and vagal tone have been induced in vitro when cardiac myocytes are exposed to massive concentrations of AAS… talking micro-molar concentration… granted X amount of test/tren/whatever equates to differing concentrations in differing tissues, I’d hypothesise the concentrations cells exposed to would be astronomical… furthermore what happens on a macro vs microbiological scale can differ wildly, antioxidant enzymes, drug elimination etc playing roles)
Sympathetic nervous system upregulation (beta adrenergic receptor upregulation) increases sensitivity at the binding site (beta adrenergic receptor) for catecholamines, AAS increase the sensitivity/bodily response to epinephrine and norepinephrine… It is well known epinephrine can induce PVC’s/PAC’s… endothelial dysfunction, alterations in cardiac morphology (cardiac enlargement) induced by anabolic steroids can predispose an individual to lethal arrhythmia. Should be noted the cardiac enlargement is potentially permanent (if it occurs) and exponentially increases the chance of HF as one gets older.
will lowering the dose help? Perhaps, perhaps not… for someone with pre-existing autonomic dysfunction such as myself, these side effects induced by AAS can be irritating. I very rarely get premature ventricular contractions (or at least very rarely notice them), for me this typically manifests as an inappropriately high resting heart rate when going from sitting to standing (absent of an increase in BP), somewhat delayed HR recovery post exercise etc. Beta blockers help tremendously, though I take them to aid with generalised anxiety, they help this aspect tremendously (by acting on the receptor sites of which epinephrine and norepinephrine bind to), if you’re just worried about cardiac dysthymia or fast HR second generation cardioselective beta blockers are more relevant… for anxiety (if you’re prone) first gen beta blockers do a better job as they bind to beta adrenergic receptors all over the body (but will deleteriously impact sub maximal exercise capacity)… but both do a fairly good job at extinguishing the physiological effects of anxiety
What would definitely help… for certain… is going off entirely
The fact that you thought you were getting arrhythmias due to estrogen is astounding… shows the level of demonisation this hormone has unfairly copped within society. If anything it would’ve exerted a deterrant/protective mechanism against them
Furthermore if you’ve got an undiagnosed cardiac defect (everyone should get screened before using AAS, but since the ignorance is so large regarding ignoring/simply not knowing about the risks involved, many don’t even go as far as to get bloodwork) then AAS would/could make a previously asymptomatic defect unbearable, that or the incredibly unlikely scenario in which you’ve developed a cardiomyopathy from one cycle (this is like… unheard of…)
1 Like
first of all thank you for putting in the time for this well thought out response and after reading it I’m almost certain that I need to drop the gear. I even got myself an appointment with the cardiologist for today. I will be very open with my AAS use. I honestly don’t want anything to do with this anymore
1 Like