Sorry I never got around to posting my own experiences with this! Anyway, it doesn't matter now. Someone on /r/Nootropics has been hospitalized for possible heart damage after combining hydrafinil with some other (mild) stimulants.
As they say on 30 Rock: shut it down.
he had a bout of sympathetic overstimulation. this causes myocardial oxygen demand ischaemia, which is not rare. A sustained tachycardia would do that. I don't see why he was placed on aspirin and maintained on it after discharge. I guess they erred on the side of caution and treated him as an acute coronary syndrome. I'd love to know if he was placed on the full acute coronary syndrome cocktail of anticoagulants (heparin, clopidogrel)
I bet his ecg showed no signs of ischemia, and if he did a nuclear scan, I am positive it will be completely normal. What happened isn't due to something inherent to hydrafanil. It is probably just a by-product of sympathetic overstimulation which can occur with any stimulant.
Sorry I never got around to posting my own experiences with this! Anyway, it doesn't matter now. Someone on /r/Nootropics has been hospitalized for possible heart damage after combining hydrafinil with some other (mild) stimulants.
As they say on 30 Rock: shut it down.
he had a bout of sympathetic overstimulation. this causes myocardial oxygen demand ischaemia, which is not rare. A sustained tachycardia would do that. I don't see why he was placed on aspirin and maintained on it after discharge. I guess they erred on the side of caution and treated him as an acute coronary syndrome. I'd love to know if he was placed on the full acute coronary syndrome cocktail of anticoagulants (heparin, clopidogrel)
I bet his ecg showed no signs of ischemia, and if he did a nuclear scan, I am positive it will be completely normal. What happened isn't due to something inherent to hydrafanil. It is probably just a by-product of sympathetic overstimulation which can occur with any stimulant.
Even if you're right that this "can occur with any stimulant," the question is whether we should consider hydrafinil in particular "safe," even though a moderate quantity of hydrafinil + moderate quantity of another stimulant + physical activity = "sympathetic overstimulation" and a trip to the hospital. If the two stimulants in question were, e.g., caffeine and nicotine, there wouldn't have been a hospital visit and we wouldn't be having this discussion. That's why I consider those substances safe.
P.S. The Mayo Clinic says that myocardial ischemia "can damage your heart muscle, reducing its ability to pump efficiently." Do we know whether this statement is equally valid for ischemia caused by a stimulant and for ischemia caused by heart disease?
Mayo Clinic is referring primarily to ischemic cardiomyopathy secondary to coronary vessel disease. This is completely different to what the OP of the reddit post suffered. His troponin bump is most likely demand ischemia, secondary to increased workload on the heart via sympathetic stimulation. His condition would probably have resolved on his own without much sequelae. Had his palpitations persisted, he would risk developing a tachycardia induced cardiomyopathy, which is enlargement of the heart (especially the left side) but it is unlikely that his palpitations would have persisted after he completely clears the stimulants from his system.
Troponin bump does not equal heart attack. A heart attack requires ECG changes, typical pain patterns, and a troponin rise. He only fulfils one of the 3 (you need at least two) and his troponin bump is mild, and has settled within two to three days (half-life of troponin is 7-10 days) which indicates that he had a minor leak (insignificant damage) due to increased workload.
I am not saying I am positive that he is fine (but I'm willing to bet money that a nuclear scan would be negative) and I am glad he went to the hospital (everyone who suspects something is not quite right, should immediately go to the hospital). I am just saying what most likely happened. Anyways, erring on the safe side, keep your doses ultra low, take serial measurements of your heart rate and BP, or just don't take it.
I would have to disagree. What you are refering to is what anesthesiologists know as the difference between type I and type II myocardial ischaemia.
Type I is the atherosclerotic patient presenting to ER with chest pain, ST segment modification on EKG, troponin elevation. The mechanism is vulnerable plaque rupture inducing thrombosis, the damage is vascular, this is what in France we call "infarctus" (i don't know if in English the term infarction is strictly equivalent, or if infarction is general term for all types of ischaemia).
Type II is haemodynamic or hypoxic type. This is not always a known coronary patient, with moderate coronary stenosis that can be asymptomatic. During general anesthesia, especially in haemorragic surgery, arterial hypotension and anemia induce a decreased blood flow to the coronary vessels, especially if a moderate stenosis is present. Sympathetic reaction to tissular hypoperfusion induce tachycardia that increase myocardial oxygen consumption, further widening the gap between myocardial oxygen demand vs delivery. This mechanism, ishaemia without thrombosis is called "apoplexie" in french.
Both are ACS, and both need aspirin therapy, betablochers, conversion enzyme inhibitors, and an emergent coronarography. I honestly don't think a healthy adult can develop a Type II ischaemia because of isolated tachycardia. There need to be a severe coronary stenosis, that would have been symptomatic, or he must be deeply anaemic or hypoxic.
Troponin elevation consequent to stimulant induced tachycardia is an acute coronary syndrom to but in don't think you can relate it to type I or II ishaemia. It is obviously a NSTEMI (non ST elevation myocardial infarction) due to coronary spasm (like in Prinzmetal's). Toxic coronary spasms were described in mephedrone abusers. Mephedrone seems to be a very potent vasoconstrictor, and a few rave party lovers with several severed fingers can attest that.
If this compound could induce coronary spasms, that would be a great reason to just pack it in a giant dong shaped gelcap and feed it to whoever sold it to you. But i find strange a compound lacking the powerful stimulant and euphoric nature of mephedrone could be an equally powerful vasoconstrictor. This said, if a guy who never had a chest pain before took this compound and had a NSTEMI, just dump this shit already, it is not worth the risk!
Ceretropic always has a message under its compounds saying : Not for human consumption.
Under Hydrafinil, it has a second message written in red saying : look guys, we REALLY don't know where we're going with this one, so even if we know you are going to eat this dope, we want to make clear we do not encourage you to do this. Except that we sell it of course...
There must be something dodgy with this one.
One last thing : Troponin elevation is never to be banalized by saying : "it is myocardial suffering, but no need to panic". In large studies in postoperative patients with troponin elevation, the group of patients in which doctors didn't aggressively manage it (aspirin, clopidogrel, betablockers, statins...) had a dramatically lower survival than the group where the treatment was optimized to the maximum extent. In the optimized group, the survival rate was similar to patients without troponin elevation.
Keep in mind it is in predominantly type II ischaemia, the difference must be even greater in NSTEMI (stimulant abuse or not). If you go to ER for chest pain, and your troponin is elevated, but the doctor says "well, that's nothing", punch him in the face and go see another doctor quick.
PS : I want to make clear that what i said about Ceretropic is to be taken as a joke. I have no problem with this company that seems serious and reputable.
Edited by ataraxis, 22 January 2015 - 12:47 PM.
