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Cocaine/Cocaethylene Cardiotoxicity, what damage is done, and how reversible is it?

Vastness

Bluelight Crew
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Hello all,

I am posting this in this forum because I would like answers from a somewhat scientific perspective. I have searched but have not really had much luck finding the sort of information I am looking for.

We all know cocaine is cardiotoxic, but what exactly does this mean? As in, what changes are occurring in the heart following administration of cocaine, and how much of this (if any) is reversible?


I have tried to look into this myself, but I have no biological science background and thus almost all of the studies I've seen are not easy to interpret. I have seen this one - http://www.ncbi.nlm.nih.gov/pubmed/19463023 - referenced elsewhere on the site, but again, the explanation of the mechanisms for cocaine toxicity are lost on me.

What I am essentially asking admittedly is "How much cocaine is too much?"


I know this question is impossible to answer as everyone is different - but I would hope that there is enough information available to give some numbers that are accessible to the layperson.

Again, what changes are occurring in the heart? Are these changes immediate following a single dosing, or do they manifest with prolonged dosing? How much of this change is reversible? At what point, and following what pattern of usage, do they become irreversible? What (if any) lifestyle choices can be made to improve cardiac resilience and mitigate the aforementioned cardiotoxic damage?

Again, I would personally love to see some numbers in reference to the above questions. I know I have seemingly asked a lot of questions, but it seems to me that at the moment although everyone knows that cocaine is cardiotoxic and perhaps cardiac specialists may understand in more detail what this means, there is just very little information available in a form that everyone can understand. I know exact figures are probably impossible to give at the moment, but some sort of range would suffice.


I don't want this thread to be too focused on myself as I think the answers to the above questions would be useful to everyone who uses cocaine, but I will nonetheless include myself for example ;). I am male in my mid-twenties, otherwise in (probably) good health and who does several hours of intense cardiovascular exercise a week. I use cocaine (almost always with alcohol, I know that this is even more cardiotoxic), perhaps a little less than once a month for probably around 2 years now. Have I already irreversibly damaged my heart, and/or am I already putting myself at risk of cardiac health issues in later life?


Any responses at all would be much appreciated.
 
I could be mistaken, but the main problem is the Na channel blocking properties (local anaesthetic action, local anaesthetics are antiarrythmic agents, such as IV lidocaine, but can also CAUSE arrythmias)
 
Thanks for taking the time to respond - however, I have read similar things before, but (and I'm sure this is true for many other people as well) I honestly have no idea what exactly that means.

Why is Na channel blocking bad for the heart? Obviously we all know that cocaine significantly increases heart rate, but is the particular method by which this occurs inherently more dangerous than other stimulants? If so, why?

More importantly - how reversible is the damage that this causes?
 
The article you linked states that in the articles they reviewed there were few that could provide images of irreversible physical to the hear caused by cocaine. You might infer from that, that permanent damage from cocaine is unlikely. That does not mean it's not possible though.

F1.medium.gif
(from: http://circ.ahajournals.org/content/122/24/2558.full)

This image summarizes the effects cocaine has on the cardiovascular system. Catecholamines is collective term for dopamine, adrenaline and noradrenaline which stimulate the sympathetic nervous system (your "fight or flight" system). This increases the contractive force of the heart as well as the speed at which it pumps, hereby increasing blood pressure and demand for energy (oxygen and glucose). By constriction blood vessels less oxygen will be available to the receiving tissue.

Cocaine also activates blood platelets (the things that make your blood go solid when you've cut yourself), hereby increasing the chance of blood clots (thrombus) forming in blood vessels. When a blood clot blocks larger arteries it can prevent oxygenated blood from reaching tissue causing ischaemia. If it is not resolved quickly enough the affected tissue will die (infarction).

PQRST.png

Na+ uptake inhibition decreases contractility of the left ventricle, decreasing its output. It also increases the QRS and QT intervals of the heart action potential, which correlate with contraction and relaxation of the ventricles.

Basically cocaine places a lot of stress on the CV system, which drastically increases your chances of getting an acute heart attack or other heart problem. Increased doses and frequency of use will probably further increase the chance of something going wrong!
 
Thanks, that was the sort of response I was looking for.

Something that worries me a little though is that I read a while ago that many cocaine users have scar tissue on their heart that they don't even know about. Presumably this is not something that would be reversible, so what kind of usage pattern would be required to form this scar tissue?

I guess that these questions are difficult to answer quantitatively as everyone is different.
 
I have a question, slightly related and I wonder if anyone knows anything conclusive about this.

I read recently (from a non verifiable source) that Oxytocin (especially when released as a result of stress) counteracts damage to the heart caused by stress and repairs it (I do not know the mechanisms for this, and would assume it's highly probable that it's working on a different mechanism to cocaine damage, and thus has no real impact). If this is remotely true, wouldn't cocaine itself induce a physiological stress response, would this have any positive effect towards counteracting damage from cocaine?

Please excuse me if I'm off the mark, and do count this post as fictitious as I have read nothing credible to back up these thoughts, I just wondered if any of you boffins could set me straight, or give me a better understanding.

I'd also like to say thank you to st3ve for you post, I found it most informative.
 
Thanks, that was the sort of response I was looking for.

Something that worries me a little though is that I read a while ago that many cocaine users have scar tissue on their heart that they don't even know about. Presumably this is not something that would be reversible, so what kind of usage pattern would be required to form this scar tissue?

I guess that these questions are difficult to answer quantitatively as everyone is different.

Presumably this will be at least somewhat dose dependent... I can't stick any numbers on it like "1 gram every week is too much". Depending on genetics and other factors you might be able to take cocaine frequently without too much damage to the heart, or you may suffer damage from relatively little. Undoubtedly the more you use and the more frequent you use the higher your chances of something going wrong. The only way to find out is to get your heart examined at the hospital for tissue damage.

Isthisincognito, I'm not sure if I understand your question correctly. But if the stress caused by cocaine facilitated the release of oxytocin and repaired heart damage, people wouldn't be getting heart damage from cocaine would they? Although, if you were to somehow block the oxytocin release, it's possible the heart damage could be worse...
 
^ My question is purely clutching at straws, kind of putting 2+2 together when the answer is quite possibly completely unrelated.

I read that high stress induces heart damage, but simultaneously releases Oxytocin as a way to repair the damage caused by stress.

I was wondering as cocaine would induce stress (it may not be the same kind of stress per se), then would oxytocin be released to assist in countering the damage. The type of damage caused by cocaine may different than that which would be caused by stress and thus oxytocin would have no effect, or it could be that due to the amount of cocaine being higher than oxytocin and would render its repairing properties negligible in comparison to the damage being caused. Does that make a little more sense?

Assume I'm coming from a completely ignorant knowledge (which I am) and thus I may be way off the mark, and I was just seeking to see if anyone could set me straight.

I'm not saying cocaine facilitates the release of oxytocin, I'll try and bullet point my train of thought


  1. Does stress release oxytocin?
  2. Does cocaine induce the correct stress for the release of oxytocin?
  3. What kind of damage does cocaine cause to the heart?
  4. What kind of repair does oxytocin cause on the heart?
  5. Would oxytocin then counteract, or reduce damage as a result of cocaine?
  6. How limited would the supply of oxytocin in the body be? - would its present be insignificant in comparison to the presence of cocaine
 
Cocaine damages the heart by constricting blood vessels, making the heart work harder, and messing with electrical conduction in the heart. Cocaine is much more destructive to cardiac tissue than a stressful lifestyle is and the damage cannot be reversed by oxytocin.

Oxytocin does not prevent all cardiac tissue damage, it may just reduce the damage seen associated with living a stressful lifestyle. But cocaine usage is a totally different set of stressors and is not comparable to just having high baseline cortisol.
 
Is it possible for one-time or occasional use of cocaine to inflict testable and verifiable cardiotoxicity?
 
Yes. Look for "cocaine sudden death" on google scholar or any other academic database...

Fatal cocaine intoxication presenting as an excited delirium is described in seven recreational cocaine users. Symptoms began with the acute onset of an intense paranoia, followed by bizarre and violent behavior necessitating forcible restraint. The symptoms were frequently accompanied by unexpected strength and hyperthermia. Fatal respiratory collapse occurred suddenly and without warning, generally within a few minutes to an hour after the victim was restrained. Five of the seven died while in police custody. Blood concentration of cocaine averaged 0.6 mg/L, about ten times lower than that seen in fatal cocaine overdoses. Police, rescue personnel, and emergency room physicians should be aware that excited delirium may be the result of a potentially fatal cocaine intoxication; its appearance should prompt immediate transport of the victim to a medical facility. Continuous monitoring, administration of appropriate cocaine antagonists, and respiratory support will hopefully avert a fatal outcome.
http://europepmc.org/abstract/MED/4031813
 
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