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Cocaine induced Cx pain.


Wraith

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I know there's an actual name for this condition but I cant for the life of me find it in any searches that I have done. It's not that big of a deal but it's just something that's been bugging me for the past few days. Does anyone know the name for this? Thanks in advance.

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I have never herd of a special word per say. There are types of vasopsastic angina that present with similar findings. They include: Prinzmetal angina, variant angina, and vasospastic angina. They are often used interchangeably.

Take care,

chbare.

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That's it!!!!! Prinzmetal Angina. Thanks guys. That was bugging the %^&$&* out of me. You know how it goes.

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That's it!!!!! Prinzmetal Angina. Thanks guys. That was bugging the %^&$&* out of me. You know how it goes.

Prinzmetal's is NOT the same as a cocaine induced MI. Prinzmetal is vasospasm of the coronary arteries. Cocaine does not do this.

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Cocaine does cause coronary vasospasm.

http://www.mja.com.au/public/issues/177_05...as10632_fm.html

There are a number of proposed mechanisms of cocaine-induced myocardial infarction. Firstly, in-vitro studies have shown that cocaine activates platelets, increases platelet aggregation and potentiates platelet thromboxane production. The mechanism is thought to be by induction of α-granule release from platelets leading to subsequent thrombosis — a recent randomised, double-blind, crossover study found that there was a fourfold increase in both platelet factor 4 and thromboglobulin and an increase in platelets containing microaggregates (α-granules) at 40 and 80 minutes.10 This is supported by the postmortem findings of acute platelet-rich thrombi in fatal cocaine-related infarcts in both normal and atherosclerotic coronary vessels.11 A further procoagulant effect has also been demonstrated by the finding of lower protein C and antithrombin III levels among cocaine users.10 This anticlotting-factor deficiency predisposes to in-situ thrombosis, causing acute myocardial infarction in the presence of previously normal or minimally diseased coronary arteries. Finally, no increase in von Willebrand factor is found in cocaine users.10

Secondly, the sympathomimetic effects of cocaine induce an increase in heart rate and blood pressure, leading to a resultant increase in oxygen demand by the heart. Cocaine could lead to myocardial ischaemia and subsequent infarction, particularly in the presence of underlying coronary artery disease.2

Thirdly, coronary artery vasospasm has been suggested as another mechanism for cocaine-induced AMI. The mechanism by which cocaine may induce vasospasm is not understood. There are two schools of thought suggesting a wide role for cocaine as a general vasoconstrictor, and another suggesting a more specific role for cocaine on the vascular smooth muscle leading to vasoconstriction.2 Of particular note is a study showing the possible role of endothelin-1, the most potent endogenous, endothelium-derived vasoconstrictor factor.12 That study showed a significantly increased concentration of endothelin-1 in actively intoxicated and chronic users of cocaine over healthy control subjects. However, it was difficult to determine whether this increase alone was sufficient to induce coronary vasospasm. The study went on to hypothesise that, because endothelin-1 increases the calcium sensitivity of arteries, it may sensitise the vasculature to other vasoconstrictor stimuli and prolong coronary vasoconstriction or vasospasm, causing acute myocardial infarction even in people without coronary stenosis.12

Fourthly, several recent autopsy reports suggest prolonged cocaine misuse causes intimal hyperplasia and premature atherosclerosis in young patients who die from AMI following cocaine use.11 Similarly, endomyocardial biopsy specimens from patients with cocaine-induced chest

I agree that this is not Prinzmetal's angina, but a more broad vasospastic event. Perhaps someone was trying to simplify things and cut too much of the information out.

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God that's what I love about this forum. You ask a simple question and there are not quick, one sentence answers. The combined knowledge and experience of the readers and posters makes this a great place to burn time. Thanks for everyones time and answers.

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Funny you should ask about cocaine because after a recent call I've been doing some research into the differing pharmacodynamics of cocaine.

Cocaine is interesting because it has two different effects that almost seem contradictory. Cocaine is first a potent central nervous system stimulant. It accomplishes this partially by blocking reuptake of dopamine at the transporter protein level, causing dopamine to accumulate in the extracellular space, prolonging the dopaminergic signaling of the post synaptic cleft, or at least that's what my book tells me.

The other effect comes from its sodium channel blocking qualities. Cocaine's use as an anesthetic comes from its ability to raise the action potential of nerve cells, providing local anesthetic properties. Neat, ain't it?

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