The American Heart Association (AHA) early this month (April 2008) has just came out with a guidelines on the management of cocaine induced myocardial infarction.
Cocaine can cause myocardial ischemia because it blocks the reuptake of norepinephrine and dopamine at the presynaptic adrenergic terminals, thus results in an accumulation of catecholamines at the postsynaptic receptor (powerful sympathetic activities).
The effects of this increased sympathetic activity include:
1. including increased chronotropy and inotropy
2. coronary vasospasm
3. prothrombotic state, and
4. accelerated atherosclerosis — and, in some individuals, can actually cause MI.
But in terms of the symptoms, signs, and diagnostic workup in patients with cocaine-associated MI are similar to those in patients with MI unrelated to cocaine.
However, treatment of cocaine-triggered ischemia and infarct differs in several ways, but the two most important differences are:
1. Benzodiazepines should be given very early; administration of these agents can dramatically reduce and counteract the sympathomimetic effects of cocaine.
2. Beta blockade, because of its unopposed alpha-adrenergic effects, leads to coronary vasoconstriction, increased blood pressure, and increased mortality in cocaine-associated ischemia, and so beta blockers must be avoided in the acute treatment of these patients.
Other than that, management strategies are almost similar with non-cocaine induced MI (e.g. nitrates and aspirin)
In the setting of ST-segment-elevation acute coronary syndromes, primary PCI is better than fibrinolytics because of the relatively high incidence of false-positive ST elevations in patients who have used cocaine.
You can download the AHA guidelines on cocaine induced MI here.
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