Difference between revisions of "Cocaine-associated chest pain"

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==Background==
 
==Background==
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Cocaine is a catalyst for CAD &amp; up to 6% of cocaine related chest pain develop an MI, however, a 9-12 hour period of ECG's and serial troponins can be safe. Of the 334 patients studied, if both were negative, no deaths from cardiovascular events occurred at 30 days. 4 patients did have non-fatal MI's but were using coc at the time.<ref>Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.</ref>  
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*Cocaine causes vasoconstriction, which can precipitate MI
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**Cocaine metabolites can persist for up to 24hrs and cause delayed or recurrent coronary vasoconstriction<ref name="McCord">McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.</ref>
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===Epidemiology===
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*Causes vasculitis
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*6% incidence of AMI with cocaine chest pain  
 
*6% incidence of AMI with cocaine chest pain  
 
*Cocaine associated with 24x risk of true MI
 
*Cocaine associated with 24x risk of true MI
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==Clinical Features==
 
==Clinical Features==
 
*[[Chest pain]] in the setting of cocaine or related stimulant use
 
*[[Chest pain]] in the setting of cocaine or related stimulant use
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*Cocaine metabolites can persist for up to 24hrs and cause delayed or recurrent coronary vasoconstriction<ref name="McCord">McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.</ref>
 
  
 
==Differential Diagnosis==
 
==Differential Diagnosis==
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==Disposition==
 
==Disposition==
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*May discharge after: 9-12 hour period of ECG's and serial troponins, if both are negative
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*Consider discharge after 9-12 hour observation if pain free, no EKG changes and negative serial troponin
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**In NEJM 2/03; n=334; outcome of zero events at 30dys if no more cocaine
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**In NEJM study, 334 patients studied. If both EKG and troponins negative, no deaths from cardiovascular events at 30 days. 4 patients did have non-fatal MI's but were using cocaine at the time.<ref>Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.</ref>
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*Otherwise admit
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===Consider Admission===
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*Persistent chest pain
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*[[ECG]] changes
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*[[Arrhythmia]]
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*[[CHF]]
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*Elevated [[troponin]]
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==See Also==
 
==See Also==
 
*[[Cocaine]]
 
*[[Cocaine]]
 
*[[Cocaine toxicity]]
 
*[[Cocaine toxicity]]
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*[[Cocaine Withdrawal]]  
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*[[Cocaine withdrawal]]  
 
*[[Acute Coronary Syndrome (Main)]]
 
*[[Acute Coronary Syndrome (Main)]]
  
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<references/>
 
<references/>
  
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[[Category:Cardiology]] [[Category:Toxicology]]
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[[Category:Cardiology]]
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[[Category:Toxicology]]

Latest revision as of 01:43, 10 May 2017

Background

  • Cocaine causes vasoconstriction, which can precipitate MI
    • Cocaine metabolites can persist for up to 24hrs and cause delayed or recurrent coronary vasoconstriction[1]
  • 6% incidence of AMI with cocaine chest pain
  • Cocaine associated with 24x risk of true MI

Clinical Features

  • Chest pain in the setting of cocaine or related stimulant use

Differential Diagnosis

Chest pain

Critical

Emergent

Nonemergent

Sympathomimetics

Evaluation

  • 1-3hrs onset from last use
    • If >3 hrs = lower risk of AMI
  • Most with characteristic pain
    • Dyspnea, diaploresis, and nausea
  • Most have normal vitals
  • ECG

Management

  • ASA
  • Benzos directed at symptom relief, not necessarily hypertension and tachycardia[1]
  • Consider Nitroglycerin, Nitroprusside, Phentolamine (1mg IV), or CCB (in benzodiazepine non-responders)
  • Avoid beta-blockers due to the possibility of unopposed alpha activity. Labetolol although offering the theoretical advantage of blocking both alpha and beta receptors does not reverse coronary artery vasoconstriction[2][3]
    • Though not accepted in common practice, new evidence suggest no significant risk and a benefit to using beta blockade in these patients[4][5][6]
  • Consider NaHOC3 for Ventricular Arrythmias immediately following cocaine use
    • Reverses cocaine induced QRS prolongation by Na channel blockade

Disposition

  • Consider discharge after 9-12 hour observation if pain free, no EKG changes and negative serial troponin
    • In NEJM study, 334 patients studied. If both EKG and troponins negative, no deaths from cardiovascular events at 30 days. 4 patients did have non-fatal MI's but were using cocaine at the time.[7]
  • Otherwise admit

See Also

References

  1. ↑ 1.0 1.1 McCord J, et al. Management of cocaine-associated chest pain and myocardial Infarction. Circulation. 2008; 117:1897-1907.
  2. ↑ Boehrer JD. et al. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. Am J Med. 1993; 94: 608– 610
  3. ↑ Lange RA. et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Intern Med. 1990; 112: 897–903
  4. ↑ Dattilo PB et al. β-blockers are associated with reduced risk of myocardial infarction after cocaine use. Ann Emerg Med. 2008; 51:117.
  5. ↑ Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011; 86(12):1198-1207.
  6. ↑ Rangel C, et al. Marcus GM. Beta-blockers for chest pain associated with recent cocaine use. Arch Intern Med. 2010; 170(10):874-879.
  7. ↑ Kloner RA and Rezkalla SH. Cocaine and the heart. N Engl J Med. 2003; 348:487-488.
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