• Cocaine is a sympathomimetic that blocks catecholamine reuptake and leads to a hyper-adrenergic state.^1-4 At higher doses it may also disrupt sodium channels and ion transport.^1-4
• In cases of Cocaine-Associated Chest Pain (CACP) incidence of true MI is low (0.7-6%).^1-7
• Cocaine use was reported in 2% of aortic dissections.^1-3
• Cocaine accounts for ~25% of MIs in patients between 18 and 45 years of age.^1-4
• Complications are rare when the ECGs and biomarkers are normal.^2-5 If complications do occur, it is usually < 12hours of their ED presentation.²

Disposition:

• Low-risk patients (normal biomarkers, nondiagnostic ECGs, and responsive to treatment) can be observed for 6-8hrs and may be safety discharged if they remain symptom free.^1-7
• High-risk patients (positive biomarkers, persistent ECG changes, and/or don’t respond to treatment) should be admitted to monitored beds and managed per local protocols.^1,3,5,6
• Cessation of cocaine is the most effective secondary prevention strategy as recurrent chest pain, MI, and death are rare in patients who discontinue use.¹

History & Physical and Limitations:

• All patients with chest pain should be asked directly about cocaine use.^1-4
• There are no presenting features or historical clues that can help distinguish MI from non-MI CACP.³
• Absence of pre-existing cardiovascular factors does not help to rule out MI.^2,3

Signs and Symptoms: ^1,3

• CACP will usually occur within the first hour of use (58%) but can occur up to 18 hours later.³
  • Cocaine combined with alcohol forms the active metabolite coca-ethylene which is more potent and takes 2-3x longer to clear.²

Investigations and Limitations:

• • 12-lead electrocardiogram (ECG)
    • The ECG is an unreliable tool to predict acute MI.^1-6
      • Sn 36%, Sp 90%, PPV 18%, NPV 96% ^2-4
    • Serum biomarkers
      • Troponins should be collected in all adults with CACP.⁵
    • Radiography
      • CXR is limited in predicting aortic dissection (Sn 64%).⁸
      • CT Angiography should be used if there is suspicion for aortic dissection.⁵

• Urine Toxicology
  • When exposure to cocaine requires confirmation, does not need to be routine.⁵

Differential Diagnosis related to cocaine includes:^1-5

• Acute Coronary Syndrome
• Aortic Dissection
• Spontaneous Coronary Artery Dissection
• Hypertensive Crisis
• Pulmonary Embolism

Pharmacologic Management of CACP and CAMI:

• First Line Therapy:
  • Aspirin (162-325mg) is recommended (unless dissection is suspected).^1,3,5,9
  • Benzodiazepines^3,5,6
    • Diazepam 10 mg IV, then 5-10 mg IV q3-5 minutes; OR
    • Lorazepam 1-2mg IV q5-10 minutes.
    • No IV access:
      • Lorazepam 1-2mg IM q5-15m PRN; OR
      • Midazolam 1-5mg IM q5-10m PRN.

• Second Line Therapy for refractory symptoms and/or hypertension: ^1-6
  • Vasodilators such as nitroglycerine (NTG) and nitroprusside.

• NTG SL 0.4mg q5m x3 doses. If >3 doses are required, consider infusion.
• NTG Infusion: Start 5-10mcg/min and titrate 5-20mcg/min q5min
  (Max dose 400mcg/min).
• Nitroprusside infusion: 0.5-10mcg/kg/min (doses above 2mcg/kg/min will cause cyanide toxicity).

• Combination therapy (benzodiazepines and NTG) is thought to work better than NTG alone.⁷
• Phentolamine (a-blocker) can help oppose cocaine’s a-mediated constriction, but tends to increase heart rate and worsen myocardial oxygen demand.^6,10
  • Dosing: 1-2.5mg IV Bolus q5-15minutes prn.

• For patients with persistent ST-segment elevation or depression:
  • NTG and calcium channel blockers (CCBs) are safe and efficacious to reduce ischemic symptoms.^4,5
    • CCBs should be used as an adjunct for patients with ongoing ischemic symptoms despite NTG administration.^4,5
    • Dosing: Diltiazem25 mg/kg IV (average dose 20 mg) or Verapamil 2.5-5mg IV. Repeat either agent q15 min PRN.⁵
• Coronary angiography with PCI is preferred over fibrinolytics.^4,5 If ST-elevation and/or ischemic symptoms persist despite therapy, cardiology should be consulted to help guide these treatment decisions.
• Use of beta blockers for acute CACP is controversial and currently not recommended due to concerns that the beta blockade may result in unopposed alpha constriction.^2-6
  • The 2010 ACC/AHA guidelines state that nonselective b-blockers can be considered in patients with CACP who demonstrate persistent hypertension or tachycardia, if they were treated with a vasodilator.⁴

1. McCord J, Jneid H, Hollander JE, de Lemos JA, Cercek B, Hsue P, Gibler WB, Ohman EM, Drew B, Philippides G, Newby LK; American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation. 2008 Apr 8;117(14):1897-907. doi: 10.1161/CIRCULATIONAHA.107.188950. Epub 2008 Mar 17. PMID: 18347214.

   
   

2. Agrawal PR, Scarabelli TM, Saravolatz L, Kini A, Jalota A, Chen-Scarabelli C, Fuster V, Halperin JL. Current strategies in the evaluation and management of cocaine-induced chest pain. Cardiol Rev. 2015 Nov-Dec;23(6):303-11. doi: 10.1097/CRD.0000000000000050. PMID: 25580707.

   
   

3. Schwartz BG, Rezkalla S, Kloner RA. Cardiovascular effects of cocaine. Circulation. 2010 Dec 14;122(24):2558-69. doi: 10.1161/CIRCULATIONAHA.110.940569. PMID: 21156654.

   
   

4. Havakuk O, Rezkalla SH, Kloner RA. The Cardiovascular Effects of Cocaine. J Am Coll Cardiol. 2017 Jul 4;70(1):101-113. doi: 10.1016/j.jacc.2017.05.014. PMID: 28662796.

   
   

5. Morgan JP.  Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse. In: Dardas T, editor. UpToDate. [Internet]. Waltham, Mass.: UpToDate; 2022 [cited April 10, 2022]. Available from: www.uptodate.com

   
   

6. Nelson LS, Oladapo O. Cocaine: Acute intoxication. In: Grayzel J, editor. UpToDate. [Internet]. Waltham, Mass.: UpToDate; 2022 [cited March 15, 2022]. Available from: www.uptodate.com

   
   

7. Finkel JB, Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011 Dec;86(12):1198-207. doi: 10.4065/mcp.2011.0338. PMID: 22134939; PMCID: PMC3228621.

   
   

8. Coyle S, Moriarty T, Melody L, Ryan D. Diagnostic Testing in Acute Aortic Dissection. Curr Emerg Hosp Med Rep. 2014;2: 97–103. https://doi.org/10.1007/s40138-014-0044-8.

   
   

9. Wright RS, Anderson JL, Adams CD, et al; American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. 2011 ACCF/AHA focused update incorporated into the ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the American Academy of Family Physicians, Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons. J Am Coll Cardiol. 2011 May 10;57(19):e215-367. doi: 10.1016/j.jacc.2011.02.011. PMID: 21545940.

   
   

10. Richards JR, Garber D, Laurin EG, Albertson TE, Derlet RW, Amsterdam EA, Olson KR, Ramoska EA, Lange RA. Treatment of cocaine cardiovascular toxicity: a systematic review. Clin Toxicol (Phila). 2016 Jun;54(5):345-64. doi: 10.3109/15563650.2016.1142090. Epub 2016 Feb 26. PMID: 26919414.