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    Cocaine-Associated Chest Pain – Diagnosis and Treatment

    Cardiovascular, Toxicology

    Last Reviewed on Feb 13, 2023
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    • Cocaine is a sympathomimetic that blocks catecholamine re-uptake 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


    • Low-risk patients (normal biomarkers, non-diagnostic 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

    Diagnostic Process

    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.

    Recommended Treatment

    Harmacologic Management of CACP and CAMI

    • First Line Therapy:
      • Aspirin (162-325mg) is recommended (unless dissection is suspected).1,3,5,9
      • Benzodiazepines3,5,6
        • 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
        • 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.
          • 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
                • 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
                    • 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).
        • 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

    Quality Of Evidence?


    Most evidence is level B or C, and derived from animal observation, laboratory-based catheterization experiments, observational studies, case series, and case reports.


    Related Information

    Reference List

    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.


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