Cocaine to Crashing: Management of Cocaine Induced Chest Pain
By Harriera Siddiq
Case
· 55-year-old male with PMH of prior myocardial infarction w/stent placement arrived via EMS for chest pain (CP) of 30-minute duration; agitated and diaphoretic, clenching fist over chest (Levine’s sign.)
· Prior to EMS arrival, he took five 81mg aspirin and four expired nitroglycerin tabs of unknown strength, with minimal relief.
· On repeat questioning, patient admitted to heroin and cocaine use just prior to onset of sharp chest pain radiating to left shoulder. Additionally, patient reported non-adherence to prescribed Plavix.
· Vitals: BP 138/85, P 66, T 97.5, RR 26, O2 sat 100% on room air
· Exam was positive for minimally reactive dilated pupils, diaphoresis, tachypnea.
· EKG obtained by EMS in the field is below:
· Prior to labs resulting, patient’s telemetry showed episodes of non-sustained ventricular tachycardia (VT) and the patient was noted to be less agitated.
· During repeat EKG, patient became unresponsive, pulseless, and telemetry showed VT. ACLS was initiated—patient had agonal respirations and went into ventricular fibrillation. After 2 rounds of compressions and defibrillation x 1, return of spontaneous circulation (ROSC) was achieved, airway secured, and patient was accepted to cath lab. Repeat EKG during this event indicated STEMI with anterior ST elevations.
· No electrolyte abnormalities were noted after labs resulted. Cath found 100% Left Anterior Descending (LAD) artery occlusion proximal to stent. Percutaneous coronary intervention (PCI) was successful and LAD was re-stented.
Clinical Question: How does cocaine increase MI risk, and what interventions lower risk of progression to MI? Summary of Evidence
In 2021, approximately 4.8 million people used cocaine within the past 12 months; [1]24,538 people died secondary to cocaine overdose.[2]
Cocaine’s role in spurring MI is related to its sympathomimetic properties—increases in Heart rate, blood pressure, and contractility. These effects increase O2 demand, potentially leading to O2 supply/demand imbalance and therefore MI. Cocaine has been implicated in increased coronary vasoconstriction, coronary spasm, increased platelet aggregation, and arrythmias—all potential etiologies of MI.[3]
Increased hazard of MI in cocaine users who are otherwise low risk for CAD was noted in the Determinants of Myocardial Infarction Onset Study. 9 of 3946 patients interviewed 4 days after MI reported cocaine use within an hour of onset of infarct symptoms, and the study concluded that the risk of MI onset was elevated 23.7 times (95% CI 8.5 to 66.3) in the hour after cocaine use. Limitations of the study included potential underreporting about cocaine use, and lack of data on method of cocaine use (IV, intranasal, etc).[4]
The COCaine Associated CHest PAin (COCHPA) study, a multicenter study that analyzed CK-MB levels in 246 patients presenting to the ED with chest pain s/p cocaine ingestion, found that the incidence of cocaine-associated MI varies from as low as 1% in the Determinants of Myocardial Infarction Study (Mittleman et al) to 6%.[5]
AHA’s statement on cocaine-associated CP and MI endorsed the use of benzodiazepines (Class I/Evidence B)[6] for pain and hemodynamic effects. Nitroglycerin was also endorsed (Class I/Evidence B) for persistent HTN.[7] A 2006 review by Bhangoo et al of 2 studies examining benzos vs nitrates found equal effectiveness in combination or alone, and recommended considering CNS symptoms when making a decision on agent to use.[8]
The long-held notion of avoiding beta-blockers in the setting of cocaine-induced ACS was examined in a systematic review and meta-analysis published in The American Journal of Medicine by Lo et al, which found no link between beta blocker use and risk of MI in patients presenting with cocaine associated CP. Five studies with 1447 patients were examined; 536 were treated with beta blocker therapy in the ED up to 24 hours after admission and 911 patients were not treated with beta blocker therapy. The rate of in-patient myocardial infarction was 9.5% (51/536) in the beta-blocker group and 13% (119/911) in the non-beta-blocker group (RR 1.08; 95% CI, 0.61-1.91).[9]
Recommendations
· Timeline of cocaine use is important in stratifying MI risk. Cocaine use within an hour of chest pain may warrant close telemetry monitoring, serial EKGs, and priority IV access.
· Classic vital signs of a patient with cocaine-intoxication can be masked by co-ingestants. Chest pain, especially in patients with few risk factors, likely warrants careful inquiries into drug/medication use and adherence.
· Benzodiazepines and nitrate administration have the same class/evidence categorization (Class 1/Evidence B). Agents can be used in combination or selectively depending on presentation (CNS depression, prior nitro use—as in this case). While avoidance of beta blockers is still widely adhered to, newer evidence is challenging its deleterious effects in cocaine-induced chest pain.
References
[1] Substance Abuse and Mental Health Services Administration. (2022). Key substance use and mental health indicators in the United States: Results from the 2021 National Survey on Drug Use and Health (HHS Publication No. PEP22-07-01-005, NSDUH Series H-57). Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration. https://www.samhsa.gov/data/report/2021-nsduh-annual-national-report
[2] U.S Overdose Deaths in 2021 Increased Half as Much as in 2020 – But Are Still Up 15%. (2022, May 11). CDC. https://www.cdc.gov/nchs/pressroom/nchs_press_releases/2022/202205.htm
[3] Mittleman, M. A., Mintzer, D., Maclure, M., Tofler, G. H., Sherwood, J. B., & Muller, J. E. (1999). Triggering of Myocardial Infarction by Cocaine. Circulation, 99(21), 2737–2741. https://doi.org/10.1161/01.cir.99.21.2737
[4] Mittleman, M. A., Mintzer, D., Maclure, M., Tofler, G. H., Sherwood, J. B., & Muller, J. E. (1999). Triggering of Myocardial Infarction by Cocaine. Circulation, 99(21), 2737–2741. https://doi.org/10.1161/01.cir.99.21.2737
[5] Hollander, J. E., Hoffman, R. S., Gennis, P., Fairweather, P., DiSano, M. J., Schumb, D. A., Feldman, J. A., Fish, S. S., Dyer, S., & Wax, P. (1994). Prospective multicenter evaluation of cocaine-associated chest pain. Cocaine Associated Chest Pain (COCHPA) Study Group. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine, 1(4), 330–339. https://doi.org/10.1111/j.1553-2712.1994.tb02639.x
[6] Class I: Conditions for which there is evidence for and/or general agreement that the procedure or treatment is beneficial, useful, and effective. Evidence B: Data derived from a single randomized trial or nonrandomized studies.
[7] McCord, J., Jneid, H., Hollander, J. E., de Lemos, J. A., Cercek, B., Hsue, P., Gibler, W. B., Ohman, E. M., Drew, B., Philippides, G., Newby, L. K., & American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology (2008). 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, 117(14), 1897–1907. https://doi.org/10.1161/CIRCULATIONAHA.107.188950
[8] Bhangoo P, Parfitt A, Wu T. Best evidence topic report. Cocaine induced myocardial ischaemia: nitrates versus benzodiazepines. Emerg Med J. 2006 Jul;23(7):568-9. doi: 10.1136/emj.2006.038497. PMID: 16794106; PMCID: PMC2579557.
[9] Lo, K. B., Virk, H. U. H., Lakhter, V., Ram, P., Gongora, C., Pressman, G., & Figueredo, V. (2019). Clinical Outcomes After Treatment of Cocaine-Induced Chest Pain with Beta-Blockers: A Systematic Review and Meta-Analysis. The American journal of medicine, 132(4), 505–509. https://doi.org/10.1016/j.amjmed.2018.11.041
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