Back in January 2020, I was doing my Sub-I rotation with the cardiology team at Jackson Memorial Hospital in Miami. One day, we were suddenly paged by the EM team for a suspected myocardial infarction. When we arrived to the ED, a complete history was taken and that is when we realized the chest pain was more likely produced by cocaine consumption. While reviewing this case next day after a didactical and interesting discussion, I found that this patient had previous history of CAD that was treated with PTCA. He was also a regular cocaine user. This fact is a potential risk factor for the development of CAD secondary to cocaine in an already weakened heart (EF 10-15% for this patient). That is when an intriguing question came to my mind- should beta blockers be used to treat patients with cocaine induced chest pain? Nowadays, there is a big debate whether or not beta blockers should be used in patients with cocaine induced chest pain especially in this patient where Coreg was prescribed as part of a GDMT regime.
Cocaine acts by inhibiting the reuptake of serotonin, norepinephrine and dopamine, resulting in increased concentrations of these neurotransmitters in the brain. This drug can also easily cross the blood-brain barrier and may lead to the breakdown of the barrier (Sharma et al 2009). In regards to the heart, cocaine is known to be a powerful vasoconstrictor of the coronary arteries leading to CAD secondary to cocaine. For those populations at high risk for CAD who used cocaine, tend to experience coronary atherosclerosis, whereas for populations at low risk did not, implying that the long-term effects of cocaine were more likely to be more detrimental among individuals with higher CAD risk like the patient mentioned on this paper (Kim et Park, 2019).
In regards to pharmacology, there is still a considerable controversy of whether or not beta-blockers should be used in the setting of cocaine-related chest pain as Beta blockers remain a standard therapy in the early treatment of acute coronary syndrome. A study conducted by Sen et al (2006) concluded that beta blockers should not be used in the treatment of cocaine induced myocardial ischemia as cocaine tends to affect both alpha and beta receptors, and that by giving a beta blocker the effects of alpha blockade on the heart may become unopposed. This effect can further decrease myocardial blood flow and increase coronary vasoconstriction. Furthermore, Simons et Breall (2018) suggest that beta blockers should not be used in the setting of acute MI in patients where cocaine could have been the underlying cause due to the likelihood of exacerbation of coronary artery vasospasm. On the other hand, other studies suggest some specific beta blockers could be beneficial in some specific circumstances. For example, a prospective study conducted by Hoskins et al (2010) found that labetalol decreased the heart rate and blood pressure without adverse effects in patients that presented to the ED with a positive drug screen for cocaine after 48 hours. In addition, a retrospective cohort study conducted by Rangel et al. (2010) found that patients who received beta-blockers in the setting of chest pain associated with cocaine in the ED and that were discharged on such a regime demonstrated an acceptable decrease in mortality from cardiovascular causes over 972 days. Moreover, carvedilol has recently been found to be safe and may be effective among heart failure patients who use cocaine as it reduced cardiovascular mortality and readmission (Raza et al, 2019).
In conclusion, there is still a huge debate on beta blockers as regular therapy for patients with cocaine induced chest pain. Clinicians should consider the evidence behind withholding or giving patients beta-blockers as part of their medical treatment, especially to those patients that can benefit from it, such as patients with left ventricular systolic dysfunction and ventricular arrhythmias. In addition, new studies suggest that beta blockers such as labetalol and more recently carvedilol could benefit patients in specific scenarios. More studies are needed in order to determine which beta blockers may be beneficial for patients in terms of timing, administration, comorbidities in relation to cocaine. Beta blockers should not be absolutely contraindicated as we learn in medical school, but we still need to take into consideration potential harms of a medication that has not been approved for a specific medical condition. This is the time time when ethics take over in terms of decision-making.
Hoskins M, Leleiko R, Ramos J, Sola S, Caneer P, Khan B (2010). Effects of labetalol on hemodynamic parameters and soluble biomarkers of inflammation in acute coronary syndrome in patients with active cocaine use. J Cardiovasc Pharmacol Ther. 15(1): 47-52
Kim S, Park T (2019). Acute and Chronic effects of cocaine on cardiovascular health. International journal of molecular sciences. 20(3): 584
Rangel C, Shu R, Lazar L, Vittinghoff E, Hsue P, Marcus G (2010). Beta Blockers for chest pain associated with recent cocaine use. Arch Intern Med. 170(10): 874-9
Raza M. Alvi, Dahlia Banerji, Noor Tariq, Malek Z.O. Hassan, Magid Awadalla, Lili Zhang, Connor P. Mulligan, Adam Rokicki, Maryam Afshar and Tomas G. Neilan. (2019). Safety of Carvedilol in management of heart failure among cocaine users. Journal of American College of Cardiology. DOI: 10.1016/S0735-1097(19)31328-2
Sen A, Fairbairn T, Levy F (2006). Beta-blockers in cocaine induced coronary syndrome. Emergency Medicine Journal. 23(5): 401-402
Sharma HS, Muresanu D, Sharma A, Patnaik R (2009). Cocaine-induced breakdown of the blood brain barrier and neurotoxicity. International Review of Neurobiology. 88: 297-334
Simons M, Breall J. (2018). Overview of the acute management of non-ST elevation acute coronary syndromes. UpToDate