It is believed that administration of beta-blocker administration in patients with cocaine chest pain will produced increased vasoconstriction due to “unopposed alpha effect.”

 

Several retrospective studies on the use of beta-blocker in patients with cocaine-induced chest pain concluded the use of beta-blocker to be safe.

 

So is the unopposed alpha effect just a theory?

 

Lange RA et al. 1990 Ann Internal Med

Design: randomized, double-blind, placebo controlled trial.

 

30 (38- 68 years old) patients undergoing cardiac catherization for chest pain evaluation were studied.

 

Cocaine (intranasal administration) resulted in:

• Increased myocardial oxygen demand
• Increased coronary vascular resistance 22%
• Decreased coronary sinus blood flow: 10%

 

Administration of propranolol (intracoronary infusion) resulted in additional:

• Increase coronary vascular resistance 19%
• Decrease coronary sinus blood flow by 15%
• No additional change in myocardial oxygen demand

 

Complete coronary occlusion observed in 1 patient with ST elevation

Epicardial coronary arterial segment constriction >10% in 5 patients.

 

Bottom Line: Lange RA et al. 1990 demonstrates that the “unopposed alpha effect” does occur in coronary artery when beta-blocker is administered in a setting of acute cocaine exposure.  Overall, the use of beta-blocker in the ED management of cocaine-induce acute chest pain is not a prudent option.  It is unknown if the cocaine dose, last use of cocaine (days), or CAD history influence the “safety” of beta-blocker initiation/use during inpatient hospitalization.

References

Lange RA, Cigarroa RG, et al. Pontetiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Ann Internal Med 1990;112:897-903