Update on Cocaine and Beta-Blockers

Motivation: Cocaine use in Baltimore is unfortunately common.  During my sub-I in medicine, I met more than a couple of patients presenting with chest-pain after cocaine use.  If I did not know that the patient had been using cocaine, I would have suggested beta-blocker for its anti-arrythmic and anti-hypertensive effects.  But, the traditional teaching is that beta-blockers are contraindicated after cocaine use.  Just searching Google for "cocaine beta blocker" pulls up many sites warning against beta-blocker use - including trusty Wikipedia.

The traditional teaching is that since cocaine is a norepinephrine reuptake inhibitor, blocking the beta-receptor sites would lead to "unblocked" alpha-adrenergic effect of increased hypertension.  Beta-receptors (esp. Beta2 receptor) have some vasodilatory effect.  But, is this all theory or are there trials? Despite decades of official warning against beta-blocker use, the following paper is the first paper to assess use of beta-blockers in clinical chest pain.

Paper: Beta-blockers for Chest Pain Associated with Recent Cocaine Use. Rangel, C. et. al. Arch. Intern. Med. 2010 (170): 874-879.  http://archinte.ama-assn.org/cgi/content/full/170/10/874

Method: In a retrospective study, authors looked at patients admitted to San Francisco General Hospital with chest pain and U-tox positive for cocaine.  The authors primarily examined association between cocaine use and death.  Secondary outcomes were blood pressure levels, troponin levels, occurrence of v-fib/v-tach, intubation, or need for vasopressors.  Patients with clearly documented pulmonary etiologies such as pneumonia or pulmonary embolus were excluded.  331 patients met criteria of chest pain with positive urine toxicology.

Results:
Characteristics: Of 331 patients with chest pain and cocaine use, 46% got beta-blocker in the ED - mostly IV metoprolol.   Patients who got beta-blockers tended to be a little bit older (51 years versus 49 years) and likely to have higher blood pressure (SBP of 159 versus 141), history of HTN (70% vs 58%) and coronary bypass grafting (6% vs 1%), and have concurrent use of ace inhibitor (42% vs 29%) and statin (17% vs 8%).

Death: 45 patients died during follow-up after hospitalization.  12% of those who received beta-blocker died compared to 15% of those not getting beta-blockers (p = 0.38).  After adjusting for confounding variables, being discharged on a beta-blocker was associated with 70% reduction in risk of cardiovascular death (HR: 0.29 CI: 0.09-0.98).

Secondary outcomes: After adjusting for other medications received, patients on beta-blockers had a mean 8 mmHg greater decrease in systolic blood pressure compared to patients who did not get beta-blockers.  Receiving beta-blocker did not result in meaningful ECG differences, differences in peak troponin levels or incidence of malignant ventricular arrythmias.

Conclusion:   Beta-blockers did not seem to harm patients with positive cocaine use history.  In particular, beta-blocker administration in the ED resulted in lower rather than the hypothesized higher blood pressure!  Also, being discharged on beta-blockers significantly decreased risk of cardiovascular death.  What I found remarkable was that in general, the patients given beta-blockers might have been unhealthier in terms of age, blood pressure, and bypass history.

Being a retrospective study, of course, imposes some significant limitations on the study.  The group getting beta-blocker and the group not getting beta-blocker were different, and these differences may have influenced the results in unforseen ways not easily corrected by statistical adjusting.  Also, some of the confidence intervals were rather large.  The confidence interval showing 70% risk reduction in CVD death had an upper limit confidence interval of the hazard ratio at 0.98.