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Beta-blockers in cocaine induced acute coronary syndrome

Three Part Question

In [cocaine users with chest pain suggestive of acute coronary syndrome] does [beta-blocker administration]cause [potentiation of coronary vasoconstriction]

Clinical Scenario

A 25 year old male is brought to the emergency department after he dialled 999 following sudden onset of crushing chest pain. He admitted to snorting cocaine before the episode but did not have any other past medical history. His blood pressure was 180/100 and he had been given aspirin and GTN spray by the paramedic crew. 12-lead ECG in A/E showed 1 mm ST-depression in V5-V6.You make a diagnosis of acute coronary syndrome and decide to give the maximum medical treatment for ACS including beta-blocker atenolol. An irate cardiology SpR calls you up the next day to ask you whether you haven't heard of beta-blockers worsening cocaine induced coronary vasospasm. You are shocked to hear that and wonder what the evidence-base is!

Search Strategy

MEDLINE using OVID interface 1966-March 2006
Cochrane Database of Systematic Reviews 2006 Issue 1
Medline: [exp COCAINE-RELATED DISORDERS/ OR exp COCAINE/] AND[exp Chest Pain/ OR exp Angina pectoris OR exp Myocardial Infarction/ OR acute coronary] AND [exp Adrenergic beta-Antagonists/ OR OR beta]

Search Outcome

Medline: 12 references were noted out of which 2 directly related to our question
Cochrane: No new references found

Relevant Paper(s)

Author, date and country Patient group Study type (level of evidence) Outcomes Key results Study Weaknesses
Lange RA. et al
Thirty clinically stable patient volunteers referred for catheterisation for evaluation of chest pain Patients were given intranasal cocaine 2mg/Kg followed by either an IV push of saline or 2mg Propanolol over 2 minutes.Randomized, double-blind, placebo-controlled trialChange in coronary sinus blood flow after cocaineDecreased post cocaine by 10% (+/-7%)Low numbers equate to low statistical significance Age range 38-68 Only 7 of the 30 had normal coronary arteries Investigation only involved gross coronary anatomy No markers of myocardial ischaemia
Further change in coronary sinus blood flow after cocaine then salineNo change
Further change in coronary sinus blood flow following cocaine and then treated with propanololDecreased by 15% (+/- 18%)
Change in coronary vascular resistance after initial cocaineIncreased by 22% (+/- 11%)
Further change in coronary vascular resistance after cocaine then salineNo change
Further change in coronary vascular resistance after cocaine then propanololFurther increase by 19%
15 patients (7 men and 8 women) aged 40-79 years, non cocaine users undergoing catheterisation for evaluation of chest pain who were administered 2mg/kg cocaine intranasally and 15 minutes later received intravenous labetalol(n=6) or saline (n=9)Prospective clinical trialResults on angiography6 were angiographically normal and 9 had sclerotic disease (>70% narrowing)Very poor methodology, no mention of type of study or procedure of randomisation or any blinding process Very small sample size Significant number had coronary vascular disease and all were not related directly to cocaine use No markers of ischemia studied Method of reporting of data is poor and the percentages have been calculated from their tables by the reviewers The tables merely report gross change in parameters with deviations in values measured Patients were non cocaine users so validity in cocaine users can only be assumed
Change in heart rate after cocaineNo change
Change in Mean arterial pressure after cocaineIncrease of around 8% in both groups
Change in coronary arterial area after cocaineAround 6% reduction in Group 1 who got saline after compared to around 8% reduction in those who got labetalol
Change in Heart rate after saline or labetalolNo change
Change in mean arterial Pressure after saline/labetalolAlmost 3% reduction in saline and 6% in labetalol group
Change in coronary arterial area after saline/labetalolNo significant change


Beta blockade for cocaine induced myocardial infarction has been advocated in some quarters. At first sight it would seem to make sense as many of these patients will be hypertensive and suffering the effects of an adrenergic drive. However, it must be remembered that cocaine affects both alpha and beta receptors and that by giving a beta blocker the effects of alpha blockade on the heart may become unopposed. These trials seems to confirm this concern with a decrease in myocardial blood flow and coronary vasoconstriction. In a patient with myocardial ischaemia this could result in an even lower coronary blood flow thereby worsening the ischaemia. However, we must remember that this is a small study in an experimental setting with patients receiving very small amounts of cocaine (much less than the typical recreational user). It therefore makes the interpretation of these findings difficult. On balance, in light of the feasible pathophysiological argument against the use of beta blockers, and the findings of these limited studies it appears sensible not to advocate the use of beta blockers in acute myocardial pain secondary to cocaine use.

Clinical Bottom Line

Beta Blockers should not be used in the treatment of cocaine induced myocardial ischaemia.


  1. Lange RA. Cigarroa RG. Flores ED. McBride W. Kim AS. Wells PJ. Bedotto JB. Danziger RS. Hillis LD. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade Annals of Internal Medicine. 112(12):897-903, 1990 Jun 15.
  2. Boehrer JD. Moliterno DJ. Willard JE. Hillis LD. Lange RA. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans American Journal of Medicine. 94(6):608-10, 1993 Jun