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Emergency Medicine Journal : EMJ logoLink to Emergency Medicine Journal : EMJ
. 2006 May;23(5):401–402. doi: 10.1136/emj.2006.036582

Beta‐blockers in cocaine induced acute coronary syndrome

Ayan Sen, Tim Fairbairn, Freya Levy
PMCID: PMC2564096  PMID: 16627850

Beta‐blockers in cocaine induced acute coronary syndrome

Report by Ayan Sen and Tim Fairbairn, Clinical Fellow in Emergency Medicine, SHO in General Medicine

Checked by Freya Levy, Consultant in Emergency Medicine, Stepping Hill Hospital

Manchester Royal Infirmary

Abstract

A short cut review was carried out to establish whether beta blockers should be used in the treatment of chest pain associated with cocaine use. 12 papers were found, of which two presented the best evidence to answer the clinical question. The author, date and country of publication, patient group studied, study type, relevant outcomes, results and study weaknesses of these best papers are tabulated. The clinical bottom line is that Beta Blockers should not be used in the treatment of cocaine induced myocardial ischaemia.

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 (ACS) 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 and 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 syndrome.mp] AND [exp Adrenergic beta‐Antagonists/OR beta‐blockers.mp. OR beta blockers.mp.].

Search outcome

Altogether 12 references were noted, of which two directly related to our question (see table 1). No additional papers were found in the Cochrane library.

Table 1.

Author, date and country Patient group Study type (level of evidence) Outcomes Key results Study weaknesses
Lange RA et al, 1990, USA 30 clinically stable patient volunteers referred for catheterisation for evaluation of chest pain Randomised, double‐blind, placebo‐controlled trial Change in coronary sinus blood flow after cocaine Decreased post cocaine by 10% (+/−7%) Low numbers equate to low statistical significance
Further change in coronary sinus blood flow after cocaine then saline No change Age range 38–68
Further change in coronary sinus blood flow following cocaine and then treated with propanolol Decreased by 15% (+/− 18%) Only 7 of the 30 had normal coronary arteries
Patients were given intranasal cocaine 2 mg/Kg followed by either an IV push of saline or 2 mg Propanolol over 2 minutes. Change in coronary vascular resistance after initial cocaine Increased by 22% (+/− 11%) Investigation only involved gross coronary anatomy
Further change in coronary vascular resistance after cocaine then saline No change No markers of myocardial ischaemia
Further change in coronary vascular resistance after cocaine then propanolol Further increase by 19%
Boehrer JD et al, 1993, USA 15 patients (7 men and 8 women) aged 40–79 years, non cocaine users undergoing catheterisation for evaluation of chest pain who were administered 2 mg/kg cocaine intranasally and 15 minutes later received intravenous labetalol(n = 6) or saline (n = 9) Prospective clinical trial Results on angiography 6 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
Change in heart rate after cocaine No change Very small sample size
Change in Mean arterial pressure after cocaine Increase of around 8% in both groups Significant number had coronary vascular disease and all were not related directly to cocaine use
Change in coronary arterial area after cocaine Around 6% reduction in Group 1 who got saline after compared to around 8% reduction in those who got labetalol No markers of ischemia studied
Change in Heart rate after saline or labetalol No change 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
Change in mean arterial Pressure after saline/labetalol Almost 3% reduction in saline and 6% in labetalol group Patients were non cocaine users so validity in cocaine users can only be assumed
Change in coronary arterial area after saline/labetalol No significant change

Comment(s)

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.

References

  1. Lange RA, Cigarroa RG, Flores ED, et al. Potentiation of cocaine-induced coronary vasoconstriction by beta-adrenergic blockade. Annals of Internal Medicine 1990 Jun 15;112(12):897-903. [DOI] [PubMed] [Google Scholar]
  2. BoehrerJD, Moliterno DJ, Willard JE, et al. Lange RA. Influence of labetalol on cocaine-induced coronary vasoconstriction in humans. American Journal of Medicine 1993 Jun;94(6):608-10. [DOI] [PubMed] [Google Scholar]

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