Cocaine, chest pain, and beta-blockers: time for re-evaluation?
June 2, 2010, 12:34 pm
β-Blockers for Chest Pain Associated With Recent Cocaine Use. Rangel C et al. Arch Intern Med May 24, 2010;170:874-879.
It has long been taught by toxicologists and in resuscitation courses that use of beta-blockers is contraindicated in cocaine-induced chest pain, since unopposed alpha-adrenergic activity could result in dangerously increased blood pressure. This tenet was based on animal research, some human volunteer studies, and an occasional case report. This paper retrospectively reviewed 331 patients admitted to San Francisco General Hospital with chest pain and a positive urine drug screen for cocaine (this actually measures the inactive metabolic benzoylecognine). Of these patients, 151 (46%) received a beta-blocker in the emergency department. After analyzing the data and attempting to control for confounding variables, the authors conclude that “Beta-blockers do not appear to be associated with adverse events in patients with chest pain with recent cocaine use.” They go further: ” . . . administration of beta-blockers to patients with cocaine-associated chest pain appears to be safe and may even be beneficial”.
Unfortunately, this study conflates and confuses so many different clinical entities that it becomes incoherent. When attempting to parse this paper, the effort to determine exactly what the authors are talking about at any specific time induces headache. Is whatever possible benefit they detected due to beta-blockers administered in the ED, or to patients who were discharged from hospital on long-term beta-blocker therapy? If so, are the patients discharged on chronic therapy a group selected for another confounding variable? Since the definition of “recent cocaine use” was a urine drug screen — which can be positive for at least 2 or 3 days — are we really combining two different populations: patients with chest pain accompanying acute cocaine toxicity, and those with chest pain associated with somewhat recent cocaine use but without active cocaine toxicity?
It is clear to me that the authors’ stated conclusions are hopelessly simplistic. Most likely, there are two types of cocaine-chest pain patients: those who have used cocaine in the past several hours and present with acute cocaine toxicity and coronary vasospasm, and those who are not experiencing the acute effects of cocaine (although their urine drug screen may be positive). In the former, it is probably best to avoid beta-blockers, since supportive care with adequate sedation and cooling if indicated usually succeeds in stabilizing pulse and blood pressure. The latter can be treated with standard therapy, although one should note that routine use of beta-blockers even in non-cocaine-associated chest pain has been recently questioned. Unfortunately, this type of retrospective study will never be able to answer these questions, and a randomized prospective study will obviously never be done.
In an eloquest editorial reply to a similar article several years ago, Robert S. Hoffman made some crucial points. Since only about 6% of patients with cocaine-associated chest pain will rule-in for myocardial infarction, and even those who do tend to have a very good prognosis, even the theoretical chance of benefit from beta-blockers in this group is quite small. This risks have been clearly established both theoretically and — to a limit extent — clinically. I entirely agree with Hoffman’s conclusion:
” . . .when the lack of benefit is weighed against any real or perceived risk, the preponderance of evidence continues to speak against the use of beta-adrenergic antagonists in this setting. Given this analysis, the authors’ call for a prospective trial of beta-adrenergic antagonists in cocaine users seems not only premature but frankly quite dangerous. Finally, their rationale is inherently flawed in that much of the benefit for beta-adrenergic antagonists in patients with non– cocaine-related acute coronary syndromes results from continued long-term use. Because the majority of patients with cocaine-associated chest pain will continue to use cocaine after discharge, giving these patients beta-adrenergic antagonists will not only repeat a practice abandoned by its pioneers nearly 30 years ago for good reason, but also subject an unpredictable subset of these individuals to the lethal drug interaction so well described in controlled animal investigations. Failure to learn from history dooms us to repeat it.” (Ann Emerg Med. 2008;51:127-129)