Cocaine-associated chest pain: a review
December 13, 2011, 10:35 pm
Rethinking Cocaine-Associated Chest Pain and Acute Coronary Syndromes. Finkel jB, Marhefka GD. Mayo Clin Proc 2011 Dec;86:1198-1207.
Cocaine has many actions predisposing to myocardial ischemia. Raised heart rate and blood pressure, increasing myocardial oxygen demand. At the same time, cocaine can cause coronary artery vasospasm, decreasing supply. In addition, chronic cocaine use accelerates atherosclerosis, activates platelets, and increases leukocyte adhesion — all effects that promote thrombosis.
Although many patients who have acutely or chronically used cocaine present to the emergency department with chest pain, only about 6% rule in for acute myocardial infarction (AMI). This makes managing cocaine-associated chest pain (CACP) a difficult and challenging problem, since the clinician must deal the risk of undertreating patients with actual AMI or acute coronary syndrome, and inefficiently over-managing those without. Therefore, I eagerly anticipated reading this article that promised to rethink the entire problem based on recent research.
Unfortunately, I was sorely disappointed. The authors discussion seems to be based not so much on recent reliable research as extensively on a recent (2011) set of guidelines from the American College of Cardiology Foundation and the American Heart Association. As far as I can determine, there was not a single medical toxicologist who participated in writing the section related to cocaine. Therefore, although they have long been a mainstay of treating CACP, benzodiazepines have completely dropped out of the authors’ management algorithm.
There are other problems with this paper. The authors write that:
Coronary computed tomography may have a role in treating patients who present with CCP . . . Walsh et al examined 59 patients presenting with CCP. All patient had a nonischemic ECG, TIMI risk score of 2 or less, and computed tomography results showing less than 50% coronary artery stenosis. At 30-day follow-up there were not reports of fatal Mi or death in any of the patients.
In the past TPR has discussed why the Walsh study is meaningless and coronary CT is a very poor test in this setting. The fact that these authors uncritically cite Walsh’s findings suggests that they are not so much rethinking CACP as regurgitating previously flawed scientific evidence.
Mary Shue Says:
I was hoping your “discussrd” link would go to your previous discussion but it was tied to the same info as “guidelines”. Woild you mind posting that link again? Thanks
December 14th, 2011
Hossein Sanaei-Zadeh Says:
Dear Leon
What is your idea about the following article?
Relationship between cocaine use and coronary artery disease in patients with symptoms consistent with an acute coronary syndrome.
AuthorsChang AM, et al. Show all Journal
Acad Emerg Med. 2011 Jan;18(1):1-9. doi: 10.1111/j.1553-2712.2010.00955.x. Epub 2010 Dec 23.
Affiliation
Department of Emergency Medicine, University of Pennsylvania, Philadelphia, PA.
Comment in
Acad Emerg Med. 2011 Jul;18(7):771; author reply 772-3.
Acad Emerg Med. 2011 Jan;18(1):68-71.
Abstract
OBJECTIVES: Observational studies of patients with cocaine-associated myocardial infarction have suggested more coronary disease than expected on the basis of patient age. The study objective was to determine whether cocaine use is associated with coronary disease in low- to intermediate-risk emergency department (ED) patients with potential acute coronary syndrome (ACS).
METHODS: The authors conducted a cross-sectional study of low- to intermediate-risk patients<60 years of age who received coronary computerized tomographic angiography (CTA) for evaluation of coronary artery disease (CAD) in the ED. Patients were classified into three groups with respect to CAD: maximal stenosis <25%, 25% to 49%, and ≥50%. Prespecified multivariate modeling (generalized estimating equations) was used to assess relationship between cocaine and CAD.
RESULTS: Of 912 enrolled patients, 157 (17%) used cocaine. A total of 231 patients had CAD ≥25%; 111 had CAD ≥50%. In univariate analysis, cocaine use was not associated with a lesion 25% or greater (12% vs. 14%; relative risk [RR]=0.89, 95% confidence interval [CI]=0.5 to 1.4) or 50% or greater (12% vs. 11%; RR=1.15, 95% CI=0.6 to 2.3). In multivariate modeling adjusting for age, race, sex, cardiac risk factors, and Thrombosis in Myocardial Infarction (TIMI) score, cocaine use was not associated with the presence of any coronary lesion (adjusted RR=0.95, 95% CI=0.69 to 1.31) or coronary lesions 50% or greater (adjusted RR=0.78, 95% CI=0.45 to 1.38). There was also no relationship between repetitive cocaine use and coronary calcifications or between recent cocaine use and CAD.
CONCLUSIONS: In symptomatic ED patients at low to intermediate risk of an ACS, cocaine use was not associated with an increased likelihood of coronary disease after adjustment for age, race, sex, and other risk factors for coronary disease.
© 2010 by the Society for Academic Emergency Medicine.
December 17th, 2011
Leon Says:
Dr. Sanaei-Zadeh:
I have discussed my thoughts about the whole issue of CTA in cocaine-associated chest pain when I commented on a “Letter to the Editor” about this article in a previous post. My discussion can be found at http://bit.ly/nUzSmd. See also the link to a discussion of the Walsh article.
January 8th, 2012
Leon Says:
Ms. Shue:
Thank you for your question — I apologize that I didn’t reply earlier. I have updated the link in the post, which should now refer back to my discussion of the Walsh study.
January 8th, 2012