Benjamin R. Kummer, MD
Case series have reported biologically plausible associations between cocaine use and stroke in young patients, but few studies have rigorously investigated this relationship or the effects of drug ingestion timing or route of ingestion in large populations. Using a case-control design, Cheng and colleagues attempted to confirm the existence of the link between cocaine use and stroke in young patients, and delineate the relationship between timing and route of cocaine on the risk of ischemic stroke (IS). In this study, the authors drew their population from an existing, prospectively collected, case-control registry of 1,100 cases between the ages of 15 and 49 with first-ever IS, and approximately 1,100 controls. Cocaine use and timing/route were recorded on the basis of individual patient recollections (a small subset of patients had urine drug screening), as was confounding clinical and demographic data.
After adjusting for age, gender, ethnicity, smoking, hypertension, and alcohol use, patients that used cocaine in the 24 hours prior (OR 5.7, 95%CI 1.7-19.7) had significantly increased odds of IS compared to controls. However, the odds ratio for IS lost its statistically significance (OR 3.5, 95%CI 0.9-12.6) after removing higher-odds study periods. Patients that had smoked cocaine in the previous 24 hours had even higher adjusted odds of IS (OR 7.9, 95% 1.8-35.0), although no adjustment was made for smoking, hypertension, or alcohol use. Patients that reported smoking cocaine at any point also had slightly increased but not statistically significant adjusted odds of IS (OR 1.2, 95%CI 0.9-1.6). Patients that reported use of at least once in the past 1-30 days had a slightly increased, non-significant adjusted odds of IS (OR 1.1; 95% CI 0.7-1.9).
Overall, the number of patients exposed to cocaine use was very small relative to the sample size. Aside from the small number of observations, which caused effect estimates to be very wide, cases also had a greater proportion of patients with stroke risk factors (HTN, DM2, smoking, black race) than controls. The determination of drug use history could have been influenced by recall bias, and there may have also been a bias in under-reporting drug use by the study population (although this would have generated a conservative bias for the effect estimates). Also, while the logistic regression model was adjusted for some confounders, it was not adjusted for income level, education, employment, and insurance status, as well as important risk factors in young patients, such as hypercoagulable state, hyperlipidemia, family history of stroke, or obesity.
Despite its small number of observations, this study by Cheng and colleagues argues for a biologically plausible relationship between acute cocaine smoking and IS in young patients. It would have been interesting to see whether the association between acute cocaine smoking and IS disappeared with further adjustment for markers of health care access. These findings support urine toxicology screening for young patients with acute IS, although the implications for acute stroke management in such cases are unclear.