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Tobacco Alcohol Cocaine Opioids Hallucinogens Amphetamine Marijuana No Marijuana 0 10% 20% 30% 40% 50% 60% 70% Recreational Marijuana Use & Acute Ischemic.

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Presentation on theme: "Tobacco Alcohol Cocaine Opioids Hallucinogens Amphetamine Marijuana No Marijuana 0 10% 20% 30% 40% 50% 60% 70% Recreational Marijuana Use & Acute Ischemic."— Presentation transcript:

1 Tobacco Alcohol Cocaine Opioids Hallucinogens Amphetamine Marijuana No Marijuana 0 10% 20% 30% 40% 50% 60% 70% Recreational Marijuana Use & Acute Ischemic Stroke: A Population-Based Analysis of Hospitalized Patients in the United States Kavelin Rumalla 1, Adithi Y Reddy 1, Manoj K Mittal, MD 2 1 University of Missouri-Kansas City School of Medicine, Kansas City MO; 2 University of Kansas Medical Center, Department of Neurology, Kansas City, KS INTRODUCTION ➢ Recreational marijuana use is considered to have few adverse effects. 1,2,4-8 ➢ The association between marijuana, the most commonly used recreational drug in the United States, and stroke has been explored in several case reports. 1 ➢ An epidemiological relationship between recreational marijuana abuse and acute ischemic stroke has not previously been reported. METHODS ➢ The incidence of AIS was significantly greater among marijuana users compared to non-users (RR: 1.13, P<0.0001) and had the greatest difference in the 25–34 age group (RR: 2.26, P<0.0001). ➢ Marijuana users were more likely to use other illicit substances but had less overall medical comorbidity. ➢ Marijuana abuse was more prevalent among younger patients, males, African American patients, and Medicaid enrollees (P<0.0001). ➢ In multivariable analysis, adjusted for potential confounders, marijuana (OR: 1.17, 95% CI: 1.15–1.20), tobacco (OR: 1.76, 95% CI: 1.74–1.77), cocaine (OR: 1.32, 95% CI: 1.30–1.34), and amphetamine (OR: 2.21, 95% CI: 2.12–2.30) usage were found to increase the likelihood of AIS (all P<0.0001). ➢ Among younger adults aged 15-54, recreational marijuana use is independently associated with 17% increased likelihood of AIS hospitalization. ➢ Data Source: The Nationwide Inpatient Sample (2004-2011) was used to create marijuana use (N=2,496,165) and non- marijuana use (N=116,163,454) cohorts. ➢ Inclusion Criteria: All patients aged 15-54 with a primary diagnosis of acute ischemic stroke (ICD-9-CM code 430). Patients with a secondary diagnosis of current marijuana use were further identified. ➢ Exclusion criteria: Patients coded as “in remission” from drug abuse. ➢ Predictor variables: Demographics, pre-existing comorbidity, substance abuse. ➢ Outcome variables: Symptomatic cerebral vasospasm, discharge disposition, in-hospital mortality. ➢ Statistical analysis: Age stratification of the population into groups of 15-24, 25-34, 35-44, and 45-54 was performed. We utilized bivariate analysis to compare demographics and comorbid risk factors of AIS. Multivariable logistic regression analyses were used to evaluate marijuana use as a risk factor of AIS and symptomatic cerebral vasospasm. P was set a priori at <0.0001 for all analyses. RESULTS CONCLUSION LIMITATIONS RESULTS The Gateway Drug Effect: Comparing the Incidence of Substance Abuse in Marijuana vs. Non-Marijuana Cohorts ➢ We were unable to account for any dose-dependent mechanisms of marijuana use due to the limitations of the ICD-9-CM coding system. ➢ The high liposolubility of cannabis metabolites allows them to persist in fatty tissues and thereby be detected in urine for weeks after use. 3 ➢ There is no information available in the NIS regarding time from last drug use to AIS occurrence. ➢ The lack of data on preadmission functional status and severity in the NIS inhibits adjustment for the severity of AIS. 1.D.G. Hackam, Cannabis and stroke: systematic appraisal of case reports, Stroke J. Cereb. Circ. 46 (3) (2015) 852–856, http://dx.doi.org/10.1161/STROKEAHA.115. 008680 2.D.Z. Rose, W.R. Guerrero, M.V. Mokin, et al., Hemorrhagic stroke following use of the synthetic marijuana “spice”, Neurology 85 (13) (2015) 1177–1179, http://dx.doi. org/10.1212/WNL.0000000000001973. 3.I. Mateo, A. Pinedo, M. Gomez-Beldarrain, J.M. Basterretxea, J.C. Garcia-Monco, Re- current stroke associated with cannabis use, J. Neurol. Neurosurg. Psychiatry 76 (3) (2005) 435–437, http://dx.doi.org/10.1136/jnnp.2004.042382. 4.P.A. Barber, H.M. Pridmore, V. Krishnamurthy, et al., Cannabis, ischemic stroke, and transient ischemic attack: a case–control study, Stroke J. Cereb. Circ. 44 (8) (2013) 2327–2329, http://dx.doi.org/10.1161/STROKEAHA.113.001562. 5.D. Renard, G. Taieb, G. Gras-Combe, P. Labauge, Cannabis-related myocardial infarc- tion and cardioembolic stroke, J. Stroke Cerebrovasc. Dis. Off. J. Natl. Stroke Assoc. 21 (1) (2012) 82–83, http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2010.04.002. 6.K. Esse, M. Fossati-Bellani, A. Traylor, S. Martin-Schild, Epidemic of illicit drug use, mechanisms of action/addiction and stroke as a health hazard, Brain Behav. 1 (1) (2011) 44–54, http://dx.doi.org/10.1002/brb3.7. 7. P. Cooles, R. Michaud, Stroke after heavy cannabis smoking, Postgrad. Med. J. 63 (740) (1987) 511-511. 8.T. Geller, L. Loftis, D.S. Brink, Cerebellar infarction in adolescent males associated with acute marijuana use, Pediatrics 113 (4) (2004) e365–e370. REFERENCES


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