Validation of a Brief Observation Period for Patients with Cocaine-Associated Chest Pain

Weber, James E.; Shofer, Frances S.; Larkin, Gregory Luke; Kalaria, Amit S.; Hollander, Judd E.

doi:10.1056/nejmoa022206

Cited by 145 publications

(66 citation statements)

References 25 publications

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“…The association of cocaine use with acute aortic dissection and the causal relationship of cocaine use with acute aortic dissection are not well defined (4,10,14). Several case reports of aortic dissection have been reported (15)(16)(17)(18)(19), but the article by Hsue et al (20) was the only study that clearly linked cocaine use and aortic dissection (20).…”

Section: Previous Studiesmentioning

confidence: 99%

Cocaine-related acute aortic dissection: Patient demographics and clinical outcomes

Singh¹,

Trivedi²,

Adhikari³

et al. 2007

Canadian Journal of Cardiology

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Section: Previous Studiesmentioning

confidence: 99%

Cocaine-related acute aortic dissection: Patient demographics and clinical outcomes

Singh¹,

Trivedi²,

Adhikari³

et al. 2007

Canadian Journal of Cardiology

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“…Cocaine causes tachycardia, and CTA images are dependent on heart rate. However, most patients in this study and prior studies of patients with cocaine-associated chest pain are not tachycardic [7,8,10,59]. There are some patients with tachycardia after cocaine use who may not be candidates for coronary CTA because most protocols for noncocaine-using patients require administration of betaadrenergic blockers for heart rate control, and these agents should be avoided in the setting of cocaine [41,50].…”

Section: Limitationsmentioning

confidence: 85%

“…Efforts to risk-stratify patients with cocaine-associated chest pain early in the ED course have been unsuccessful [7,[9][10][11]. Mittleman et al demonstrated that the greatest risk of AMI is within 60 minutes following cocaine use [12].…”

Section: Introductionmentioning

confidence: 99%

“…Based on an analysis of a large retrospective study, it was proposed that patients at risk for complications could be identified within 12 hours of presentation via an observation unit strategy [13]. A 9-to 12-hour observation period has been validated as safe and cost effective if the patient experiences no cardiac complications during that time [10].…”

Section: Introductionmentioning

confidence: 99%

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Coronary computerized tomography angiography for rapid discharge of low-risk patients with cocaine-associated chest pain

et al. 2009

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Background: Most patients presenting to emergency departments (EDs) with cocaine-associated chest pain are admitted for at least 12 hours and receive a "rule out acute coronary syndrome" protocol, often with noninvasive testing prior to discharge. In patients without cocaine use, coronary computerized tomography angiography (CTA) has been shown to be useful for identifying a group of patients at low risk for cardiac events who can be safely discharged. It is unclear whether a coronary CTA strategy would be efficacious in cocaine-associated chest pain, as coronary vasospasm may account for some of the ischemia. We studied whether a negative coronary CTA in patients with cocaine-associated chest pain could identify a subset safe for discharge.Methods: We prospectively evaluated the safety of coronary CTA for low-risk patients who presented to the ED with cocaineassociated chest pain (self-reported or positive urine test). Consecutive patients received either immediate coronary CTA in the ED (without serial markers) or underwent coronary CTA after a brief observation period with serial cardiac marker measurements. Patients with negative coronary CTA (maximal stenosis less than 50%) were discharged. The main outcome was 30-day cardiovascular death or myocardial infarction.Results: A total of 59 patients with cocaine-associated chest pain were evaluated. Patients had a mean age of 45.6 Ϯ 6.6 yrs and were 86% black, 66% male. Seventy-nine percent had a normal or nonspecific ECG and 85% had a TIMI score <2. Twenty patients received coronary CTA immediately in the ED, 18 of whom were discharged following CTA (90%). Thirty-nine received coronary CTA after a brief observation period, with 37 discharged home following CTA (95%). Six patients had coronary stenosis Ն50%. During the 30-day follow-up period, no patients died of a cardiovascular event (0%; 95% CI, 0-6.1%) and no patient sustained a nonfatal myocardial infarction (0%; 95% CI, 0-6.1%).Conclusions: Although cocaine-associated myocardial ischemia can result from coronary vasoconstriction, patients with cocaineassociated chest pain, a non-ischemic ECG, and a TIMI risk score <2 may be safely discharged from the ED after a negative coronary CTA with a low risk of 30-day adverse events.

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“…Numerous acute medical problems have been associated with cocaine abuse, including cardiac dysrhythmias [2][3][4][5][6][7]. Although the etiology of cocaine-associated dysrhythmias is complex and not fully understood, lethal ventricular dysrhythmias are a theorized cause of sudden death associated with cocaine use [8].…”

Section: Introductionmentioning

confidence: 99%

The effect of amiodarone pretreatment on survival of mice with cocaine toxicity

et al. 2005

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Introduction: Cocaine is a common drug of abuse and use has been associated with ventricular dysrhythmias. Published guidelines suggest that amiodarone is the first line antidysrhythmic for ventricular tachycardia and fibrillation. However, the effects amiodarone in the setting of cocaine toxicity are unknown and unstudied. The purpose of this study was to evaluate the safety and efficacy of amiodarone pretreatment in a murine model of acute cocaine toxicity.Methods: This was a randomized, blinded, placebo controlled investigation using male CF-1 mice weighing 29-37 g. First, the safety of an intraperitoneal dose of amiodarone (40 mg/kg) was confirmed in 5 mice. Second, based on preliminary investigations, an approximate intraperitoneal LD 50 dose of cocaine (110 mg/kg) was identified and used as the cocaine dose in this study. Animals were then randomized to 2 groups. The control group received 0.5 mL of intraperitoneal 0.9% saline 30 minutes before cocaine. The study group received 40 mg/kg of intraperitoneal amiodarone (40 mg/kg) 30 minutes before cocaine. A blinded observer monitored mice for 2 hours after cocaine administration.Results: No mice in the amiodarone-only group developed any signs of toxicity or died. In the saline ϩ cocaine group 31/32 (96.9%; 95% CI 83.8 to 99.9) mice seized with a median time to seizure of 2.5 minutes, and 23/32 (71.9%; 95% CI 52.3 to 86.3) died with a median time to death of 5.5 minutes. In the amiodarone ϩ cocaine group 31/33 (93.9%; 95% CI 79.0 to 99.3) mice seized with a median time to seizure of 2.0 minutes, and 24/33 (72.7%; 95% CI 54.5 to 86.7) died with a median time to death of 6.0 minutes. All animals that died did so within 9 minutes. The difference in the proportion of animals dying in the amiodarone ϩ cocaine group compared to the saline ϩ cocaine group was 0.008 (Ϫ21 to 22%).Conclusions: In this study, pretreatment with amiodarone in cocaine poisoned mice resulted in no change in seizure incidence or mortality. However, definite conclusions about the reason for these findings cannot be drawn from this model.

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Validation of a Brief Observation Period for Patients with Cocaine-Associated Chest Pain

Abstract: Patients with cocaine-associated chest pain who do not have evidence of ischemia or cardiovascular complications over a 9-to-12-hour period in a chest-pain observation unit have a very low risk of death or myocardial infarction during the 30 days after discharge.

Cited by 145 publications

References 25 publications

Cocaine-related acute aortic dissection: Patient demographics and clinical outcomes

Cocaine-related acute aortic dissection: Patient demographics and clinical outcomes

Coronary computerized tomography angiography for rapid discharge of low-risk patients with cocaine-associated chest pain

The effect of amiodarone pretreatment on survival of mice with cocaine toxicity

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