Cocaine-associated Chest Pain Research Articles

Management of Cocaine-Associated Chest Pain and Myocardial Infarction

The goals of the present article are to provide a critical review of the literature on cocaine-associated chest pain and myocardial infarction (MI) and to give guidance for diagnostic and therapeutic interventions. Classification of recommendations and levels of evidence are expressed in the American College of Cardiology/American Heart Association (ACC/AHA) format as follows: The Writing Committee conducted a comprehensive search of the medical literature concerning cocaine-associated chest pain and MI. The literature search included English-language publications on humans and animals from 1960 to 2007. In addition to broad-based searching concerning cocaine, specific targeted searches were performed on cocaine and the following topics: MI, chest pain, emergency department (ED), aspirin, nitroglycerin, calcium channel blocker, benzodiazepine, thrombolytics, phentolamine, heparin, primary angioplasty, ECG, and stress testing. Literature citations were generally limited to published articles listed in Index Medicus. The article was reviewed by 4 outside reviewers nominated by the AHA. Cocaine is the second most commonly used illicit drug in the United States, with only marijuana …

Application of the TIMI risk score in ED patients with cocaine-associated chest pain

Objective The TIMI risk score has been validated as a risk stratification tool in emergency department (ED) patients with potential acute coronary syndrome. The goal of this study was to assess its ability to predict adverse cardiovascular outcomes in cocaine-associated chest pain. Methods This was a prospective cohort study of ED patients with chest pain with cocaine use. Data included demographics, medical history, and TIMI risk score. The main outcomes were acute myocardial infarction, revascularization, or death within 30 days of ED presentation. Results There were 261 patient visits. Patients were 43.2 +8 years old, 73% male, 92% black, and 75% smokers. There were 33 patients with the composite outcome. The incidence of 30-day outcomes according to TIMI score is as follows: TIMI 0, 3.7% (95% CI, 0.1-8.3); TIMI 1, 13.2% (5.7-20.7); TIMI 2, 17.1% (4.3-29.8); TIMI 3, 21.4% (4.4-38.4); TIMI 4, 20.0% (0.1-43.6); TIMI 5/6, 50.0% (0.1-100). Conclusions The TIMI risk score has no clinically useful predictive value in patients with cocaine-associated chest pain.

Caring for patients with cocaine-associated chest pain

Cocaine use in Ireland has increased signifi cantly and poses considerable physical and psychological distress for drug users. Most patients who seek help for cocaine-associated complaints present with chest pain. However, many nurses in acute hospital facilties have limited knowledge of the management of cocaineassociated chest pain. This article will provide background information on the illicit drug cocaine and will focus on the holistic management of the patient who presents with cocaine-associated chest pain.

Caring for patients with cocaine-associated chest pain

Cocaine use in Ireland has increased signifi cantly and poses considerable physical and psychological distress for drug users. Most patients who seek help for cocaine-associated complaints present with chest pain. However, many nurses in acute hospital facilties have limited knowledge of the management of cocaineassociated chest pain. This article will provide background information on the illicit drug cocaine and will focus on the holistic management of the patient who presents with cocaine-associated chest pain.

Traditional Risk Factors and Acute Myocardial Infarction in Patients Hospitalized with Cocaine‐Associated Chest Pain

Cocaine causes coronary artery constriction and may cause acute myocardial infarction (AMI). The role of traditional coronary risk factors in cocaine-associated myocardial infarction is unclear. We hypothesized that traditional risk factors play a major role in predicting AMI in patients admitted with cocaine-associated chest pain After reviewing 165 admissions for chest pain in patients with a history of recent cocaine use and/or a positive drug screen from January 2001 to December 2004, we identified 151 patients with information available on at least 6 of the following 7 risk factors: gender, hypertension, hyperlipidemia, diabetes, smoking, family history of coronary artery disease (CAD) and known CAD. AMI was diagnosed using WHO criteria. A risk score was calculated on the basis of the number of risk factors, gender and age. Association of AMI was evaluated with the individual risk factors and with the risk score. AMI was identified in 21 patients (14%). All patients diagnosed with AMI were smokers. Continuous risk score (p < 0.0001), highest vs. lowest quartile of risk score (p = 0.007), known CAD, age, hyperlipidemia and family history of CAD were individually associated with the diagnosis of AMI (p>or=0.05). Each quartile of risk score was associated with increased odds of the diagnosis of AMI and score of 8 or higher was statistically significant. Several traditional risk factors are associated with the diagnosis of AMI among patients hospitalized with cocaine-associated chest pain and increasing risk factor score was associated with increasing odds of AMI diagnosis.

The Thrombolysis in Myocardial Infarction (TIMI) Risk Score Does Not Predict Outcome in Patients with Cocaine-associated Chest Pain

The Thrombolysis in Myocardial Infarction (TIMI) Risk Score Does Not Predict Outcome in Patients with Cocaine-associated Chest Pain

The cardiovascular effects of cocaine

Cocaine use continues to be prevalent among all races and socioeconomic groups in the United States. Patients presenting to emergency departments after cocaine ingestion frequently present with a chief complaint of chest pain. Although acute myocardial infarction is perhaps the most concerning diagnosis in this setting, there are many other potential causes of chest pain after cocaine ingestion. This article reviews the pharmacology of cocaine, as well as the etiologies and treatment of cocaine-associated chest pain, with an emphasis on this drug’s range of cardiovascular effects.

Trends in Clinical Toxicology: Advances That May Change Your Practice

Recent studies have had a significant impact on the practice of Medical Toxicology. We review selected articles that have advanced our thinking about consequential issues such as gastrointestinal decontamination, paracetamol poisoning, ethanol withdrawal, cocaine-associated chest pain, carbon monoxide poisoning and over-anticoagulation.

Characteristics of Cocaine Users Presenting to an Emergency Department Chest Pain Observation Unit

This report examines the sociodemographic and substance use characteristics, co-occurring psychological status, substance abuse consequences, and prior experiences with substance abuse treatment among patients with cocaine-associated chest pain presenting to an emergency department chest pain observation unit. This was a consecutive cohort of patients in the emergency department chest pain observation unit aged 18-60 years with low to moderate risk for acute coronary syndrome and recent cocaine use. Responses on standardized and validated instruments were used to examine demographic and clinical characteristics of the sample and to compare patients who met Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) criteria for past three-month substance abuse or substance dependence with patients who did not. Of 145 eligible patients identified between June 1, 2002, and February 29, 2004, 86% met criteria for a lifetime DSM-IV substance use disorder and 50% met past three-month criteria. Approximately one half of the total sample reported substantial symptoms of depression. Substance use frequency and consequences, depression, and psychological distress were significantly more severe among those with past three-month substance use diagnoses; however, most sociodemographic characteristics were not associated with substance use diagnoses. Interest in treatment services and treatment history was also significantly associated with the presence of a substance use disorder diagnosis. Findings regarding diversity in alcohol and drug involvement, current level of psychological functioning, depressive symptomatology, and interest in treatment services provide useful information for designing emergency department-based interventions for this population.

Validation of a brief observation period for patients with cocaine-associated chest pain

Weber JE, Shofer FS, Larkin GL, et al (University of Michigan, Ann Arbor, MI; Hurley Medical Center, Flint, MI; University of Texas, Dallas, TX; et al) Retrospective studies of patients with cocaine-related chest pain treated by a strategy of discharge from the ED after 12 hours of observation and no evidence of ischemia have been reported. The complication rate in these reports appears to be very low. The safety of a 9- to 12-hour observation period for patients with cocaine-related chest pain at low to intermediate risk for cardiovascular events was assessed prospectively. Three hundred forty-four patients with cocaine-related chest pain receiving protocol-driven care in a chest-pain observation unit were included. These were consecutive patients who had reported or tested positive for cocaine use. Patients with normal troponin I levels, with no new ischemic changes on ECG, and who had no cardiovascular complications during 9 to 12 hours of observation were discharged. Death from cardiovascular causes at 30 days was the main outcome measure. Twelve percent of the patients were admitted directly to the hospital. Thus, 302 patients remained in the study cohort. None of the patients died of cardiovascular causes within 30 days of discharge. Of 256 patients with detailed follow-up data, only 4 (1.6%) subsequently had a nonfatal myocardial infarction. All 4 of these patients had continued to use cocaine. For patients with cocaine-related chest pain, a policy of 9 to 12 hours of observation followed by discharge appears to be safe. However, such patients should still be examined for potential acute coronary syndromes. Those who do not have recurrent symptoms, increased levels of markers of myocardial necrosis, or dysrhythmias may be safely released after 9 to 12 hours of observation. Strategies for substance abuse treatment are needed for such patients, as their likelihood of nonfatal myocardial infarction is increased if they continue to use cocaine.

Validation of a brief observation period for patients with cocaine-associated chest pain

Validation of a brief observation period for patients with cocaine-associated chest pain

Managing Patients with Cocaine-Associated Chest Pain

In this prospective study, investigators evaluated an observation protocol for patients with cocaine-associated chest pain. Over a 2-year period,

A prospective, randomized, controlled trial of benzodiazepines and nitroglycerine or nitroglycerine alone in the treatment of cocaine-associated acute coronary syndromes

The purpose of the present study was to compare the use of lorazepam plus nitroglycerine (NTG) versus NTG alone in the reduction of cocaine induced chest pain in the emergency department. The secondary objective of the study was to help determine the safety of lorazepam in the treatment of cocaine- associated chest pain. The study was a prospective, randomized, single-blinded, controlled trial conducted at an university-affiliated urban emergency department (ED). All patients who presented with cocaine-associated chest pain were enrolled. Exclusion criteria included age greater than 45 years, documented coronary artery disease, chest pain of more than 72 hours duration, or pretreatment with nitroglycerin. Patients were given either sublingual nitroglycerine (SL NTG) (Group 1) or SL NTG plus 1 mg of lorazepam intravenously (Group 2) every 5 minutes for a total of 2 doses. Chest pain was recorded on an ordinal scale of 0 to 10 at baseline, and then at 5 minutes after each dose. Adverse reactions to medication were also recorded. Twenty-seven patients met the inclusion criteria and were enrolled in the study. The average age of these subjects was 34.1 years, and 67% were men. The NTG-only group consisted of 15 patients and the NTG-plus-lorazepam group consisted of 12 patients. Baseline mean chest-pain scores were 6.87 in Group 1 and 6.54 in Group 2, with no differences between groups. Five minutes after initial treatment, mean scores for the two groups were 5.2 and 3.9, respectively, with a difference in means of 1.24 (95% confidence interval [CI] −0.8-3.8). Five minutes after the second treatment, the mean scores were 4.6 and 1.5, respectively, with a difference in means of 3.1 (95% CI 1.2-5). Kruskal-Wallis testing showed a significant difference in pain relief between the two study groups (P =.003), with greater pain relief noted at 5 and 10 minutes in the NTG-plus-lorazepam group (P =.02 and P =.005, respectively). All patients in the study were admitted to the hospital, but no patient in either group had an acute myocardial infarction or cardiac complications in the ED. No adverse side effects were noted for either group. The early use of lorazepam with NTG was more efficacious than NTG alone, and appears to be safe in relieving cocaine-associated chest pain. (Am J Emerg Med 2003;21:39-42. Copyright 2003, Elsevier Science (USA). All rights reserved.)

Coronary angiographic findings in patients with cocaine-associated chest pain

Patients who present to the Emergency Department (ED) with chest pain associated with cocaine use are a common problem. The incidence and predictors of underlying significant coronary disease in patients with and without myocardial infarction (MI) has not been well described. Patients who underwent coronary angiography within 5 weeks of an ED evaluation for cocaine-associated chest pain were studied. Significant disease was defined as ≥ 50% stenosis of a coronary artery or major branches or bypass graft. A total of 90 patients underwent coronary angiography. Significant disease was present in 45 (50%), with 1-vessel disease in 32%, 2-vessel disease in 10%, 3-vessel disease in 6%, with significant graft stenosis in 3%. Significant disease was present in 77% of patients with MI or troponin I elevations, compared to only 35% of patients without myonecrosis. Predictors of significant coronary disease included MI or troponin I elevations, prior MI, known coronary disease (prior MI or revascularization), and elevated cholesterol. Only 7 of the 39 patients (18%) without myonecrosis or a history of coronary disease had significant disease on angiography. In conclusion, significant disease is found in the majority of patients with cocaine-associated MI or troponin elevations. In contrast, only a minority of those without myonecrosis have significant coronary disease.

Utility of Troponin I in Patients with Cocaine‐associated Chest Pain

AbstractBaseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine‐associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. Objective: To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. Methods: Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule‐in protocol that included serial sampling of creatine kinase (CK), CK‐MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK‐MB MI (CK‐MB ≥ 8 ng/mL with a relative index [(CK‐MB × 100)/total CK] ≥ 4, cardiac death, and significant coronary disease (≥50%). Results: Of the 246 admitted patients, 34 (14%) met CK‐MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI‐positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK‐MB criteria for MI, and the other had a peak CK‐MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK‐MB MI and cTnI and were not significantly different. Conclusions: Most patients with cTnI elevations meet CK‐MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK‐MB for diagnosing necrosis in patients with cocaine‐associated chest pain and suspected MI.

Utility of troponin I in patients with cocaine-associated chest pain.

Baseline electrocardiogram abnormalities and market elevations not associated with myocardial necrosis make accurate diagnosis of myocardial infarction (MI) difficult in patients with cocaine-associated chest pain. Troponin sampling may offer greater diagnostic utility in these patients. To assess outcomes based on troponin positivity in patients with cocaine chest pain admitted for exclusion of MI. Outcomes were examined in patients admitted for possible MI after cocaine use. All patients underwent a rapid rule-in protocol that included serial sampling of creatine kinase (CK), CK-MB, and cardiac troponin I (cTnI) over eight hours. Outcomes included CK-MB MI (CK-MB >or= 8 ng/mL with a relative index [(CK-MB x 100)/total CK] >or= 4, cardiac death, and significant coronary disease (>or=50%). Of the 246 admitted patients, 34 (14%) met CK-MB criteria for MI and 38 (16%) had cTnI elevations. Angiography was performed in 29 of 38 patients who were cTnI-positive, with significant disease present in 25 (86%). Three of the four patients without significant disease who had cTnI elevations met CK-MB criteria for MI, and the other had a peak CK-MB level of 13 ng/mL. Sensitivities, specificities, and positive and negative likelihood ratios for predicting cardiac death or significant disease were high for both CK-MB MI and cTnI and were not significantly different. Most patients with cTnI elevations meet CK-MB criteria for MI, as well as have a high incidence of underlying significant disease. Troponin appears to have an equivalent diagnostic accuracy compared with CK-MB for diagnosing necrosis in patients with cocaine-associated chest pain and suspected MI.

Cocaine-Associated Chest Pain

Recreational cocaine use dates back more than 5000 years among the Incas, and since then, its popularity has been waxing and waning. Sigmund Freud popularized the drug in Europe in the late 1800s. Cocaine reached the United States in the early 1900s and its immediate popularity led President Taft to declare it public enemy no. 1 in 1910. Cocaine became popular again in the 1980s and has since reached epidemic proportions. An estimated 23 million persons have used cocaine at least once (30% of men and 20% of women between the ages of 26 and 34 years) and 1.5 million are regular users.12 Cocaine produces potent euphoric effects rapidly, which probably explains its popularity; however, its actions on the central nervous and cardiovascular systems can also result in significant morbidity and occasional mortality.

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

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

A pilot study to assess the safety of dobutamine stress echocardiography in the emergency department evaluation of cocaine-associated chest pain

Study Objective: Chest pain in the setting of cocaine use poses a diagnostic dilemma. Dobutamine stress echocardiography (DSE) is a widely available and sensitive test for evaluating cardiac ischemia. Because of the theoretical concern regarding administration of dobutamine in the setting of cocaine use, we conducted a pilot study to assess the safety of DSE in emergency department patients with cocaine-associated chest pain. Methods: A prospective case series was conducted in the intensive diagnostic and treatment unit in the ED of an urban tertiary-care teaching hospital. Patients were eligible for DSE if they had used cocaine within 24 hours preceding the onset of chest pain and had a normal ECG and tropinin I level. Patients exhibiting signs of continuing cocaine toxicity were excluded from the study. All patients were admitted to the hospital for serial testing after the DSE testing in the intensive diagnostic and treatment unit. Results: Twenty-four patients were enrolled. Two patients had inadequate resting images, one DSE was terminated because of inferior hypokinesis, another DSE was terminated because of a rate-related atrial conduction deficit, and 1 patient did not reach the target heart rate. Thus, 19 patients completed a DSE and reached their target heart rates. None of the patients experienced signs of exaggerated adrenergic response, which was defined as a systolic blood pressure of greater than 200 mm Hg or the occurrence of tachydysrhythmias (excluding sinus tachycardia). Further suggesting lack of exaggerated adrenergic response, 13 (65%) of 20 patients required supplemental atropine to reach their target heart rates. Conclusion: No exaggerated adrenergic response was detected when dobutamine was administered to patients with cocaine-related chest pain. [Dribben WH, Kirk MA, Trippi JA, Cordell WH. A pilot study to assess the safety of dobutamine stress echocardiography in the emergency department evaluation of cocaine-associated chest pain. Ann Emerg Med. July 2001;38:42-48.]

COCAINE USE AND ACUTE MYOCARDIAL INFARCTION

Cocaine use in the United States is widespread, affecting more than 30 million Americans. Although many of these persons do not seek healthcare, the overriding cause for hospitalization is cocaine-associated chest pain. Because only a minority of these patients suffer myocardial injury, it is important to exclude even rarer life-threatening causes for chest pain, such as aortic dissection or pneumothorax. Following that, a thorough knowledge of the pathophysiology and existing literature helps to provide cost-effective care, which focuses resources on those patients most likely to suffer complications. Regardless of the severity of complications, referral to cocaine detoxification programs, counseling, social support, and outpatient follow-up care for modification of cardiac risk factors is a fundamental component of long-term patient care.