An evaluation of cocaine-induced chest pain.

STUDY OBJECTIVE: To determine if enzymatic evidence of acute myocardial injury is present in patients complaining of chest pain after cocaine use when the ECG is normal or nondiagnostic. DESIGN: Serial ECG and creatinine kinase (CK) and CK isoenzymes (CK-ISO) determinations were performed at time of emergency department presentation and every six hours over 12 hours on individuals complaining of chest pain within six hours of last cocaine use. SETTING: ED of an urban tertiary care center. TYPE OF PARTICIPANTS: Forty-two individuals with a mean age of 28.5 years. INTERVENTIONS: Patients with positive CK-ISOs were admitted immediately to formally rule out myocardial infarction. Patients developing ECG changes during observation period also were admitted even if CK-ISOs were normal. Patients with unchanged ECGs and normal CK-ISOs were discharged after 12 hours of observation. RESULTS: Eight patients (19%) had elevated CK and CK-ISO values at presentation. Two of these patients had elevated values on three sequential determinations and were believed to have sustained acute myocardial infarction. Six patients had elevated CK and CK-ISOs at presentation only. ECGs remained normal or nondiagnostic in all patients. CONCLUSIONS: Enzymatic evidence of acute myocardial injury may occur in patients who develop chest pain after cocaine use and have normal or nondiagnostic ECGs. This injury may reflect acute infarction or transient ischemia. Single or serial normal or nondiagnostic ECGs do not rule out ischemia or injury in this group of patients.

Chest pain and dyspnea related to "crack" cocaine smoking: value of chest radiography.

The chest radiographs of 71 patients who had chest pain or shortness of breath following the smoking of highly potent "crack" cocaine were retrospectively evaluated. Nine patients had abnormal findings on radiographs as follows: atelectasis or localized parenchymal opacification in four, pneumomediastinum in two, pneumothorax in one, hemopneumothorax in one, and pulmonary edema in one. Radiographic detection of these abnormalities was important in the clinical management of these patients. This spectrum of findings is presented with a discussion of the pathophysiologic mechanisms responsible.