Letter to the Editor Cocaine-induced coronary thrombosis and acute myocardial infarction Julio Nu´n˜ez Villota * , Lorenzo Fa´cila Rubio, Juan Sanchı ´s Fore´s, Vicent Bodı ´ Peris, Eva Plancha Burguera, Vicente Bertomeu Gonza´lez, Mauricio Pellicer Ban˜uls, Angel Lla´cer Escorihuela Servicio de Cardiologı ´a, Hospital Clı ´nico Universitario, Avda. Blasco Iba´n˜ez 17, 46010 Valencia, Spain Received 24 February 2003; accepted 21 April 2003 Keywords: Cocaine; Coronary thrombosis; Acute myocardial infarction 1. Introduction Cocaine-related heart ischemia is not an infrequent finding, particularly occurring in young male, and it has been associated with thrombosis in previously angiographic normal coronary arteries [1]. In the present report we describe a case of a patient with an acute myocardial infarction secondary to cocaine toxicity. 2. Clinical case A 26-year-old man was admitted to our hemodynamic laboratory because of an anterior AMI and post myocardial infarction angina. He is an active smoker (10 cigarettes/day) and consumes inhaled cocaine during weekends (the last consumption of cocaine was 1 week ago). No others risk factors were recorded. Initial electrocardiogram shows sinus rhythm and anterior QS complex (V1–V3) with antero- lateral ST segment elevation (V1–V5, D1 and aVL). Cre- atine-kinase isoenzyme MB and Troponin I were elevated at arrival. Upon admission, the patient was normotensive but with signs of pulmonary congestion. Ventriculography showed anterolateral and apical hypokinesia with an ejec- tion fraction of 21%. Coronariography revealed a massive thrombosis and distal vasoconstriction of the left anterior descending coronary artery. Circumflex and right coronary artery were angiographically normals (Fig. 1). Recombinant tissue plasminogen activator was started by intracoronary infusion (50 mg) with additional 50 mg via systemic. Clinical evolution was satisfactory without new ischemic events. Four days later, a second coronariography was performed showing a thrombus resolution in the left anterior descending coronary artery; a ventriculography showed an improvement in ejection fraction. The patient has remained asymptomatic at 6 months (Fig. 2). 3. Discussion Cocaine has been associated with myocardial ischemia and infarction independently of the administration route, the amount ingested and the frequency of use [2,3]. The medical literature contains numerous cases of acute myocardial infarction after cocaine use. With this case we want to stress that the risk of acute myocardial infarction remains elevated after acute cocaine use, and occurs in subjects with previously ‘‘normal’’ angiographycally coronary arteries (as has been described in about half of acute myocardial infarctions cocaine-relat- ed). Most patients with cocaine-related infarction are young, male and heavy smokers but without other risk factors for atherosclerosis [2,4,5]. The pathogenesis of cocaine-related infarction is multifactorial and includes an increased myo- cardial oxygen demand, marked vasoconstriction of the coronary arteries, enhanced platelet aggregation and throm- bus formation [2,3]. Although the risk of acute myocardial infarction is highest within the first hour [4,5], it may also occur as late as a few days after cocaine consumption (like in this case). One possible explanation may be the rise in cocaine metabolites after several hours with the deleterious vascular effect described above. It is important to identify patients with cocaine-related ischemia and acute myocardial infarction because the diag- 0167-5273/$ - see front matter D 2003 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2003.04.071 * Corresponding author. Tel.: +34-96-3347133; fax: +34-96-3862658. E-mail address: julionv@terra.es (J.N. Villota). www.elsevier.com/locate/ijcard International Journal of Cardiology 96 (2004) 481 – 482