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Case Reports
. 2025 Mar 25;17(3):e81158.
doi: 10.7759/cureus.81158. eCollection 2025 Mar.

Chasing the High, Losing the Beat: A Case of Cocaine-Induced Myocardial Infarction

Saurabh Kumar Singh  1 , Chirag Agrawal  1 , Anbhigya Kumar Arya  1 , Satyajit Padhiary  1 , Devesh Kumar  1
Affiliations
Case Reports

Chasing the High, Losing the Beat: A Case of Cocaine-Induced Myocardial Infarction

Saurabh Kumar Singh et al. Cureus. .

Abstract

Cocaine use is a well-established risk factor for various cardiovascular complications, including acute myocardial infarction (MI). The pathophysiological mechanisms responsible for cocaine-induced MI are multifactorial, encompassing coronary vasoconstriction, increased myocardial oxygen demand, and thrombosis. While cocaine-related cardiovascular events are more commonly seen in individuals with pre-existing risk factors, cases involving young, otherwise healthy individuals remain rare, yet they present a significant concern. We present the case of a young male in his late teens who presented to the emergency department with acute-onset chest pain that began two hours following his first-time use of cocaine. On evaluation, it was an anterior wall MI. Urgent coronary angiography was performed, which showed an ostial cut-off in the left anterior descending artery, along with a Thrombolysis in Myocardial Infarction (TIMI) grade V thrombus. Percutaneous coronary intervention (PCI) was successfully performed, and TIMI III flow was achieved. He was discharged on day five post-procedure, and at a six-month follow-up, he was doing well. This case highlights the need for early recognition and prompt intervention, including coronary angiography and PCI, to improve outcomes. Furthermore, it emphasizes the potential for long-term success with proper follow-up care and adherence to prescribed therapies.

Keywords: acute myocardial infarction; cardiovascular complications; chest pain; first-time cocaine use; young male.

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Conflict of interest statement

Human subjects: Consent for treatment and open access publication was obtained or waived by all participants in this study. Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work.

Figures

Figure 1
Figure 1. (A) A standard 12-lead electrocardiography showing anterolateral wall myocardial infarction (QRBBB with ST elevation in chest leads V1-V6 and I, AVL with reciprocal ST depression in Il/lIl/AVF). (B) Coronary angiography right anterior oblique caudal view showing the left anterior descending artery 100% cut-off from the ostia. (C and D) After balloon dilatation flow achieved with thrombus. (E and F) Final flow achieved post-stenting in right anterior oblique cranial and right anterior oblique caudal view, respectively.
Figure 2
Figure 2. Transthoracic M-mode echocardiography from parasternal long-axis view showing a left ventricular ejection fraction of 30%.
IVS = interventricular septum; LVPW = left ventricular posterior wall; LVEDD = left ventricular end-diastolic diameter; LVESD = left ventricular end-systolic diameter
See this image and copyright information in PMC

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