2019 Research Forum

A Case of Meth-Induced Cardiomyopathy and Acute Myocardial Infarction David Aguirre MD, Jeffrey Coleman MD R2, Sarah El-Halees MS IV Department of Internal Medicine, Kern Medical

LHC noted a proximal LAD lesion of about 80% and left ventriculography showed an LV EF of 20% and global hypokinesis. An outside facility agreed to perform percutaneous coronary intervention (PCI) of the critical LAD lesion, however, while awaiting transfer he remained in the ICU for intense cardiac monitoring with continued medical management for ACS with heparin drip and started on nitroglycerin drip. Patient underwent revascularization and bare metal stenting of proximal LAD baring no complications and followed up in cardiology clinic. Medications on discharge were aspirin, clopidogrel, carvedilol, lisinopril, furosemide, atorvastatin, and spironolactone. Eight months later, repeated TTE revealed significant improvement of the LV EF of 40-45% from 20-25% permitting the discontinuation of spironolactone. Dual antiplatelet therapy with aspirin and clopidogrel was given for a duration of 12 months. Patient is now 14 months post PCI and is remaining clinically asymptomatic while maintaining his lifestyle modifications and medication compliance. The common side effects of hypertension and tachycardia will worsen with increasing doses of methamphetamine due to adrenergic stimulation. Amphetamine associated acute myocardial infarction may become more common if the rate of amphetamine abuse continues to increase. All physicians, particularly emergency medicine and cardiologists should be aware of such complications so early diagnosis and management may be provided. Methamphetamine associated cardiomyopathy appears to be potentially reversible upon cessation of methamphetamine and guideline directed management for heart failure. 1. Won S., Hong R., Shohet R., Seto T., Parikh N. Methamphetamine associated cardiomyopathy. Clin Cardiol. 2013 Dec: 36(12): 737-742 2. Substance Abuse and Mental Health Services Adminstration. Results from the 2013 national Survey on Drug Use and Health, Http://Samhsa.gov/data/NSDUH/2013SummNatFindDetTables/Index.aspx. 3. Borders T.F., Booth B.M., Han X., et al. Longitudinal changes in methamphetamine and cocaine use in untreated rural stimulant users: racial differences and the impact of methamphetamine legislation. Addiction. 2008;103(5):800-808 4. Sinha Q., Lewis O., Kumar R., Yeruva S., Curry B. Amphetamine abuse related acute myocardial infarction. Case Rep Cardiol. 2016; 2016: 7967851 5. Lopez J., Yeo K., Caputo G, et al. Recovery of methamphetamine associated cardiomyopathy predicted by late gadolinium enhanced cardiovascular magnetic resonance. J Cardiovasc Magn Reson. 2009;11:46. CASE PRESENTATION CONT’D CONCLUSION

INTRODUCTION

IMAGES

Methamphetamine abuse is now the second most commonly used illicit substance worldwide, after cannabis. Yet, the documented treatment and management of cardio toxic manifestations, such as acute myocardial infarction, is a rare event. The purpose of this case report is to discuss the diagnosis, evaluation, and management of methamphetamine- induced acute myocardial infarction in the presence of methamphetamine induced cardiomyopathy. A 35-year-old male with no medical history who has a social history significant for tobacco, alcohol, methamphetamine, cocaine, and PCP abuse presented to the emergency department with 2-3 days of shortness of breath accompanied by new and abrupt onset of pressure-like chest pain. The pain was described as constant 7/10 and non-radiating with no noted alleviating or aggravating factors. On arrival, he was afebrile, stating 100% oxygen on room air with no signs of cardiopulmonary distress. Upon evaluation, patient disclosed that over the past week he excessively used methamphetamine and PCP, with his last methamphetamine use within hours prior to his arrival. A chest x-ray obtained was unremarkable. EKG was not suggestive of any ST segment elevations or depressions. Initial serum troponin was elevated at 0.63 and urine toxicology was positive for methamphetamine and PCP. The diagnosis of non-ST elevation myocardial infarction (NSTEMI) was made. He was admitted and started on medical management for acute coronary syndrome (ACS) with orders placed to obtain a transthoracic echocardiogram (TTE) and trend serum troponins every 4 hours. The repeated troponin increased to 2.45, and the TTE revealed a severely reduced left ventricular ejection fraction (LV EF) of 25-30%. This was concerning and prompted further investigation of his unstable angina with a left heart catheterization. CASE PRESENTATION

EKG completed at initial presentation in the ED with no ST segment changes.

Above image reveals the stent placement.

Pre-stenting of the proximal LAD artery lesion of 80%

Above image depicts revascularization of the artery.

Post-stenting of the proximal LAD artery

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