2019 Research Forum

Department of Internal Medicine

Applicant: Sarah El-Halees MS IV Principal Investigator & Faculty Sponsor: David Aguirre MD A Case of Methamphetamine Induced Cardiomyopathy and Myocardial Infarction

David Aguirre MD, Jeffrey Coleman MD R2, Sarah El-Halees MS IV

INTRODUCTION Methamphetamine is now the second most commonly used illicit substance worldwide, after cannabis. Yet, the treatment and management of its cardio toxic manifestations, such as acute myocardial infarction, is rarely documented. PURPOSE To discuss the diagnosis, evaluation, and management of methamphetamine-induced acute myocardial infarction in the presence of methamphetamine induced cardiomyopathy. DISCUSSION 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 a 2 to 3 day history of shortness of breath accompanied by new and abrupt onset of pressure-like pain in his chest. The pain was described as constant 7/10 in intensity, non-radiating with no noted alleviating or aggravating factors. On arrival, the patient was afebrile, had 100% oxygen saturation 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 was obtained and was unremarkable. The 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) A transthoracic echocardiogram (TTE) was requested and serum troponin levels were obtained 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 which found the proximal left anterior descending (LAD) artery to have a lesion of 80% with the left ventriculography estimating a LV EF of 20%. This patient was relocated to the ICU pending transfer to another institution for percutaneous coronary intervention (PCI); he was immediately restarted on ACS protocol with initiation of a heparin and nitroglycerin drips. This patient underwent revascularization and bare metal stenting of the proximal LAD baring no complications and was closely followed up in the cardiology clinic. Medications on discharge were aspirin, clopidogrel, carvedilol, lisinopril, furosemide, atorvastatin, and spironolactone. Eight months later a repeat TTE showed significant improvement of the LV EF of 40-45% from 20-25% permitting discontinuation of spironolactone. Dual antiplatelet therapy with aspirin and clopidogrel were given for a duration of 12 months. This patient is now 14 months post PCI and he remains clinically asymptomatic while maintaining his lifestyle modifications and medication compliance. CONCLUSION 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 its usage and guideline directed management for heart failure.

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