Acute Myocardial Infarction In A Young Man In The Covid-19 Era: A Case Report

Introduction: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects host cells through ACE2 receptors, leading to coronavirus disease (COVID-19)-related pneumonia, as well as significant cardiovascular complications, such as acute myocardial infarction (AMI). There is controversy on the mechanism and management of AMI during the COVID-19 era. We describe a case of a 22 year old patient with no past medical history who presents with an acute myocardial infarction, who was found to be COVID-19 positive. Investigations: Patient’s vitals were: temperature 99.3F, blood pressure 136/99 mmHg, heart rate 80 bpm, respiratory rate 16 breaths/minute, SpO2 96% on room air. There were no abnormalities on pulmonary or cardiovascular exam. Initial laboratory testing showed elevated inflammatory markers such as ferritin, IL-6, C-reactive protein, lactate dehydrogenase, and an elevated white blood cell count with a neutrophilic predominance. LDL was normal. There was also an initial elevated troponin T. A chest radiograph was without abnormalities. EKG was notable for ST elevations in leads II, III, aVF, with depressions in leads V1, V2, V4, V5 accompanied by hyperacute T waves. Echocardiogram was notable for inferior and infero-lateral wall hypokinesis. COVID-19 PCR resulted positive. Management: Coronary angiography revealed one hundred percent stenosis of proximal left circumflex artery. The lesion was a total thrombotic occlusion with an organized thrombus. Aspiration thrombectomy was performed, and an Onyx 2.5x26 stent was placed and TIMI III flow achieved. Discussion: This is a very unique case of COVID-19 in a young patient with no co-morbidities who presented with an acute myocardial infarction. Plaque instability and rupture due to cytokine release in patients with existing atherosclerosis is a common hypothesis. It is also postulated that direct endothelial injury can occur via entry of the SARS-CoV-2 virus, with activation of the renin-angiotensin-aldosterone system causing widespread endothelial dysfunction and multiple organ injuries. This issue warrants further study, as well as discussion regarding post- intervention care in this population who are at significant thrombotic risk.