Acute myocardial infarction in a 26-year-old patient as the first manifestation of protein C deficiency.

Abstract

Introduction: Acute coronary syndrome is the leading cause of death worldwide. However, myocardial infarction in young patients (under 40 years old) in the absence of coronary artery atherosclerosis is an infrequent phenomenon. In addition to traditional risk factors, it is associated with a variety of contributing factors, including drug abuse such as cocaine or marijuana, Leiden factor V mutation, oral contraceptives in young women, protein C and S deficiency, and excessive consumption of energy drinks. Protein C (PC) is an essential coagulation component, dependent on vitamin K and requiring thrombin on the surface of endothelial cells to form activated PC, which exerts its anticoagulant effect by inhibiting factors Va and VIIa. A deficiency of plasma PC results in a prothrombotic state. PC deficiency occurs in 0.02-0.05% of the general population, is found in 2-5% of incident thromboembolic events, and up to 10% of recurrent events. In 1993, PC deficiency was first described, and its primary clinical presentation is venous thromboembolism; however, acute arterial thromboembolic events linked to this disease have been increasingly described.

Case report: A 26-year-old man presented to the emergency department with chest pain after ingesting an energy drink and engaging in swimming exercises. The electrocardiogram showed ischemia with hyperacute T waves in V2-V4 and ST-segment elevation in V2-V6 with ventricular extrasystoles. Echocardiography showed hypokinesia of the mid-apical inferolateral and anterolateral walls, with an ejection fraction of 50%. Troponin I was >40, and Troponin T was 5814. Management included analgesics, nitroglycerin, and intervention. Coronary angiography revealed a 95% critical lesion in the proximal left anterior descending artery with a sizeable luminal thrombus, and percutaneous coronary intervention with drug-eluting stent placement was performed. The urine drug screen was negative, a rheumatic panel of 9 antibodies was negative, and C3 and C4 were regular. Protein C: 62.5 (low), Protein S, cardiolipin IgM, cardiolipin IgG, and D-dimer were normal. During hospitalization, he developed acute kidney injury stage II and atypical pneumonia, which were successfully treated. He was managed with enoxaparin 60 mg twice daily, clopidogrel 75 mg, aspirin 100 mg, colchicine 0.5 mg, and amiodarone 200 mg.

Conclusion: Protein C deficiency is an infrequent cause of myocardial infarction. As a thrombotic disorder, it is essential to follow up with hematology.