SESSION TITLE: Cardiovascular Disease 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Sudden onset of chest pain accounts for 10% of Emergency Department visits. Although MI’s more commonly present in older patients, practitioners may question the urgency as well as the necessity for cardiac catherization in young individuals with elevated troponins without ST elevations on EKG. We present a case of an acute MI and significant LAD occlusion in a 26-year-old male with no prior medical history. CASE PRESENTATION: A 26-year-old male presented to the ED after 8 hours of mild, persistent substernal chest pain. He denied any previous episodes, and denied alcohol or drug usage. He reported a 5 pack year smoking history. EKG showed RBBB with T wave inversions in V1, V2, & V3. Initial troponin was 9.5. A few hours later, his pain worsened. Echocardiogram revealed moderate anterolateral, septal, & apical hypokinesis with an LVEF of 40%. Repeat troponin was 36.5. Coronary angiogram showed extensive non-occlusive thrombus in the proximal LAD with embolization and 100% occlusion of the distal LAD. Extensive mid-LAD myocardial bridging was also found. PCI was performed with a bare metal stent. The following day the patient’s symptoms resolved. Hypercoaguable workup showed a significant acquired protein C and S deficiency. He was discharged on DAPT and Coumadin. DISCUSSION: Myocardial bridging (MB) is a congenital abnormality in which a coronary artery tunnels through the myocardial fibers. Studies suggest MB having a correlation between various CV pathologies such as acute MI, ventricular rupture, life-threatening arrhythmias, hypertrophic cardiomyopathy, apical ballooning or sudden death. The majority of MI’s with MB are caused by atherosclerotic plaque rupture, fissure, or erosion with occlusive thrombus formation. One mechanism is the MB produces systolic retrograde flow and overall flow disruption, leading to the development of atherosclerosis. Due to these pressure gradients, the resulting coronary endothelial dysfunction also adds to early atherosclerosis. MB therapy remains unclear in complicated patients. Beta blockers are first line in symptomatic patients without obstructive CAD whereas surgical myotomy or CABG can be considered in patients with significant disease. Angioplasty with stenting has shown to have a high frequency of repeated revascularization. Protein C & S deficiencies have a known increased risk of venous thrombosis. However, there are numerous reports regarding these deficiencies being linked to coronary thrombosis as well as MI in young adults. These deficiencies alone may not significantly increase the risk of arterial thrombosis; however, when coupled with smoking and myocardial bridging, there's a higher incidence of premature MI. CONCLUSIONS: There are numerous etiologies for elevated troponins in young individuals, including cardiac and non-cardiac causes. Early recognition and diagnosis can lead to long-term benefits in morbidity and mortality. Reference #1: Loukas M, Curry B, Bowers M, et al. The relationship of myocardial bridges to coronary artery dominance in the adult human heart. J Anat. 2006;209:43-50. Reference #2: Arbab-Zadeh A, Nakano M, Virmani R, Fuster V. Acute coronary events. Circulation. 2012;125:1147-1156. Reference #3: Coller et al. Deficiency of plasma protein S, protein C, or antithrombin III and arterial thrombosis. Arteriosclerosis 1987;1:456-462. DISCLOSURES: No relevant relationships by Jeffrey Roan, source=Web Response