Abstract 4145465: A Bridge from Sweet to Sour: A Case of Recurrent Myocardial Stunning in Diabetic Ketoacidosis

Background: Myocardial bridging (MB) is a common congenital anomaly wherein a coronary artery segment takes an intramyocardial course. While often benign, MB may be associated with myocardial ischemia/stunning (MS), acute coronary syndromes (ACS), or even sudden cardiac death during periods of increased cardiac demand. Case presentation: A 47-year-old male with a history of type 1 diabetes mellitus was admitted to the Intensive Care Unit for diabetic ketoacidosis (DKA). He complained of epigastric pain with an electrocardiogram showing transient ST-elevation in the anterior and inferior leads. Cardiac troponin showed an upward trend with a peak of 0.202 ug/L and an elevated NT-proBNP of 5,014 pg/mL. A transthoracic echocardiogram (TTE) revealed left ventricular systolic dysfunction (LVEF 40%) with akinesis of the mid to apical anterior and septal walls, consistent with the left anterior descending (LAD) artery territory. Emergent left heart catheterization (LHC) revealed patent coronary arteries with severe mid-LAD MB with TIMI 3 flow. He was managed conservatively with guideline-directed medical therapy for heart failure, and subsequent TTE nine months later showed normalization of LV wall motion (LVEF 65%). Five months later, the patient was readmitted for DKA with elevated troponin. A repeat TTE demonstrated LV systolic dysfunction (LVEF 35%) with wall motion abnormalities (WMA) mirroring the initial presentation. Discussion: Our patient presented with recurrent episodes of ACS/MS complicated by LV systolic dysfunction along the LAD territory during periods of DKA, a known stressor for myocardial ischemia. The absence of obstructive coronary atherosclerosis on LHC, coupled with severe mid-LAD MB, suggests that the MB was the likely culprit for recurrent ACS/MS. Although stress cardiomyopathy was considered a differential diagnosis, this was less likely given the uncharacteristic pattern of WMA sparing the apical lateral and inferior walls as opposed to apical ballooning and the presence of an alternative diagnosis. Conclusion: This unique case underscores the importance of recognizing MB as a rare but potential cause of ACS/MS and LV dysfunction in patients with precipitating stressors such as DKA.