Abstract 17117: Hyperhomocysteinemia Associated St Elevation Myocardial Infarction In A Young Male

Case Presentation: A 24-year-old male with a medical history of Crohn’s on mesalamine presented to the emergency room with crushing substernal chest pain at rest. Electrocardiogram revealed ST elevations in Lead V2-V5 (Figure-1a). He was taken emergently to the catheterization laboratory and had 100% thrombotic occlusion of his proximal left anterior descending coronary artery (LAD) (Figure-1b). Intravascular ultrasound (IVUS) confirmed the presence of soft atheromatous lipid-rich plaque in the proximal LAD with heavy thrombus burden (Figure-1c/d). He underwent aspiration thrombectomy and IVUS guided percutaneous coronary intervention with a 4.5 mm x 32 mm drug-eluting stent. Echocardiogram revealed an akinetic anterior wall with an ejection fraction of 35% without a patent foramen ovale. Hypercoagulable workup was initiated and showed a significantly elevated homocysteine level of 84.4 umol/L (normal:3.5-10.4). Family history, drug screen, hemoglobin A1C, and lipid profile were unremarkable. Discussion: The differential diagnosis in a young male presenting with a STEMI includes thromboembolism versus plaque rupture. IVUS showed clear evidence of a lipid-rich plaque demonstrating premature atherosclerotic vascular disease rather than a thromboembolic event. His most striking risk factor was hyperhomocysteinemia with a level of 84.4 umol/L. Elevations in homocysteine plasma concentration has been identified as an independent risk factor for atherosclerosis due to its atherogenic and prothrombotic properties. To date lowering homocysteine levels with folate and additional therapies have not shown to reduce the risk of coronary disease. Our case stresses the importance of intravascular imaging, especially in atypical cases such as a young male presenting with a STEMI to differentiate plaque rupture versus thromboembolism. Further studies are needed to identify risk modifying therapies for hyperhomocysteinemia associated vascular disease.

Age and Phenotype of Patients With Plaque Erosion

Background A recent study reported that the outcome of patients with plaque erosion treated with stenting is poor when the underlying plaque is lipid rich. However, the detailed phenotype of patients with plaque erosion, particularly as related to different age groups, has not been systematically studied. Methods and Results Patients with acute coronary syndromes caused by plaque erosion were selected from 2 data sets. Demographic, clinical, angiographic, and optical coherence tomography findings of the culprit lesion were compared between 5 age groups. Among 579 erosion patients, male sex and current smoking were less frequent, and hypertension, diabetes, and chronic kidney disease were more frequent in older patients. ST‐segment–elevation myocardial infarction was more frequent in younger patients. Percentage of diameter stenosis on angiogram was greater in older patients. The prevalence of lipid‐rich plaque (27.3% in age <45 years and 49.4% in age ≥75 years, P <0.001), cholesterol crystal (3.9% in age <45 years and 21.8% in age ≥75 years, P =0.027), and calcification (5.5% in age <45 years and 54.0% in age ≥75 years, P <0.001) increased with age. After adjusting risk factors, younger patients were associated with the presence of thrombus, and older patients were associated with greater percentage of diameter stenosis and the presence of lipid‐rich plaque and calcification. Conclusions The demographic, clinical, angiographic, and plaque phenotypes of patients with plaque erosion distinctly vary depending on age. This may affect the clinical outcome in these patients. Registration URL: https://www.clinicaltrials.gov . Unique identifiers: NCT03479723, NCT02041650.