Case Report: Coronary plaque rupture following glucocorticoid tapering in a high-risk CAD patient with immune nephritis: mechanistic insights and clinical implications.

Background: Glucocorticoids (GCs) exhibit metabolic risks that may accelerate atherosclerosis. However, their Case summary: A 51-year-old male with immune nephritis, chronic kidney disease (CKD), and poorly controlled hypertension presented with unstable angina. Coronary angiography revealed multivessel disease [70% stenosis in the proximal left anterior descending artery (LAD) and 90% in the posterior descending artery]. Initial treatment included angioplasty with a drug-coated balloon in the posterior descending artery, dual antiplatelet therapy, statins, and prednisone (10 mg/day). Seven months later, after self-reducing GCs to 5 mg/day, he suffered an acute myocardial infarction due to LAD plaque rupture, confirmed by optical coherence tomography (OCT) showing fibrolipid-rich plaques, deep calcifications, and minimal lumen area (0.67 mm Discussion: This case underscores the mechanistic duality of GCs. Chronic GC therapy suppresses pro-inflammatory cytokines and macrophage activity, stabilizing plaques by reducing oxidized LDL uptake. However, abrupt tapering may trigger rebound vascular inflammation, destabilizing high-risk lesions. OCT imaging proved critical in identifying vulnerable plaque morphology, emphasizing its role in guiding urgent interventions.