Renal transplant recipients with a history of coronary artery disease (CAD) remain at significant risk for perioperative cardiovascular complications, with myocardial ischemia potentially occurring despite the absence of new obstructive coronary lesions. A 64-year-old male with diabetes mellitus, end-stage renal disease on hemodialysis, and a history of coronary artery bypass grafting and percutaneous transluminal coronary angioplasty underwent a successful living donor renal transplant. Early postoperative recovery was stable, with excellent graft function (serum creatinine 0.85 mg/dL). On postoperative day 3, he developed acute chest pain. Electrocardiogram showed ST depressions in V3–V6, and echocardiography revealed anterior-lateral wall hypokinesia with an ejection fraction (EF) of 45%. Coronary angiography showed patent grafts without new stenoses. A diagnosis of Type II myocardial infarction (MI), likely from increased myocardial oxygen demand and perioperative stress, was made. Management included dual antiplatelet therapy, beta-blockers, anticoagulation, nitrates, and careful volume control. The patient stabilized clinically, with EF improving to 55%–60%, and maintained good graft function at discharge. This case highlights the occurrence of demand ischemia posttransplant despite angiographically patent grafts. Type II MI should be considered in the differential for postoperative chest pain in high-risk renal transplant patients. Surgical stress, hemodynamic shifts, and autonomic activation in the early posttransplant period can precipitate myocardial injury even without plaque rupture. Prompt recognition and tailored management are crucial to preserve both cardiac and graft function.
Dudem et al. (Thu,) studied this question.