Transient ST-segment elevation following coronary artery bypass grafting in a patient with immune thrombocytopenia treated with romiplostim: a case report

Abstract Introduction ST-segment elevation following coronary artery bypass grafting (CABG) is a clinically important postoperative finding that may indicate perioperative myocardial infarction, early graft failure, or acute coronary compromise. However, non-ischemic postoperative processes may produce similar electrocardiographic abnormalities, creating diagnostic uncertainty, particularly in clinically stable patients. Patients with immune thrombocytopenia (ITP) undergoing cardiac surgery present an additional therapeutic challenge because of the competing risks of bleeding and thrombosis. Thrombopoietin receptor agonists (TPO-RAs), such as romiplostim, may be used to increase platelet counts before invasive procedures, but their use requires careful assessment in patients with concomitant cardiovascular disease. Case presentation A 47-year-old man with chronic ITP and multivessel coronary artery disease underwent elective CABG following preoperative administration of romiplostim for platelet optimization. Forty-eight hours after receiving romiplostim, his platelet count increased from 57 × 10⁹/L to 125 × 10⁹/L. Four-vessel CABG was performed, with a pedicled left internal mammary artery (LIMA) grafted to the left anterior descending artery (LAD) and a right internal mammary artery (RIMA) used as a Y-graft arising from the LIMA and directed sequentially to the diagonal branch, ramus intermedius, and posterior descending artery (PDA). The operation was initially attempted off-pump but was converted to cardiopulmonary bypass because of challenging coronary anatomy and inadequate target-vessel exposure. On postoperative day one, routine electrocardiography demonstrated new ST-segment elevation in leads II, III, and aVF, accompanied by PR-segment depression. A pericardial friction rub was documented. The patient remained clinically asymptomatic and hemodynamically stable. Transthoracic echocardiography showed preserved left ventricular systolic function without new regional wall motion abnormalities or pericardial effusion. High-sensitivity cardiac troponin I (hs-cTnI) was 0.9 ng/mL on postoperative day one and declined to 0.3 ng/mL on postoperative day three (laboratory reference range, 0–0.6 ng/mL). C-reactive protein and erythrocyte sedimentation rate were elevated to 120 mg/L and 68 mm/h, respectively; preoperative inflammatory marker values were unavailable.Given the absence of clinical or echocardiographic evidence of ongoing ischemia, declining cardiac biomarkers, preserved ventricular function, and the additional procedural bleeding risk associated with ITP, immediate coronary angiography was deferred. The patient was managed with close monitoring, aspirin, prophylactic low-molecular-weight heparin, indomethacin, and intravenous nicorandil during the initial assessment. The ST-segment elevation resolved by postoperative day three without clinical evidence of ongoing myocardial ischemia. Conclusion Transient ST-segment elevation after CABG requires systematic evaluation for both ischemic and non-ischemic causes. In this patient, the combination of inferior ST-segment elevation, PR-segment depression, a documented pericardial friction rub, preserved ventricular function, absence of regional wall motion abnormalities, declining hs-cTnI, elevated inflammatory markers, and spontaneous ECG resolution favored an early postoperative inflammatory process. Romiplostim should be regarded as part of the patient’s overall thrombotic-risk profile rather than as a proven direct cause of the transient ECG abnormality.