Pregnancy-related acute myocardial infarction after treatment with ritodrine hydrochloride: A case report

Pregnancy-associated myocardial infarction (PAMI) is a rare but potentially life-threatening condition for the mother and fetus. Pregnancy also confers a three- to fourfold increased risk of MI compared with the non-pregnant state. However, recognizing PAMI promptly in obstetric settings remains challenging. A 34-year-old Japanese primigravida at 30 weeks of gestation had been receiving ritodrine for preterm labor. On hospital day 2, approximately 4 h after discontinuation of tocolytics, repeat electrocardiography (ECG) indicated new ST-segment elevation in leads I, aVL, and V3-V6 without chest pain. High-sensitivity troponin I was 5392 pg/mL, CK-MB was 21 IU/L, and transthoracic ECG revealed mild apical hypokinesis. That night, prolonged fetal bradycardia prompted emergency Cesarean delivery. Maternal cardiac biomarkers then declined rapidly, and the ECG and wall-motion abnormalities resolved. Myocardial perfusion scintigraphy (day 5) and coronary computed tomography angiography (day 6) showed no perfusion defect or obstructive coronary disease. The infant, weighing 1546 g, was admitted to the neonatal intensive care unit. No adverse effects attributable to ritodrine were observed, and the infant was discharged on postnatal day 58. The report describes probable drug-induced PAMI temporally associated with β₂-agonist tocolysis, with plausible mechanisms including transient coronary vasospasm and supply-demand mismatch in the hemodynamic milieu of pregnancy. This case suggests that women receiving β₂-agonist tocolysis should be monitored for vital signs, electrolytes, and ECG changes. Even without chest pain, new ECG abnormalities or palpitations warrant immediate cardiac evaluation.