Key result
Prolonged ritodrine infusion linked to SVT and tachycardia-induced cardiomyopathy with LVEF 30%.
Why the study?
Beta-adrenergic agonists during pregnancy are linked to maternal cardiac systolic dysfunction and potential tachycardia-induced cardiomyopathy, yet prolonged ritodrine infusion remains in use for preterm labor.
Case Report (n=1)
No
Prolonged ritodrine infusion for preterm labor can trigger severe tachycardia-induced cardiomyopathy, highlighting the critical need for careful maternal heart rate monitoring and prompt intervention for persistent tachycardia.
May warrant cardiac monitoring during prolonged ritodrine tocolysis; hypothesis-generating for drug-induced cardiomyopathy incidence in pregnancy.
Preterm birth remains a leading cause of neurodevelopmental disability in offspring, prompting various preventive measures. However, controversies persist surrounding these approaches, particularly regarding beta-mimetic drugs. In Japan, it remains a concerning reality that ritodrine infusion continues to be used for long-term tocolysis in preterm labor, despite the warning issued by the US Food and Drug Administration. Growing evidence suggests that the use of beta-adrenergic agonists during pregnancy is associated with an increased risk of maternal cardiac systolic dysfunction. Furthermore, tachycardia-induced cardiomyopathy (T-CM), a rare etiology of cardiomyopathy, can also be triggered by beta-adrenergic stimulation. Here, we present a case of a 35-year-old pregnant woman without prior arrhythmias who developed T-CM following prolonged ritodrine infusion for preterm labor. The patient experienced persistent, exacerbated tachycardia under continuous ritodrine infusion starting at 20 weeks of gestation and developed supraventricular tachycardia with an impaired left ventricular ejection fraction of 30% and an elevated N-terminal prohormone of brain natriuretic peptide (NT-proBNP) level of 2,122 pg/mL, at the time of transfer at 36 weeks of gestation. Administration of adenosine and verapamil revealed atrial tachycardia or flutter, and the patient was diagnosed with tachycardia-induced cardiomyopathy, which was confirmed by a dramatic improvement in systolic function following maternal heart rate control using a bisoprolol patch. The patient delivered a healthy female via cesarean section at 37 weeks of gestation and was discharged from the hospital with favorable maternal and neonatal outcomes. This report highlights another potential risk of maternal cardiac deterioration due to beta-adrenergic effects, emphasizing the importance of reconsidering the long-term use of ritodrine infusion, as well as the need for dose titration, discontinuation, or switching to the alternative agent in cases of persistent or exacerbated tachycardia. Careful monitoring, including more frequent daily checkups to assess pulse rate and respiratory changes, along with the use of early warning systems and occasional BNP or NT-proBNP measurements, should be considered to ensure the timely detection of deterioration and the implementation of earlier preventive interventions.
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Nakao et al. (2024) conducted a case report in Tachycardia-Induced Cardiomyopathy (n=1). Ritodrine infusion was evaluated on Development of tachycardia-induced cardiomyopathy. Prolonged ritodrine infusion for preterm labor in a 35-year-old pregnant woman triggered supraventricular tachycardia and subsequent tachycardia-induced cardiomyopathy with a left ventricular ejection fraction of 30%.
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