Objectives: To describe the time of detection, electrophysiologic mechanism, and severity of hemodynamic sequelae of arrhythmias in infants and children prenatally exposed to cocaine and to determine whether the incidence of severe neonatal arrhythmia is related to prenatal exposure to cocaine.
Design: Characteristics of arrhythmias are described for all significant arrhythmias detected at Boston (Mass) City Hospital in infants and children with known cocaine exposure, as well as a convenience sample of children from Children's Hospital, Boston. A historical cohort was used to calculate the rates of cardiac consultation for arrhythmia among children prenatally exposed to cocaine and among children with no known cocaine exposure.
Study population: Characterization of the arrhythmias is based on case studies of 18 children. The rate of arrhythmia consultation was calculated from 554 infants who had urine toxic screens for cocaine and from 13 arrhythmias detected between 1988 and 1991.
Outcome measures: Prenatal cocaine exposure; the time of detection, electrophysiologic mechanism, and severity of hemodynamic sequelae of arrhythmias; and the incidence of cardiology consultation for arrhythmia in infants and children prenatally exposed to cocaine.
Results: Fetal arrhythmia persisted into the neonatal period in three cocaine-exposed infants; two were delivered via emergency cesarean sections for presumed fetal bradycardia and were subsequently found to have asymptomatic frequent and blocked atrial premature beats. Including these three infants, arrhythmia was observed in 13 cocaine-exposed neonates; 12 had a variety of supraventricular arrhythmias and four had low-grade ventricular ectopy. Arrhythmia resulted in congestive heart failure in five (38%) of 13 neonates. Six occurrences of arrhythmia were observed beyond the neonatal period among five cocaine-exposed infants. Late arrhythmias included high-grade ventricular arrhythmias and resulted in two cardiorespiratory arrests. In addition, neonates with known exposure to cocaine were more likely to have a consultation for arrhythmia than neonates without known exposure.
Conclusions: Sustained arrhythmias may result from an increased number of potential initiating premature beats in children prenatally exposed to cocaine. These effects persist beyond the period of exposure and are associated in some children with congestive heart failure, cardiorespiratory arrest, and death. Prenatal cocaine exposure increases the incidence of consultation for atrial and ventricular arrhythmias.