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Ventricular septal thickness and cardiac function in neonates after in utero ritodrine exposure
Insights
In utero ritodrine exposure can cause cardiac septal hypertrophy in newborns. Cardiac evaluation is recommended for neonates exposed to ritodrine for over 7 weeks due to potential heart function changes.
Area of Science:
- Neonatal cardiology
- Fetal medicine
Background:
- Maternal exposure to ritodrine during pregnancy is known to cause cardiac septal hypertrophy in neonates.
- The impact of this hypertrophy on neonatal cardiac function requires further investigation.
Purpose of the Study:
- To assess the effect of in utero ritodrine exposure-induced septal hypertrophy on cardiac function in neonates.
- To determine the correlation between the duration of ritodrine exposure and the severity of septal hypertrophy.
Main Methods:
- M-mode echocardiograms were performed on day 1 of life in 41 ritodrine-exposed infants and 22 matched control infants.
- Disproportionate septal hypertrophy (DSH) was defined by an interventricular septal thickness/posterior wall thickness ratio (ST/PW) > 1.3.
- Echocardiographic parameters, including ST/PW and systolic time intervals, were analyzed.
Main Results:
- Infants exposed to ritodrine in utero exhibited DSH and increased right systolic time intervals compared to controls (P < 0.05).
- Neonates exposed for ≥2 weeks showed absolute increases in septal thickness.
- ST/PW strongly correlated with ritodrine exposure duration (r = 0.96).
Conclusions:
- In utero ritodrine exposure leads to cardiac septal hypertrophy and altered cardiac function in neonates.
- Cardiac evaluation is advised for neonates with >7 weeks of in utero ritodrine exposure pending further long-term safety data.
Abstract:
Cardiac septal hypertrophy occurs after in utero ritodrine exposure. To assess the effect of septal hypertrophy on cardiac function we obtained M-mode echocardiograms on day 1 of life in 41 infants exposed to ritodrine and 22 control infants matched for gestational age. Mean duration of ritodrine exposure was 16.2 +/- 13.2 days (range 1 to 49 days). Disproportionate septal hypertrophy (DSH) was defined as an interventricular septal thickness/posterior wall thickness ratio (ST/PW) of greater than 1.3. Infants exposed to ritodrine in utero had DSH and increased right systolic time intervals compared with control values (P less than 0.05). A subgroup, those infants exposed for 2 weeks or longer, had not only DSH but also an absolute increase in septal thickness compared with control infants and infants exposed to ritodrine for less than 2 weeks. ST/PW correlated well with the duration of ritodrine exposure (r = 0.96); the longer the exposure the thicker the septum. Although all echocardiographic changes lasted for less than 3 months, we have no information regarding the effect on the fetus of maternal ritodrine exposure for longer than 7 weeks. Until such information is available, cardiac evaluation is recommended in neonates exposed to ritodrine in utero for longer than 7 weeks.