Safety of nifedipine in threatened preterm labor: Investigation by three-dimensional echocardiography.

OBJECTIVE

To evaluate atrial and ventricular parameters using real time three-dimensional transthoracic echocardiography (RT3DTTE) in women treated with nifedipine in the early third trimester (III-T) of pregnancy.

METHODS

A prospective single-subject design study in a university-affiliated hospital, where each participant served as her own control. We studied 25 pregnant women at a gestational age of 25-33 weeks with TPTL prior to vs 48 hours postnifedipine treatment. Two-dimensional transthoracic echocardiography (2DTTE) and RT3DTTE were used to study 3D left atrial (LA) volumes and indexes, emptying fraction, left ventricular and LA cavities, and total vascular resistance (TVR).

RESULTS

Two-dimensional transthoracic echocardiography showed a significant increase in LA area (from 15.2 ± 2.62 to 16.16 ± 2.21 mm2 , P = .02) before vs after nifedipine; RT3DTTE showed a significant change in LA end-diastolic volume index (from 23.7 ± 4.2 to 26.75 ± 3.8 mL/m2 , P = .008). LA end-systolic volume and index were not significantly different before vs after nifedipine (from 24.56 ± 8 to 25.3 ± 5.5 mL, from 13.6 ± 5.3 to 14.8 ± 3.4 mL/m2 ); P > .05, respectively. E/a ratio, E-tdi, and E/E-tdi did not change significantly ([from 2.54 ± 4.46 to 2.54 ± 4.1], [from 11.9 ± 1.9 to 11.9 ± 2], [from 7.8 ± 1.4 to 7.6 ± 1.1], respectively, P > .05). Tricuspid annular plane systolic excursion (TAPSE) did not change significantly from 23.77 ± 4.2 to 23.9 ± 3.3, P = .1. There was a significant decrease in pulmonary pressure (from 25.4 ± 4.2 to 23 ± 2.5 mm Hg, P = .02), in mean arterial pressure (from 80 ± 4 to 76 ± 3 mm Hg, P < .001) and in TVR (from 1160 ± 260 to 1050 ± 206 dyne s/cm-5 , P = .04).

CONCLUSIONS

According to RT3DTTE measurements, in pregnant women treated with nifedipine for tocolysis, there were no detrimental cardiovascular effects detected 48 hours postnifedipine treatment. RT3DTTE could show accurately the compensatory response of the left heart to the cardiovascular changes induced by treatment with nifedipine.