BackgroundConsidering the limited information available on right cardiac remodelling during gestation, we aimed to characterise the right cardiovascular (CV) remodelling and reverse remodelling (RR) induced by pregnancy and postpartum, respectively, and the impact of perinatal CV risk (CVR) factors on these processes. MethodsThis prospective cohort was recruited at two tertiary centres during 2019–2022, including 51 healthy pregnant women and 79 with perinatal CVR factors. Participants were evaluated by transthoracic echocardiography during pregnancy (1st[1T] and 3rd[3T] trimesters) and postpartum (one-month[PP1], six-months[PP2], and one-year postpartum[PP3]). Generalised linear mixed-effects models were used for statistical analysis. ResultsSimilar enlargement of the right atrium (RA) and right ventricle (RV) dimensions was observed throughout pregnancy, normalising at PP2 values similar to PT1. This anatomical postpartum recovery was accompanied by an increase of RV global longitudinal strain, being statistically significant in perinatal CVR group. Interestingly, at 3T, this group revealed lower RV and RA strain compared to healthy participants. Despite both groups maintained preserved RV systolic function from 1T to PP3, a significant reduction of TAPSE and tricuspid S’ velocity was observed at PP1. Concomitantly, all participants showed a significant increase of E/A at the same time-point, suggesting the recovery of diastolic deterioration seen from 1T to 3T that was persistingly higher in the perinatal CVR group througout the postpartum. Constant pulmonary artery systolic pressure (PASP) was documented throughout follow-up time, showing consistently higher values in the perinatal CVR group. All these echocardiographic index changes were within the normality range. ConclusionThis study described subtle right cardiac changes within the normal/physiological range, recovering six-months after delivery. Coexisting perinatal CVR factors seem to affect the magnitude of RV diastolic function changes, PASP and myocardial deformation without any impact on other RV systolic function indexes.
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