Impact of cardiovascular risk factors in cardiac (reverse) remodelling induced by pregnancy

Abstract Introduction Haemodynamic overload during pregnancy induces cardiac remodelling, characterised by cardiac hypertrophy and chamber enlargement, associated with deterioration of diastolic function, despite preservation of the systolic function. After delivery, the woman's heart undergoes reverse remodelling(RR), and myocardial function and structure normalise to their pre-gravid state. The impact of cardiovascular risk factors(CRF) in cardiac remodelling and RR, namely, on cardiac function and structure, is variable and remains to be clarified. Purpose To characterise cardiac remodelling and RR during pregnancy and postpartum, respectively, and to investigate CRF's impact in these processes. Methods This prospective cohort study included volunteer pregnant women (healthy [H group] or obese and/or hypertensive and/or with gestational diabetes [CRF group]) recruited in two tertiary centres between 2019 and 2022. Women were evaluated by transthoracic echocardiography at the 1st trimester [1T,10-15 weeks, baseline], 3rd trimester [3T,30-35 weeks, peak of cardiac remodelling] of pregnancy as well as at the 1st, 6th and 12th month after delivery (during RR). Blood samples were collected in each evaluation moment to quantify plasma troponin I (cTnI), procollagen I COOH-terminal propeptide (PICP), ST2/IL33-receptor, C-reactive protein (CRP) and relaxin-2 by ELISA. Generalised linear mixed-effects models were used to evaluate the extent of RR and its potential predictors. Results We included 130 pregnant women with a median age of 33 [30,36] years, 41.5% with at least one CRF. As shown in Table 1, pregnant women developed cardiac hypertrophy with significant atrial and ventricular enlargement from 1T to 3T in both groups. A significant rise in filling pressures was also documented. During postpartum, a significant regression of cardiac hypertrophy and dilation was verified in the two study groups, accompanied by a significant decrease of E/e’ as soon as 1 month after delivery. These cardiac anatomical and functional adaptations induced by pregnancy were accompanied by a significant reduction in plasma cTnI, PICP, ST2/IL33-receptor, CRP and relaxin-2 levels from 3T to 6-months after delivery. Compared to the healthy pregnant women, the CRF group showed higher relative wall thickness (RWT) for all time points of the follow-up period, with similar values of indexed cardiac mass and volumes. Pregnant women with CRF revealed higher E/e’, contrasting with lower ejection fraction and worse global longitudinal strain. Conclusion The significant cardiac reverse remodelling occurred as soon as 1 month after delivery, returning to basal values 6 months postpartum, supported by a significant reduction of levels of plasma biomarkers related to myocardial injury, repair, fibrosis, and inflammation. Pregnant women with CRF showed higher RWT, impaired relaxation and subclinical LV dysfunction when compared with healthy women at all time points of the study.