Does the coupling between respiration, blood pressure, and heart rate differ in pregnant women with pre-eclampsia compared to healthy pregnant women?
Pre-eclampsia is associated with altered short-term cardiovascular couplings, specifically an increased respiratory influence on diastolic blood pressure and altered respiratory influence on heart rate, highlighting the potential role of respiration in its pathogenesis.
Pre-eclampsia (PE), a serious pregnancy-specific disorder, causes significant neonatal and maternal morbidity and mortality. Recent studies showed that cardiovascular variability parameters as well as the baroreflex sensitivity remarkably improve its early diagnosis. For a better understanding of the dynamical changes caused by PE, in this study the coupling between respiration, systolic and diastolic blood pressure, and heart rate is investigated. Thirteen datasets of healthy pregnant women and 10 of subjects suffering from PE are included. Nonlinear additive autoregressive models with external input are used for a model-based coupling analysis following the idea of Granger causality. To overcome the problem of misdetections of standard methods in systems with a dominant driver, a heuristic ensemble approach is used here. A coupling is assumed to be real when existent in more than 80 per cent of the ensemble members, and otherwise denoted as artefacts. As the main result, we found that the coupling structure between heart rate, systolic blood pressure, diastolic blood pressure and respiration for healthy subjects and PE patients is the same and reliable. As a pathological mechanism, however, a significant increased respiratory influence on the diastolic blood pressure could be found for PE patients (p=0.003). Moreover, the nonlinear form of the respiratory influence on the heart rate is significantly different between the two groups (p=0.002). Interestingly, the influence of systolic blood pressure on the heart rate is not selected, which indicates that the baroreflex sensitivity estimation strongly demands the consideration of causal relationships between heart rate, blood pressure and respiration. Finally, our results point to a potential role of respiration for understanding the pathogenesis of PE.
Riedl et al. (Mon,) studied this question.