CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 2, March/April 2022 70 AFRICA pre-eclampsia.35,36 The less pronounced inflammatory response in late-onset pre-eclampsia and gestational hypertension could also explain the known lower frequency of maternal and foetal complications compared to the early-onset forms.37,38 Conversely to Xiao et al.,34 we did not find a significant difference between the mild and severe forms in both the gestational hypertension and the pre-eclampsia groups, which could be due to the fact that most of the women, by the time of inclusion in the study, had only blood pressure values as an indicator of severity. The authors of an extensive review39 dealing with differences and similarities between early- and late-onset pre-eclampsia commented on the more pronounced immunological response in early-onset pre-eclampsia most likely explaining the higher probability of multi-organ damage. They consider the studies comparing early- and late-onset pre-eclampsia to be limited, especially when it comes to interleukin-6 levels. Studies focusing on interleukin-6 levels, specifically in women with gestational hypertension, are rare and usually those women are part of a larger hypertension-in-pregnancy group.40,41 Nonetheless evidence of an inflammatory response in such women does exist. Zhang et al.42 found significantly higher levels of interleukin-6 in women with gestational hypertension compared to the controls, but unlike in our study, in their study the levels of interleukin-6 in gestational hypertension were significantly lower than in the pre-eclampsia group. Most studies deal with early- and late-onset forms of pre-eclampsia, however, our study proved a more pronounced inflammation in the earlyonset forms of gestational hypertension as well, which we believe to be an important finding. It is interesting to note that in our study, in the control group, the levels of interleukin-6 were positively correlated with a number of parameters: pre-pregnacy and current BMI, weight gain and gestational age, while in the hypertensive groups, such correlations did not exist. This result could lead to the conclusion that during a hypertensive pregnancy, higher levels of interleukin-6 are mostly determined by the presence of the hypertensive disorder of pregnancy itself, and the influence of other factors is negligible. Similar to our study, Friis et al. found higher levels of interleukin-6 and other inflammatory markers in pregnant women with a higher BMI.43 Another group of authors found a positive correlation between foeto-maternal adiposity and inflammatory markers, including interleukin-6.44 The levels of interleukin-6 were higher in smokers for our whole study group, the controls and the gestational hypertension group, but not for the pre-eclampsia group. This result corresponds to a 2017 study45 in which the authors found higher interleukin-6 levels in non-pregnant smokers, as well as a moderate positive correlation between its levels and serum amyloid A:low-density lipoprotein levels, a marker for oxidative stress. Sunyer et al.46 also proved that interleukin-6 levels were significantly higher in the group of ever-smokers from a total of 1 003 people who survived myocardial infarction. With regard to the echocardiographic examination in our study, in the whole study group, higher levels of interleukin-6 correlated with more pronounced structural changes of the LV and also with some parameters indicating worse diastolic function as well as worse longitudinal strain of the LV. Indexing to BSA led to the disappearance of the correlations between interleukin-6 and the EDD and ESD of the LV and the ESA of the RV. This is likely due to the moderate positive correlation between interleukin-6 and BSA. In the pre-eclampsia group, however, where higher interleukin-6 levels did not correspond to higher BSA, the indexing to BSA rendered the correlation with the EDD of the LV non-significant, but enhanced the correlation with the ESD and the EDD of the LV. In the combined hypertension group, the correlation with EDD remained weaker but significant after indexing. However, it is worth noting that interleukin-6 had a positive correlation with RV FAC and a negative correlation with the E/e′ ratio of the tricuspid valve for the pre-eclampsia group alone. Those correlations were not present for the gestational hypertension group and the correlation with FAC in the controls was negative. Although these particular results might seem paradoxical, they could be explained by the presence of an increased contractility, which is believed to be the initial RV response to a higher afterload,47,48 likely happening as a result of the generalised vasoconstriction in pre-eclampsia, which is not as pronounced in gestational hypertension.49 Therefore higher levels of interleukin-6 could indicate the initial compensatory stages of RV involvement in the systemic syndrome of pre-eclampsia, despite corresponding to a seemingly better function. Interleukin-6 had very few correlations in the gestational hypertension group, which could lead to the conclusion that despite significantly higher interleukin-6 levels in this population, the biomarker does not seem to directly correspond to cardiac changes as assessed echocardiographically. We are not aware of another study examining correlations between interleukin-6 levels and echocardiographic changes in human pregnancy, normotensive or otherwise. Table 7. Correlation coefficients between interleukin-6 levels and right-sided echocardiographic parameters Parameters Whole study group Controls GH PE GH + PE Ind RA volume 0.133 0.024 0.253 0.178 0.199 EDA 0.071 0.097 –0.121 0.110 –0.001 ESA 0.120 0.286* –0.058 –0.046 –0.066 Ind EDA –0.058 –0.249 –0.106 0.203 0.067 Ind ESA –0.004 0.022 –0.010 –0.036 –0.029 FAC –0.139 –0.389** –0.146 0.325* 0.072 TAPSE 0.021 –0.046 0.008 0.255 0.114 TV E –0.020 0.010 0.136 –0.248 –0.050 TV E–DT –0.046 0.031 –0.313 0.002 –0.152 TV E/A –0.034 0.001 0.134 –0.159 0.007 TV e′ –0.033 –0.052 0.157 0.125 0.112 TV E/e′ –0.021 –0.010 –0.007 –0.367* –0.168 TV e′/a′ –0.018 0.049 0.023 –0.020 –0.024 TV S wave –0.052 0.057 0.049 –0.122 –0.026 RV GLS 0.147 0.139 0.078 –0.094 –0.019 AT of PV –0.016 –0.074 0.106 –0.052 0.040 *p < 0.05, **p < 0.01, ***p < 0.001, GH: gestational hypertension; PE: pre-eclampsia; Ind: indexed to BSA; RA: right atrial; EDA: end-diastolic area of the right ventricle; ESA: end-systolic area of the right ventricle; FAC: fractional area change of the right ventricle; TAPSE: tricuspid annular plane systolic excursion; TV E: peak velocity of early tricuspid inflow wave; TV E–DT: deceleration time of the E wave; TV E/A: the ratio between the peak velocities of the early and late tricuspid inflow waves; TV e′: peak early diastolic velocity of the tricuspid annulus; TV E/e′: the ratio of the E wave of the tricuspid flow and the e′ of the tricuspid annulus; TV e′/a′: the ratio between the peak velocities of the early and late velocities of the tricuspid annulus; TV S wave: peak systolic velocity of the tricuspid annulus; RV GLS: global longitudinal strain of the right ventricle (free wall); AT of PV: acceleration time of the pulmonary valve.
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