Adriëtte Oostvogels

2 53 pBMI, lipids and BP during pregnancy Underlying mechanisms Obese pregnant women have increased lipids, 10-12 and a dysregulated vascular and immune system. 28 All three factors can contribute to the development of hypertension or pre-eclampsia. Obesity affects endothelial dysfunction, 28 whereas lipids have a direct and also an indirect effect on endothelial dysfunction. 18 Proper endothelial function is important as the endothelium produces (amongst others) nitric oxide (NO), a vasodilator which decreases BP. In non-pregnant women, ApoA1 was found to be positively correlated with elastin peptides, 29 which induce NO-dependent vasodilatation. 30 On the other hand, although TG are not atherogenic by itself, high levels of non-fasting TG are an indicator of cytotoxic remnants of ApoB-lipoproteins like chylomicron and very low density lipoproteins. 31 Moreover, TG-rich ApoB- lipoproteins can penetrate the arterial intima, promoting endothelial damage. 32 FFA plays an important role here, as they promote low-density lipoprotein and cholesterol-rich remnant particles to enter the intima. 18 Moreover, FFA can increase oxidative stress, 18 causing oxidation of ApoB-lipoproteins like LDL, which decreases vasodilatation through decreased NO synthesis and release and degradation of NO. 33 Furthermore, also a dysregulated immune system can contribute to an increased BP. Inflammatory factors are increased to a greater extent in women with overweight or obesity compared to women with normal weight. 28,34 These inflammatory markers (TNF- α and interleukin-6) can be secreted from adipocytes and stimulate the liver to produce C-reactive protein (CRP). 35 Our study shows that lipids do not mediate the association between obesity and BP course during pregnancy. CRP was reported to be positively associated with BP in pregnancy, but correcting for pBMI attenuated these associations. 36,37 This suggests a mediating role for the inflammatory markers, like CRP, in the association between pBMI and BP course during pregnancy, apart from the independent role of obesity and lipids on BP. Conclusion This study shows that women with overweight or obesity in the highest tertile of maternal lipids start their pregnancy with a 7 mmHg higher SBP and a 4.9 mmHg higher DBP. Both maternal pBMI and maternal lipids have an independent effect on BP during pregnancy. However, BP course was not changed by maternal pBMI or maternal lipids. Improving maternal pBMI and lipid profile in early pregnancy might improve BP during pregnancy.