4 years ago

Cerebral autoregulation in different hypertensive disorders of pregnancy

Cerebrovascular complications that are associated with hypertensive disorders of pregnancy (preeclampsia, chronic hypertension [CHTN], and gestational hypertension [GHTN]) are believed to be associated with impaired cerebral autoregulation, which is a physiologic process that maintains blood flow at an appropriate level despite changes in blood pressure. The nature of autoregulation dysfunction in these conditions is unclear. We therefore evaluated autoregulation in 30 patients with preeclampsia, 30 patients with CHTN, and 20 patients with GHTN and compared them with a control group of 30 normal pregnant women. Study Design The autoregulatory index (ARI) was calculated with the use of simultaneously recorded cerebral blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), blood pressure (noninvasive arterial volume clamping), and end-tidal carbon dioxide during a 7-minute period of rest. ARI values of 0 and 9 indicate absent and perfect autoregulation, respectively. We use analysis of variance with Bonferroni test vs a control group. Data are presented as mean ± standard deviation. Results ARI was significantly reduced in preeclampsia (ARI, 5.5 ± 1.6; P = .002) and CHTN (ARI, 5.6 ± 1.7; P = .004), but not in GHTN (ARI, 6.7 ± 0.8; P = 1.0) when compared with control subjects (ARI, 6.7 ± 0.8). ARI was more decreased in patients with CHTN who subsequently experienced preeclampsia than in those who did not (ARI, 3.9 ± 1.9 vs 6.1 ± 1.2; P = .001). This was not true for women with GHTN or control subjects who later experienced preeclampsia. Conclusion Pregnant women with CHTN or preeclampsia (even after exclusion of superimposed preeclampsia) have impaired autoregulation when compared with women with GHTN or normal pregnancy. Whether the decreased ARI in patients with CHTN who later experience preeclampsia is due to preexistent differences or early affected cerebral circulation remains to be determined.

Publisher URL: www.sciencedirect.com/science

DOI: S0002937814022029

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