During pregnancy, women undergo major physical changes, not least of which are those that occur within the cardiovascular system. Hypertension in pregnancy can cause serious complications for both mother and child and a more serious problem is encountered when pre-eclampsia develops.

Hypertension disorders in pregnancy can be split into (a) chronic hypertension which predates the pregnancy or has an onset before 20 weeks gestation, and (b) hypertension developing after 20 weeks gestation, which can result in hypertension alone (gestational hypertension) through proteinuria and multi-organ dysfunction (pre-eclampsia) to seizures (eclampsia)¹. Chronic hypertension can also progress to pre-eclampsia¹. The presence of mild pre-existing hypertension approximately doubles the risk of pre-eclampsia but also doubles the risk of other complications such as placental abruption and growth restriction². When chronic hypertension is severe the risk of pre-eclampsia is as high as 46% resulting in increased maternal and fetal risks².

Prevalence and Survival

In the United States and the United Kingdom approximately 5% of pregnancies are complicated by preeclampsia and of these patients, 1-2% progress to eclampsia^{2, 3}. The incidence is increased in women of low socioeconomic status, extremes of age, and primigravid state³. An estimated 50,000 women die annually from pre-eclampsia worldwide and maternal morbidity include permanent CNS damage from recurrent seizures or intracranial bleeds, renal insufficiency. Although preeclampsia is not preventable, early diagnosis, careful monitoring and aggressive treatment is crucial in preventing mortality^{3, 4}. The risks to the fetus from preeclampsia include prematurity, placental infarcts, intrauterine growth retardation, abruptio placentae, and fetal hypoxia³.

Brachial blood pressure is routinely monitored throughout pregnancy, but is not a sensitive enough measure to distinguish pre-eclampsia from other types of hypertension or to predict pre-eclampsia in those at risk¹. The ability to distinguish between hypertensive disorders and identify those women who have an increased risk of pre-eclampsia can lead to better management of hypertensive disorders during pregnancy and therefore better outcomes for both for both mother and child.

Arterial stiffening

There is a large body of evidence showing that increased arterial stiffness is a basic cause of hypertension⁵. Increased arterial stiffness is observed as an increase in aortic pulse wave velocity (PWV) and an increased aortic augmentation index (AIx) caused, in turn, by the early return of the reflected pressure wave in the stiffer arteries.  The effect of changes in arterial stiffness during pregnancy has recently been the subject of several studies ^{6, 7, 8, 9}. A normal cardiovascular response to pregnancy is seen as an increased heart rate, lower brachial blood pressures primarily due to vasodilation of peripheral vessels and the expansion of blood volume during pregnancy². Elevated endothelial release of nitric oxide is also thought to be a central factor in this haemodynamic alteration during pregnancy⁶. In addition, aortic AIx has been shown to be significantly lower in pregnant women, in each of the three stages of pregnancy, compared to non-pregnant women. The aortic systolic pressure (during the 1^st and 2^nd trimesters) and aortic augmentation pressure (during the 2^nd and 3^rd trimesters) were also significantly lower compared to non-pregnant women⁸. The SphygmoCor system measures the changes in aortic AIx during pregnancy, and therefore provides a key insight into whether observed changes in aortic AIx are consistent with normal pregnancy.

Interestingly, in normotensive pregnancies, maternal aortic PWV has also been found to be significantly associated with lower birth weight independent of mean blood pressure¹⁰. An increase of 1 m/s in aortic PWV was associated with a decrease in birth weight centiles of 17%. Fetal growth is a principal issue in antenatal observations and birth weight centiles are regarded as important measures of pregnancy outcome. Potentially, higher arterial stiffness, even in normotensive pregnancies, may reflect inadequate plasma volume expansion, that in turn impedes optimal fetal growth¹⁰.

References

1. Roberts CL, Algert CS, Morris JM, et al. Hypertensive disorders in pregnancy: a population-based study. MJA 2005;182:332-335.
2. James PR, Nelson-Piercy. Management of Hypertension before, during, and after pregnancy. Heart 2004;90:1499-1504.
3. Castro LC: Hypertensive Disorders of Pregnancy. In: Hacker N, Moore JG, eds. Essentials of Obstetrics and Gynecology. 3rd ed. Philadelphia, Pa: WB Saunders Inc; 1998: 196-207.
4. Wagner LK. Diagnosis and Management of Preeclampsia. American Family Physician 2004;70:2317-2324.
5. Nichols WW, O’Rourke MF. McDonald’s blood flow in arteries. Theoretical, experimental and clinical principles. 5^th Edition Hodder Arnold London pp 370-3.
6. Ronnback M, Lampinen K, Groop P, et al. Pulse wave velocity in currently and previously pre-eclamptic women. Hypertens Pregnancy 2005;24:171-180.
7. Elvan-Taspinar A, Franx A, Bots M L, et al. Central hemodynamics of hypertensive disorders in pregnancy. Am J Hypertens 2004;17:941-946.
8. Smith SA, Morris JM, Gallery EDM. Methods of assessment of the arterial pulse wave in normal human pregnancy. Am J Obstet Gynecol 2004;190:472-6.
9. Spasojevic M, Smith SA, Morris JM, et al. Peripheral arterial pulse wave analysis in women with pre-eclampsia and gestational hypertension. BJOG 2005;112:1475-1478.
10. Elvan-Taspinar A, Franx A, Bots M L, et al. Arterial stiffness and fetal growth in normotensive pregnancy. Am J Hypertens 2005;18:337-341.

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