Page 187 - Read Online

Page 4 of 8 Vakhtangadze et al. Vessel Plus 2019;3:19 I http://dx.doi.org/10.20517/2574-1209.2019.07

the American Heart Association is considering eclampsia and preeclampsia as gender-specific risk factors of
[3]
CVD .

Preeclampsia itself is the risk factor for the other complications, including life-threatening complications.
A population based study conducted in Sweden of 1,003,489 deliveries showed that preeclampsia, multiple
childbearing, caesarean deliveries are important risk factors for pulmonary embolism and stroke [33,38] ; On the
background of preeclampsia increases the incidence of pulmonary embolism and stroke 3-12 times in late
pregnancy, at delivery, and in the puerperium, and similar increases in risks were also observed for multiple
pregnancies and caesarean delivery. At the time of pregnancy physiologically develops hypercoagulation
state, rise of D-dimer; continuous rise of these markers can lead to or is associated with vein thrombosis and
[39]
pulmonary thromboembolism .

Hypertension can occur firstly in postpartum period as well, the pathophysiology of this condition is
not clear. In retrospective study of 988 women showed that women with postpartum hypertension have
clinical risk factors and an antepartum plasma angiogenic profile similar to those found in women with
[40]
preeclampsia what could be sign of subclinical or unresolved preeclampsia .
Development of hypertension later in the life seems is clearly linked to complications and hypertension
during pregnancy; thus a population-based study of 146,748 women showed that hypertension during
pregnancy was associated with an elevated risk of future CVD or hypertension during life-time, irrespective
[41]
of time of development of hypertension .

Physiology
Normal physiologic changes during pregnancy are expressed in rise of cardiac output (CO) up to 20%-50%
starting by 6 week of gestation and reaching maximum by 16-28 weeks (usually around 24 week); all of this
[42]
is followed by rise of heart rate and stroke volume. It remains near peak levels up to 30 week . CO is rising
by another 30% during labor but then rapidly drops after delivery and reaches 15%-25% above normal level
because of contraction of the uterus. Then continues gradual reduction (mostly over the next 3 to 4 weeks)
and reaches the pre-pregnancy level at about 6 week postpartum. The rise of CO during pregnancy is
mostly determined by increased requirements of the utero-placental circulation; Rise of cardiac output
is determined also by the needs of skin to regulate the temperature and kidneys to excrete fetal wastes as
well. Changes in cardiac function are associated with changes in renal function, thus glomerular filtration
rate (GFR) rises by 30%-50%, reaching maximum again by 16-24 week gestation, and remains at same level
almost until term [42-44] .

Gestational Hypertension and Preeclampsia/Eclampsia are associated with impairment of cardiac function
longer than in normal pregnancy. A prospective longitudinal case-control study showed that in one year
postpartum, preeclampsia is associated with diastolic dysfunction, asymptomatic left ventricular moderate-
severe dysfunction/hypertrophy, functional/geometric abnormality, which is even more expressed in women
[45]
with preterm preeclampsia (56%) than with term preeclampsia (14%) or matched controls (8%; P < 0.001) ,
This study showed that majority of preterm preeclamptic women have stage B asymptomatic heart failure
postpartum, and 40% develop essential hypertension within 1 to 2 years after pregnancy.

Fibrinoid necrosis with a perivascular mononuclear cell infiltrate vessel wall in early phase of preeclampsia,
[46]
later lipophages are found in vessels of these women . These changes are quite close to atherosclerotic
process. Acute atherosis is not found in normal pregnancies including normal pregnancies in diabetic
women, but can develop in vessels of women with preeclampsia or in women with small-for-gestational-age
infants, or both.

Pregnancy leads to response from endocrine glands as well, partly because the placenta produces hormones
and partly because most hormones circulate in protein-bound forms and this protein binding increases