MAP, a feasible tool and part of antenatal surveillance, has remained the target of scientific research in the prediction of pregnancy-related diseases [17, 22]. The association between first trimester MAP and placenta accreta is still unclear. In our retrospective case–control study, we investigated the association between first trimester MAP and placenta accreta. Our results showed that elevated first trimester MAP remained significantly positively associated with placenta accreta. Furthermore, first trimester MAP, smoking during pregnancy, and previous cesarean section history were significantly positively associated with placenta accreta, indicating that they may be probable risk predictors of placenta accreta.
Strengths and Limitations
The strength pertains to the availability of data on a wide range of maternal characteristics on an individual level. In addition, the early accurate risk assessment of placenta accreta would identify high-risk women for targeted early prevention. Despite our findings, our study has several limitations. One limitation is the small number of cases, which possibly introduces selection bias. Another limitation is that all pregnant women were from China, which fully minimized the confounding effects of ethnic background. Whether our results can be extended to other ethnic groups remains to be confirmed.
Placenta accreta refers to abnormal placental invasion to the uterine wall, which is characterized by invasion of trophoblasts into the myometrium, but not beyond [23, 24]. Placenta accreta is a life-threatening obstetrical disease and has a high maternal morbidity and mortality rate, presenting specific intrapartum challenges [25, 26]. Placenta accreta affects about 2% of singleton deliveries, and its incidence is gradually increasing . Considering the rising incidence and associated severe adverse outcomes of placenta accreta, methods that can accurately diagnose placenta accreta in the prenatal period before patients develop symptoms need to be developed so that plans for the prevention of bleeding and related complications and individualized treatment can be made. Currently, ultrasound and MRI are the methods used to diagnose placenta accreta. The diagnostic factors include the presence of placental lacunae, loss of the hypoechoic retroplacental interface, and hypervascularity of the interface between the placenta and the bladder or uterine wall. However, the effectiveness and accuracy of the above mentioned methods are controversial. Recently, an increasing number of studies showed that first trimester MAP is associated with adverse pregnancy outcomes [28, 29].
In the present study, we observed that elevated first trimester MAP remained significantly positively associated with placenta accreta. Previous studies showed that first trimester MAP values may change in pregnant women who have already developed or are destined to develop placenta accreta. First trimester MAP may be helpful to improve the antenatal diagnosis of placenta accreta. Furthermore, knowing the risks early may contribute to explain the MRI or sonogram findings more accurately.
MAP, the mean value of arterial pressure in one cardiac cycle, is a part of antenatal surveillance. In addition, higher levels of MAP are related to the increased risk of developing hypertension during pregnancy, pre-eclampsia, and gestational diabetes [15, 16, 19]. All these pregnant outcomes and placenta accreta belong to the disorders of placental development. Placenta accreta starts to develop in the first trimester .
In women with pre-eclampsia, the values of uterine artery pulsatility index and mean arterial pressure are increased. Interestingly, our findings showed that first trimester MAP is significantly increased in the placenta accreta group compared with that in the healthy control group. However, all the values are within normal range. Uteroplacental vasculature circulation undergoes significant structural and functional modifications to ensure an adequate blood supply to the developing placenta and the fetus in the first trimester . In early stages of pregnancy, trophoblasts invade the uterine spiral arteries, replacing muscular and endothelial cells of the arterial wall and transforming them in low resistance vessels with an increased blood flow . As mentioned above, placenta accreta starts to develop in the first trimester . Thus, the probable mechanisms underlying this phenomenon may be that increased MAP within normal limits may provide more blood supply to the placental circulation and other organs of placenta accreta patients .
Considering the excessive trophoblast invasion and abnormal vascular remodeling of placenta accreta patients, these patients need more blood supply. Hence, factoring first trimester MAP into the risk assessment could better identify patients who are at risk of developing placenta accreta, and placenta accreta patients would be subjected to closer and refined monitoring and treatment.
In addition, we found that the incidence of smoking during pregnancy was significantly positively associated with placenta accreta in our study, suggesting that smoking during pregnancy may be related to the occurrence and development of placenta accreta. A potential mechanism is that cigarette smoke increases placental adrenomedullin expression and aggravates trophoblast invasion via the adrenomedullin pathway . Excessive invasion of trophoblast cells leads to the occurrence and development of placenta accreta eventually.
The incidence of placenta accreta is increasing every year . There are parallels between the increasing number of caesarean section cases and the increasing incidence of placenta accreta [34, 35]. Evidence shows that women with a history of caesarean delivery have the highest risk of developing placenta accreta [36-38]. In the present study, we found a significant positive association between previous cesarean section history and the incidence of placenta accreta. Our results also echo those of previous studies, suggesting that previous cesarean section history may be an important factor of placenta accreta [33, 39, 40]. The probable mechanisms underlying this phenomenon may include abnormal angiogenesis, abnormal trophoblast differentiation, and oxygen tension in the uterine scar [41, 42].