Mid-trimester blood pressure in pregnancy. Blood pressure fall or fall of a myth?

Yet we have always seen it. If we look carefully at our patients' medical records we may still see it. Or at least, we are convinced to see it. Now, it is like a ghost, a mirage. An unidentified entity that comes and goes, although we were used to see. It cannot be so any longer. The work by Nama et al. [1] undermines all our basic beliefs. The entity that vanishes is the mid-trimester blood pressure (BP) drop that for many years we used to consider a milestone of our obstetric knowledge. It was widely and undisputedly described in the late 1960s by MacGillivray et al. [2]. Measuring BP throughout pregnancy in 226 women over an 18-month period, they found a 15 mmHg BP drop in the second trimester at around 18 weeks and a subsequent rise to the prepregnant levels during the third trimester. This observation was also enforced by the work of Page and Christianson [3]. They showed a similar trend for the mean arterial pressure (MAP) prospectively studied on 14 833 singleton pregnancies and gave prognostic meaning to 90 mmHg mid-trimester MAP in terms of subsequent intrauterine mortality, intrauterine growth restriction and maternal occurrence of preeclampsia. We must admit that these old observations were rather descriptive and, probably because of the numerosity of the sample, were never questioned thereafter. They really became a dogma in obstetric medicine, were reported in many classifications [4], and were considered a robust milestone of our knowledge. We taught that and generations of obstetricians have grown up with such information. Furthermore, it had a convincing physiologic background. The trophoblastic invasion, which begins at the time of implantation, produces deep modifications of the spiral arteries, migrating into their median layer, and making them insensitive to vasoconstrictors. This was beautifully described in the histological observations by Gerretsen et al. [5] and in the angiotensin sensitivity studies by the group of Professor Gant in Dallas [6]. All these findings supported the concept that the second wave of trophoblastic invasion created a low-resistance district, changing the function of the uterine spiral arteries to a ‘venous behavior’, with the consequence of a reduced (mainly diastolic) BP, just at around 20 weeks. The article by Nama et al.[1] revolutionizes the above concepts. They found an increasing continuous trend for BP to increase, and, by focusing their investigations on the mid-trimester, they did not find a drop, but rather an increase, as compared with the first trimester. Their numbers are not as large as some historic series, but their study appears well conducted and the data achieve statistical significance. We may suggest that this is the revenge of statistics over simple clinical observation. After this article, we have to abandon our romantic view of the mid-trimester BP drop, surrender to evidence and move forward to enter into a new era. Some issues will then be (re)opened. How can we interpret the trophoblastic colonization of the spiral arteries, which really occurs, and currently is not under discussion? Is an increased mid-trimester BP, whatever the limits considered, still to be considered ominous and with an unfavorable prognostic meaning? Or, should new trends be described to define maternal and fetal risks? Furthermore, what about the observation we have recently reported [7], namely that an increasing trend in mean 24-h BP, together with the analysis of the mean resistance index of the uterine arteries, is predictive for subsequent superimposed preeclampsia? Is it in contrast with the observations by Nama et al. or does it just apply to pregestational hypertensive patients? Again, the article by Nama et al.[1] may really open a new age in the study and management of pregnancy hypertension. We very much look forward to future discussion.