Elevated brachial blood pressure has traditionally been the main indicator for diagnosing hypertension, but with the increased availability of non-invasive central blood pressure (CBP) measuring devices, there is growing interest in using CBP for managing hypertension in non-pregnant and pregnant individuals.

The role of brachial blood pressure in the prediction of future cardiovascular structural damage, morbidity, and mortality among non-pregnant adult population is well-established in high-income countries (1), as well as in middle-income countries, such as China and Mexico (2, 3). Controlling brachial blood pressure can reduce the risk of cardiovascular death (4). However, peripheral hypertension does not necessarily correlate with maternal and perinatal outcomes, except for the increased risk of intracranial hemorrhage when there is severe peripheral hypertension (5). Numerous studies suggest that CBP is superior to peripheral blood pressure (PBP) in predicting cardiovascular disease among non-pregnant patients (6–9). The superiority of CBP is likely due to central pressures exhibiting lower variability and more accurately reflecting the tension levels on major target organs such as the heart, brain, and kidneys (10). CBP is defined as blood pressure readings taken from the aorta or common carotid arteries, primarily influenced by increased arterial stiffness and wave reflection (11). It represents the pressure against which the heart must pump to ensure blood flow throughout the body. Evidence indicates that preeclampsia (PE) is associated with increased CBP, pulse wave velocity, and arterial stiffness (12–14). It is known that the cerebrovascular complications of PE and eclampsia can occur in the presence of mild elevations of PBP and even in the absence of proteinuria (15, 16). Since the blood flow to the brain is controlled by the central aortic blood pressure, it is possible that under conditions when there is only mild elevation of the brachial blood pressure, the CBP may be much higher, thus accounting for the vasogenic oedema typical of eclampsia, justifying the need to know how the CBP behaves in patients with HDP and eclampsia.

To evaluate this hypothesis, it is essential to clearly define what constitutes mild and severe central hypertension. Current literature presents conflicting findings regarding the definition of central hypertension (17, 18). Notably, Cheng et al. have proposed a threshold CBP of 130/90 mmHg, which generally serves as a benchmark for central hypertension in non-pregnant women (11, 19). However, given the physiological changes that occur during pregnancy, it would be biased to apply findings from the non-pregnant population, especially those involving men (20). During pregnancy, physiological changes generally result in lower CBP readings compared with those in non-pregnant women and men (21). Therefore, it is necessary to establish the CBP threshold for diagnosing central hypertension in the pregnant population.

The primary objective of this study was to evaluate the correlation and comparative use of PBP and CBP in identifying hypertension among pregnant women. The secondary objective was to determine the threshold values for central systolic blood pressure (cSBP) and central diastolic blood pressure (cDBP) for diagnosing mild and severe central hypertension in pregnancy.

This was a cross-sectional study conducted between December 2022 and April 2024. We prospectively studied 270 inpatients diagnosed with hypertensive disorders of pregnancy (HDP) and 270 inpatient normotensive controls who were in their second and third trimesters of pregnancy. This study was conducted at the Nelson Mandela Academic Hospital, South Africa, in keeping with the principles laid down in the Helsinki Declaration (22). Walter Sisulu University and the Nelson Mandela Academic Hospital board approved this study (ethics reference number 035/2022), and informed consent was obtained from each participant before data collection.

The definitions of hypertension and HDP were based on the International Society for the Study of Hypertension in Pregnancy (23). Mild peripheral hypertension was defined as a pSBP of 110–159 mmHg and/or a pDBP of 90–109 mmHg. Severe peripheral hypertension was defined as a pSBP of 160 mmHg or higher and/or a pDBP of 110 mmHg or higher. The inclusion criteria for hypertensive patients were current hypertensive disease in pregnancy with a gestation period of ≥20 weeks. For controls, the inclusion criteria were a healthy normotensive singleton pregnancy in labor, those admitted for a repeat elective caesarean section at term, or women without hypertension presenting with particular conditions such as placenta previa, preterm premature rupture of membranes, or preterm labour. Participants were excluded if they were under 20 weeks pregnant or if they opted out of participation. Additionally, individuals with diabetes mellitus, cardiac disease, chronic renal disease, antiphospholipid syndrome, or other autoimmune diseases were also excluded from the study.

Data on the presence and type of HDP were collected from patient interviews and medical records using a standard data collection sheet. At enrolment and within 7 days after delivery, brachial and central systolic and diastolic blood pressures were measured using the Microlife WatchBP Office Central. Participants who were initially normotensive but later developed elevated blood pressure were reclassified as hypertensive, while those with gestational hypertension who later exhibited features of PE were reclassified as having PE. Before using the Microlife WatchBP Office central, the correct size of cuff was chosen and placed over the left or right upper arm so that the artery mark arrow points toward the lower arm. The cuff was wrapped around the arm, making sure that the lower edge of the cuff was approximately 2 cm above the elbow. The WatchBP Office Central device automatically measured both brachial and CBP, displaying the results on the screen once the measurement process was complete.

It is important to note that while the validity and reliability of the Microlife WatchBP Office Central have been established in the general population, its PBP measurement component lacked validation for pregnancy use (19) To address this deficiency, a pilot study was conducted involving three distinct groups of participants: 15 normotensive pregnant women, 15 women diagnosed with gestational hypertension, and 15 women with PE. Initially, PBP was measured using the pregnancy-validated Microlife WatchBP Home BT, followed by measurements with the Microlife WatchBP Office Central.

The validation process adhered to the guidelines set forth by the Association for the Advancement of Medical Instrumentation, the European Society of Hypertension, and the International Organization for Standardization (24, 25).

The results of the validation exercise demonstrated a strong correlation between the pregnancy-validated Microlife WatchBP Home BT and the Microlife WatchBP Office Central (refer to Tables 1, 2). Subsequently, the Microlife WatchBP Office Central was used to simultaneously measure both brachial blood pressure and CBP in each participant.

Historically, measuring CBP required invasive methods, which limited its application. However, recent advancements in non-invasive technologies have improved the feasibility of obtaining reliable measurements in clinical environments. This transition toward non-invasive techniques facilitates better monitoring, particularly in vulnerable groups like pregnant women.

This study aimed to assess the relationship between peripheral and CBP and to determine the thresholds for mild and severe central hypertension among pregnant women in the third trimester.

The research established that the cut-off for diagnosing central hypertension is a cSBP of 116 mmHg and a cDBP of 78 mmHg. These findings are consistent with the work of Chulkova et al. (26), who noted that a cSBP of 115 mmHg in pregnant women might indicate a risk for PE. Additionally, these results align with a study by Booysen et al. (27), which reported a cSBP upper threshold of 112 mmHg among a cohort of 311 young Black South Africans with a median age of 31. The similarity in our findings can be attributed to the younger demographic and shared background, as both studies focused on younger Black South Africans.

Conversely, research involving older populations has indicated higher thresholds for CBP. For example, a study with over 6,000 participants conducted by Hao et al. (18) established a 90th percentile cutoff for cSBP at 125 mmHg for men and 126 mmHg for women. This is consistent with previous findings from Japan, where a threshold of 129 mmHg was reported (17). Additionally, Cheng et al. (19) demonstrated through a longitudinal study involving 1,272 older participants that a central BP greater than 130/90 mmHg significantly predicts cardiovascular events over a median follow-up of 15 years. While the cut-off values determined by Cheng et al. (19) serve as important benchmarks, they may not fully apply to pregnant populations, where physiological changes result in unique cardiovascular dynamics (20). Moreover, aging is often associated with aortic stiffness, which leads to an earlier return of reflected waves in late systole, contributing to higher central BP levels (10).

For severe central hypertension, our study found that among pregnant women in their third trimester with severe brachial hypertension, cSBP was ≥148 mmHg and cDBP was ≥95 mmHg. To our knowledge, this work is the first to document the threshold for severe central hypertension. However, further studies are needed to validate these findings. These thresholds are considerably lower than those of PBP (160/110 mmHg), which is expected, as CBP is generally lower than PBP due to the inherent physiological differences between the two vascular systems.

One limitation in our calculations is that some normotensive controls displayed higher cSBP and/or cDBP values than their peripheral counterparts. Under typical conditions, cSBP should be lower than pSBP, with minimal variation between pDBP and cDBP. The possible explanation for this finding in our study is that while the participants had normal PBP, their CBP may have already been abnormal.

In comparison of peripheral and CBP, a positive correlation was found between pSBP and cSBP, as well as between pDBP and cDBP among normotensive pregnant women, aligning with previous findings by Fujime et al. (28). Importantly, Fujime et al. analyzed a larger sample of 830 participants, which adds strength to their findings. Similarly, a cross-sectional study by Priyadarsini et al. (29) involving 107 pregnant women and 53 age-matched non-pregnant women also confirmed a strong relationship between brachial systolic blood pressure and cSBP in healthy normotensive pregnant women (29).

These positive correlations could be explained physiologically by the impact of arterial elasticity on circulatory pressure distribution (30). With healthy, elastic arteries, a strong correlation between peripheral and central measurements is expected. Healthy, elastic arteries allow for a more efficient transmission of pressure waves generated by the heartbeat. When arteries are elastic, they can accommodate the surge of blood during systole, dampening the pressure peaks and maintaining a more stable blood flow throughout the body (31).

Additionally, several studies have demonstrated that CBP has a better relationship to future cardiovascular events and mortality and is also more relevant than peripheral brachial BP in predicting target organ damage, as it represents the true load imposed on the heart, brain, kidneys, and the large arteries (32–34). Nevertheless, additional research is necessary to validate these findings, given that some authors dispute the stronger correlation between CBP and cardiovascular events (35, 36).

In this study, the median cSBP among normotensive pregnant women was found to be 115 mmHg. This finding is consistent with the results of Turi et al. (37), who reported a similar mean cSBP of 115 mmHg in healthy pregnant women. However, in our study, the cSBP value was slightly higher, though not significantly, than the pSBP value of 114 mmHg that was observed. Typically, in normotensive individuals, cSBP is expected to be lower than pSBP. This atypical finding raises the possibility that individuals with higher cSBP in this study may have an underlying increase in arterial stiffness or could be at risk of developing it. As arterial stiffness increases, systolic pressure tends to rise. This is due to the early merging of the fast-reflected wave with the forward wave (38). Furthermore, increased arterial stiffness damages more elastic fibers in the blood vessel walls, leading to inadequate buffering and transmission of pulsatile pressure from the heart to target organs (39). Such changes can ultimately result in organ damage, so it is a good idea to closely monitor these patients to assess their risk of high blood pressure in the future.

In this study, cDBP in normotensive controls was less than pDBP in 159 participants, and it was greater than pDBP in 98 participants. This is again an unexpected finding in normotensive controls, as under physiological conditions, the cDBP should either be the same as the pDBP or less than the pDBP (40). This suggests that the 98 individuals with higher cDBP may be having central diastolic hypertension or are at risk of developing central hypertension, while their peripheral diastolic blood pressure puts them in the normal blood pressure category. Only a prospective follow-up study can test this explanation.

There is little correlation between the pBP and the occurrence of eclampsia. Several studies indicate that the blood pressure may be normal or only mildly elevated in women with eclampsia and even with stroke (41–43). The present study found that the median central systolic and diastolic blood pressures, as well as pDBP, were significantly higher in cases of eclampsia compared with those with other HDP and with non-hypertensive controls. This implies that CBP measurement may be better able to distinguish between the subtypes of HDP and phenotypes of PE than PBP.

In addition, the median cSBP for women with eclampsia and mild peripheral hypertension was relatively severe. This suggests that some eclamptic patients with mild pSBP actually have a cSBP that falls into the severe range. This finding may help explain why some patients with mild peripheral hypertension experience eclampsia. This implies that the cSBP might be a better predictor of eclampsia than the pSBP. Central aortic blood pressure plays a crucial role in regulating blood flow to the brain (15). Consequently, it could be inferred that in cases of eclampsia, vasogenic oedema might occur due to elevated CBP, even when brachial blood pressure remains only slightly elevated in the affected women.

The limitation of this study is that all hypertensive patients received antihypertensive treatment, which may have affected their blood pressure readings. However, patients were recruited within 24 h of admission, a time frame during which the pharmacological treatment might not have fully taken effect.

This study established the threshold values for central hypertension as 116/78 mmHg, with severe central hypertension defined as 148/95 mmHg. This study also reinforces the positive correlation between peripheral and CBP in both normotensive and hypertensive populations. Notably, women with eclampsia showed higher CBP levels compared with those having mild hypertension in the severe range. This may clarify why some patients with mild peripheral hypertension experience eclampsia and may thus indicate that CBP is a better predictor of eclampsia than PBP. Further research is needed to confirm these findings.