The contribution of mean arterial pressure to pulse pressure is greater in women than in men beginning before middle age

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The contribution of mean arterial pressure to pulse pressure is greater in women than in men beginning before middle age

https://doi.org/10.21203/rs.3.rs-3596822/v1

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The study analyses the contribution of mean arterial pressure (MAP) to pulse pressure (PP) in hypertensive men and women younger than 50 years. Central pressure waveform was obtained from radial artery applanation tonometry in 312 hypertensive patients between 16 to 49 years (134 women, mean age 35 ± 9 years). As expected, brachial PP, central PP, incident wave, and augmentation pressure were significantly higher above the mean level of MAP (≥ 100 mmHg) compared to lower levels (p values adjusted for sex, age, height, weight, and heart rate were 0.001, < 0.001, 0.005, and < 0.001 respectively). In turn, the differences observed in brachial PP, central PP, and the incident wave between the MAP subgroups were significantly greater in women than in men (p values for the interaction between sex and MAP adjusted by age, height, weight, and heart rate were 0.008, 0.004 and 0.010 respectively). When subjects were stratified by age (16–29, 30–39, and 40–49 years), the strength of the relationship between MAP and central PP increased from age 30–39 onwards in women and from age 40–49 in men (p-value for the interaction between sex, MAP, and age group: < 0.001). The sex difference was driven by a greater MAP-mediated increase in the incident wave in women (p < 0.001). In conclusion, in hypertensive subjects younger than 50 years, the contribution of MAP to PP was greater in women than in men beginning at age 30–39 years.

Biological sciences/Physiology/Circulation/Hypertension

Health sciences/Risk factors

Sex difference

young adults

middle-aged adults

pulse pressure

mean arterial pressure

augmentation pressure

pulse pressure

What is known about the topic

Women show a more pronounced rise in PP and SBP compared with men beginning decades before menopause.
This sex difference could respond to a different relationship between MAP and PP with age.

What this study adds

In individuals under the age of 50, men had higher PP and SBP than women, but the sex difference was blunted at higher levels of MAP due to a greater contribution of MAP to PP in women.
The contribution of MAP to PP increased with age in both sexes but began a decade earlier in women.
Our findings highlight the role of MAP in the steeper age-related increase in BP pulsatility in women compared to men.

Blood pressure (BP) is composed of a steady component, represented by mean arterial pressure (MAP), and a pulsatile component, represented by pulse pressure (PP). High PP, a hallmark of arterial aging (1), is also observed in young men whose underlying mechanism is a high stroke volume rather than arterial stiffness. Interestingly, brachial PP declines between early adulthood and middle age (2), despite the age-related increase in arterial stiffness and MAP (3), starting to increase again in older decades. The curvilinear change in brachial PP with age expresses a transition in the hemodynamic determinants of BP pulsatility. A gradual decline in the stroke volume along with an increase in the diameter of the ascending aorta outweighs arterial wall stiffening until middle age, beyond which the stiffening of the arterial wall outpaces the increase in diameter (2–5).

While high brachial PP in young adulthood coincides with a high peripheral amplification of the pressure wave, PP is also high at the central aorta paralleling a high stroke volume (6, 7). The transition in the underlying mechanism of PP from high stroke volume in young adults to high arterial stiffness in older age is accompanied by a change in the shape of the central aortic pressure waveform (8). In young individuals, the incident wave, recognized as the first systolic peak in the pressure contour, is the main contributor to the amplitude of central aortic PP. In the subsequent decades and up to 60 years, the contribution of the augmentation pressure (AP), recognized as a late systolic peak, becomes increasingly significant (9). The differential change of the incident wave and AP before middle age is indicative that both components of the pressure wave does not relay on a common mechanism as occurs later.

Women are at higher risk of adverse cardiovascular outcomes at lower systolic BP (SBP) thresholds than men, being the association between SBP and cardiovascular risk being more pronounced in younger versus older women (10). On the other hand, the relationship between steady state and pulsatile components of BP differs between men and women over the life course, with a more pronounced rise in PP and SBP in women compared with men beginning decades before menopause (11–18). This is also expressed in the sex difference in the transition of hypertension subtypes between young and middle adulthood. The prevalence of isolated systolic hypertension remains very low in young women until age 40 after which it shows a rapid rise while men show the opposite pattern (13, 19). Recent follow-up data from the HELIUS study showed that at age 30, isolated systolic hypertension was found in 5.4% of men and 0.7% of women, whereas, after a median follow-up time of 6 years, the prevalence halved in men and doubled in women (20).

When analyzing pulsatile parameters, it is important to take into account the differences in MAP (21). Increasing distending pressure recruits non-distensible collagen, leading to a nonlinear increase in arterial stiffness and higher BP pulsatility (22). However, despite the steeper increase in MAP during the first half of adult life, PP decreases until middle age before increasing in parallel with MAP in later decades (13). In a previous study we showed that in men, the relationship between MAP and brachial PP changed with age, from negative before age 40 to positive after that age (23). In the younger group, a reciprocal decrease in stroke volume prevented the increase in PP associated with increasing MAP despite a concomitant decrease in arterial compliance (23). Based on this background, we studied how the contribution of MAP to central PP and pulse wave morphology changes between young to middle age and how it varies with sex.

Design and Participants

We analysed the hemodynamic data of a cross-sectional nested in a prospective cohort of ambulatory patients referred to the Hypertension Section of the Hospital Italiano de Buenos Aires, Argentina between June 2011, and April 2015. Patients were included if they were over 16 years of age and younger than 49 years, with hemodynamic measurements, and referred to the Hypertension Section of the Hospital Italiano de Buenos Aires, Argentina. Exclusion criteria were participants with vascular indexes considered inconclusive, or low operator index < 70, or with extreme outliers which might lead to a methodological error.

The study protocol and patient characteristics were previously reported (24). The present study was approved by the local ethics review board Comité de Ética de Protocolos de Investigación (CEPI) (protocol number: 2911) and was conducted according to the amended declaration of Helsinki and addressing the ICH E6 Good Clinical Practice.

Measurements definitions and variables

We collected data by reviewing high-quality electronic medical records and hemodynamic secondary databases, all data was collected in form.

Demographic variables included the patient's age at the time of the referral, gender, comorbidities (arterial hypertension), vital signs (heart rate, height, weight, BMI), treatment and hemodynamic measurements. The severity of hypertension was assessed by the level of MAP rather than conventional stages based on systolic and diastolic thresholds. We used MAP to assess the severity of hypertension because it modifies PP through the distension of the arterial wall (22).

The central aortic pressure wave contour was obtained noninvasively using a SphygmoCor device (CvMS; AtCor Medical, Sydney, NSW, Australia), which uses applanation tonometry for the acquisition of the radial pressure wave. The radial pressure waveform was recorded with the subject resting supine for 5 minutes. It was calibrated with the systolic and diastolic brachial pressure (OMRON HEM 705 CP oscillometric sphygmomanometer Omron Corp., Japan) using the appropriate cuff size for the arm circumference. Only recordings with an operator index > 70% were admitted. The amplitude of the central pulse wave at the first pressure peak (non-augmented central PP) will be referred to hereinafter as the incident wave. Central AP was calculated as the second peak minus the first peak of the central pressure wave and expressed in millimeters of mercury. The AIx expresses AP as a percentage of central aortic PP. Non-augmented central PP (hereafter referred to as incident wave) was calculated as central PP subtracting AP. MAP was calculated via integration of the radial pressure waveform by the Sphygmocor software. Carotid to femoral pulse wave velocity (PWV) was measured in a subset of 238 patients.

Statistical analyses

Data are presented as mean ± standard deviation or median and range between minimal and maximal values. Analyses were stratified separately by sex. MAP was analysed as a dichotomous variable based on the mean of the sample, which was 100 mmHg, and as a continuous variable. Differences between age and MAP subgroups were evaluated using one-way ANOVA or Chi-square. Pearson correlation was used to evaluate the association between age and hemodynamic parameters, each is presented with Pearson coefficient and p-value. We use a generalized linear model to evaluate the interaction of MAP and age on central PP, incident wave, and AP, stratified by men and women. The model was adjusted for covariates (age, sex, heart rate, and antihypertensive treatment). The interaction between sex, age group, and MAP on pulsatile BP parameters was evaluated by multiple regression analyses. The role of age and MAP as predictors of central PP, the incident wave, and AP was evaluated in men and women by multiple regression analyses. Each variable is presented with its coefficient and confidence interval of 95% (CI 95%). A P value of less than 0.05 was considered to indicate statistical significance in all analyses. Statistical analyses were conducted using SPSS version 22 for Windows (IBM Corp., Armonk, NY, USA).

Participants

Between June 2011 and April 2015, 352 patients aged 16 to 49 years old were referred to the Hypertension Section for the non-invasive evaluation of central aortic BP. Of those 312 patients were included (134 women). The mean age was 35 ± 9 years (16–49 years), and the mean systolic and diastolic blood pressure were 134 ± 14 and 82 ± 10 mmHg respectively. One hundred eighty-five (59%) patients were on antihypertensive treatment.

Sex differences in hemodynamic parameters

Table 1 shows demographic and pulse wave parameters according to sex. Women had older age, lower body size, and higher heart rate. Men and women had comparable MAP, brachial diastolic blood pressure, and PWV. However, women had significantly lower brachial SBP (P < 0.001), brachial PP (P < 0.001), central PP (P < 0.05), and incident wave (P < 0.001) than men. On the other hand, measures of wave reflection such as AP and AIx were higher in women than in men (P < 0.001), blunting the sex difference in SBP and PP at the central aorta, therefore reducing peripheral amplification of PP (P < 0.001).

Table 1

Sex differences in demographic and hemodynamic parameters in patients between 16–49 years with hemodynamic measurements referred to the hypertension section (n = 312).
Parameters	Men n = 178	Women n = 134
Age, ys	34 ± 10	37 ± 9 †
Height, cm	176 ± 7	162 ± 6 ‡
Weight, Kg	86 ± 14	70 ± 16 ‡
BMI, Kg/m²	27.4 ± 4	26.7 ± 6
Antihypertensive treatment, n (%)	105 (59)	78 (58)
HR, bpm	70 ± 13	77 ± 13 ‡
Brachial SBP, mmHg	137 ± 12	129 ± 16 ‡
Central SBP, mmHg	118 ± 11	117 ± 15*
Brachial DBP, mmHg	82 ± 9	82 ± 11
Brachial MAP, mmHg	99 ± 10	99 ± 12
Brachial PP, mmHg	56 ± 12	47 ± 11 ‡
Central PP, mmHg	35 ± 7	33 ± 9*
Peripheral amplification, mmHg	20 ± 7	14 ± 6 ‡
Incident wave, mmHg	32 ± 7	26 ± 6 ‡
AP, mmHg	2.5 ± 5	7 ± 6 ‡
AIx, %	6.3 ± 13	19.0 ± 13 ‡
PWV, m/s	6.7 ± 1.3	6.8 ± 1.2
Continuous variables are presented as mean ± standard deviation. Aix; augmentation index; AP, augmentation pressure; MAP, mean arterial pressure; PP, pulse pressure, and carotid to femoral pulse wave velocity (PWV). PWV was measured in a subset of 238 patients. Mean ± SD. *P < 0.05; †P < 0.01; ‡P < 0.001.

Contribution of MAP to the sex difference in PP and pressure waveform

Figure 1 illustrates the sex difference in hemodynamic parameters stratified by MAP. When MAP was divided into two groups based on its mean value (< versus ≥ 100 mmHg), higher MAP levels were associated with significantly higher brachial PP, central PP, incident wave, and AP compared to lower MAP levels (p values adjusted for sex, age, height, weight, and heart rate were 0.001, < 0.001, 0.005, and < 0.001 respectively). Moreover, the difference observed in brachial PP, central PP, and the incident wave between the MAP subgroups was significantly greater in women than in men (p values for the interaction between sex and MAP adjusted by age, height, weight, and heart rate were 0.008, 0.004 and 0.010 respectively). High MAP was also associated with a significantly higher DBP and AP, and lower peripheral amplification, without significant sex difference. Therefore, a greater contribution of MAP to the incident wave in women blunted the sex difference in SBP and PP.

Contribution of age to the relationship between MAP and pulsatile parameters according to sex

Next, we analysed whether age modifies the strength of the relationship between pulsatile parameters and MAP. The relationship of pulsatile parameters with MAP showed a progressive age-related strengthening which was more prominent in women starting a decade earlier than in men (Table 2 and Fig. 2). Multiple regression analysis including MAP, age group, sex, and the interaction term MAP x age group x sex, indicated that the contribution of MAP to brachial, central PP, incident wave, and peripheral amplification increased significantly with age, more strongly in women than in men (P < 0.001).

Table 2

Univariate correlation analyses between MAP and hemodynamic parameters stratified by age and sex.
Hemodynamic parameters	Sex	< 30 ys	30–39 ys	40–49 ys	Interaction sex x age x MAP
Number	Male	67	48	63	-
Number	Female	31	39	64	-
Heart rate, bpm	Male	0.54 ‡	0.28	0.22	0.108
Heart rate, bpm	Female	0.58 †	0.25	0.06	0.108
Brachial PP, mmHg	Male	-0.07	-0.15	0.40 †	< 0.001
Brachial PP, mmHg	Female	0.03	0.35 *	0.57 ‡	< 0.001
Central PP, mmHg	Male	-0.06	0.03	0.49 ‡	< 0.001
Central PP, mmHg	Female	-0.01	0.44 †	0.65 ‡	< 0.001
Augmentation Pressure, mmHg	Male	0.23	0.40 †	0.46 ‡	0.767
Augmentation Pressure, mmHg	Female	0.14	0.41 *	0.58 ‡	0.767
Augmentation index, %	Male	0.22	0.39 †	0.37 †	0.249
Augmentation index, %	Female	0.19	0.27	0.44 †	0.249
Incident wave, mmHg	Male	-0.11	-0.21	0.29 *	< 0.001
Incident wave, mmHg	Female	0.06	0.27	0.53 ‡	< 0.001
Peripheral amplification, mmHg	Male	-0.08	-0.25	-0.03	0.008
Peripheral amplification, mmHg	Female	0.05	-0.06	-0.06	0.008
PWV, m/s	Male	0.45 †	0.12	0.27 *	0.744
PWV, m/s	Female	0.78 ‡	0.29	0.39 †	0.744
Values are Pearson coefficients. Abbreviations: Aix; augmentation index; AP, augmentation pressure; MAP, mean arterial pressure; PP, pulse pressure, and carotid to femoral pulse wave velocity (PWV). The PWV was measured in a subset of 238 patients. *P < 0.05; †P < 0.01; ‡P < 0.001

Figure 3 compares the age-related slopes of PP and the components of the pressure waveform between MAP subgroups according to sex. Compared to the lower MAP subgroup, elevated MAP weakened the inverse correlation between age and central PP (from r = -0.43, p < 0.001 to r = 0.00, p = ns in men; and from r = -0.10, p = ns to r = 0.32, p < 0.05 in women) and incident wave (from r = -0.56, p < 0.001 to r = 0.45, p < 0.001 in men; and from r = -0.37, p < 0.01 to r = r = 0.03, p = ns in women) while strengthened the positive correlation between age and AP (from r = 0.49, p < 0.001 to r = 0.65, p < 0.001 in men; and from r = 0.40, p < 0.01 to r = 0.52, p < 0.001 in women). The result was a progressive divergence between MAP subgroups in the corresponding age-related slopes. The divergence began at age 30 and was more pronounced in women than in men.

Predictors of central PP, the incident wave, and AP between men and women

Multivariate analyses shown in Table S1 indicated that after adjusting for age, heart rate, and antihypertensive treatment, MAP remained a stronger predictor of central PP and incident wave in women than in men. On the other hand, age was a stronger negative predictor of central PP and incident wave in men than in women. In turn, heart rate was negatively associated with central PP and AP in both sexes. Antihypertensive treatment only showed a marginal independent association with AP in men.

The present cross-sectional study analyses the influence of age and sex on the relationship between steady state and pulsatile components of blood pressure in hypertensive subjects younger than 50 years. Here we showed that the contribution of MAP to PP increased from young adulthood to middle age, more strongly in women beginning a decade earlier than men. While in men the contribution of MAP to PP was mediated by an increase in AP, in women it was driven by a combined increase in both components of the pressure wave. In young adults (< 30 years), increasing MAP was associated with higher heart rate, which, in turn, blunted the effect of elevated MAP on PP in both sexes.

The initial drop in brachial PP to a nadir in middle age contrasts with the view of a high PP as a surrogate of arterial stiffness and a hallmark of arterial aging (3). We have previously shown that both brachial PP and stroke volume are higher before age 30 than in middle age (2, 7). It is likely that the higher the stroke volume in early adulthood the greater its decline in subsequent decades, and consequently the fall in PP. It has also been proposed that the initial fall in brachial PP underlies an increase in proximal aortic diameter which, until midlife, outweighs the effect of increasing aortic wall stiffness (3, 4). Both hypotheses could be mutually complementary since a larger initial stroke volume could stimulate a greater adaptive remodelling of the aortic root diameter. Therefore, a sex difference in stroke volume in young adulthood could determine a corresponding sex difference in aortic diameter, leaving early middle-aged hypertensive women more prone to increased PP than their male counterparts. This hypothesis aligns with the observed more significant decrease in PP in men from early to midlife adulthood and the stronger positive correlation between MAP and PP in women.

High MAP weakened the negative effect of age on central PP in men and reverted it to positive in women compared to the age-related change at a lower MAP. Given a comparable MAP-dependent increase in AP, the source of the sex difference in the relationship between MAP and PP was a greater contribution of increasing MAP on the incident wave in women. Based on the study, it appears that the ability of the female proximal aorta to buffer the increase in arterial wall stiffness due to MAP is lower than that of men from early middle age. The likely mechanism underlying the higher incident wave in women with elevated MAP is a smaller aortic root diameter, a determinant of characteristic impedance. Accordingly, the CARDIA study and the Framingham Heart study showed that men experience a greater age-related remodeling of the aortic root diameter than women (25, 26). Also, the Asklepios study found that while MAP and PWV increased between the ages of 35 and 55, PP increased only in women, remaining stable in men. The sex difference was attributed to a difference in characteristic impedance, which remained unchanged in women while it decreased in men (27).

High MAP loads the stiff components of the arterial wall, leading to a nonlinear increase in arterial stiffness and higher BP pulsatility. In turn, an increase in resistance in small arteries, a determinant of higher MAP, increases wave reflection and augments central aortic PP. Here we showed that the contribution of MAP to PP is not homogeneous but rather increases between early adulthood and middle age. The pressure-dependent increase in PWV did not result in a significant contribution of MAP to PP before the age of 30. Accordingly, in a previous study in hypertensive men, a reciprocal decrease in stroke volume blunted the MAP-mediated increase in brachial PP before age 40, despite a concurrent decrease in arterial compliance (23). Similarly, in the ENIGMA study (29), young essential hypertensive subjects had 12 mmHg lower central PP despite having 11 mmHg higher MAP than their isolated systolic hypertension counterparts. The latter paralleled the 19% higher stroke volume and the six beats per-minute lower heart rate in those with isolated systolic hypertension.

The study has potential limitations. First, the participants were recruited from an outpatient setting, which may not be representative of the general population. Second, most of the patients were receiving antihypertensive medication. However, as shown in multivariable analyses, the results were independent of the use of antihypertensive medication, indicating that any influence of treatment was mediated by its effects on either MAP or heart rate.

In conclusion, the study showed that women were more susceptible than men to the effect of hypertension on PP beginning in the fourth decade. Before age 30, the effect of elevated MAP on PP was blunted by a concomitant increase in heart rate.

Perspective

Our findings highlight the role of MAP in the steeper age-related increase in BP pulsatility in women compared to men, supporting the claim of sex-specific blood pressure targets (30), to prevent the pulsatile stress from damaging target organs.

Conflicts of interest

The authors have nothing to disclose.

Funding

None

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There is NO conflict of interest to disclose.

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The contribution of mean arterial pressure to pulse pressure is greater in women than in men beginning before middle age

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Abstract

Figures

Summary Table

Introduction

Methods

Design and Participants

Measurements definitions and variables

Statistical analyses

Results

Participants

Sex differences in hemodynamic parameters

Contribution of MAP to the sex difference in PP and pressure waveform

Contribution of age to the relationship between MAP and pulsatile parameters according to sex

Predictors of central PP, the incident wave, and AP between men and women

Discussion

Perspective

Declarations

Conflicts of interest

Funding

References

Additional Declarations

Supplementary Files

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