Keywords

Pulse pressure; Obesity; Hypertension

Introduction

Hypertension (HTN) and obesity often coexist [1-4]. When hypertensive subjects are compared with normotensive, one of the main differences is the awesome increase of the prevalence of obesity among hypertensive [5]. Furthermore, weight gain seems to be one of the main determinants of blood pressure increase with age [3,4]. HTN and obesity share many socio-ecological and epidemiological similarities. First, they are diseases of civilization, corollaries of profound changes that accompanied the 45,000 years of evolution from Homo sapiens sapiens, to which physical activity was the pledge of survival [6], to the today human who uses more neurons than muscles to live and survive, and therefore, has reduced physical activity and increased energy intake. Second, the relevance of both hypertension and obesity, as important public health challenges, is increasing worldwide [4]. Third, there are ethnic disparities in the prevalence and cardiovascular health impact of both. Thus, for example, HTN is experiencing a more dramatic growth in blacks, affecting younger people, with poorer blood pressure control, and singularly moving early to cardiovascular complications [7-10]. Obesity also is more prevalent in Blacks than in Caucasians, and would be associated with a higher cardiovascular risk in Blacks [11].

The diagnosis of HTN, whether by office or by out-of-office BP monitoring is based on the values of systolic blood pressure (SBP) and diastolic blood pressure (DBP) [12,13]. The target values of the management of high blood pressure also relate these parameters. Even if no recommendation today suggests considering pulse pressure (PP), either for diagnosis or for monitoring the treatment of high blood pressure, there has been increased recognition of PP having a more important predictive value of increased cardiovascular morbidity and mortality these last years. Indeed, Epidemiologic surveys and clinical studies have demonstrated a close relationship between increased PP and target organ damage including urinary albumin excretion [14,15]. Decline in glomerular filtration rate [16,17], left ventricular hypertrophy [18,19] and endothelial dysfunction [19,20]. PP has also been recognized as predictor of atrial fibrillation [19,21], heart failure [19], impairment in neurocognitive function and dementia [22] and cardiovascular events onset and recurrence [19,23-26]. Thus, PP would prove to be a better marker of cardiovascular risk than other blood pressure parameters. Studies have demonstrated that various modalities of PP measures (central or peripheral, clinic or ambulatory) have statistically similar predictive value.

There is an association between obesity and cardiovascular risk, of which PP is a recognized marker. Whether this association differs between abdominal and general obesity is controversial. Indeed, some studies have suggest that measures of abdominal obesity are best correlated with cardiovascular risk [27-31], discouraging the use of the BMI, whereas some others have failed to demonstrate this superiority of measures of abdominal obesity to that of general obesity [32-36].

Another debate about the correlation between obesity and pulse pressure, and therefore cardiovascular risk, concerns the existence of modifying factors of this correlation. Most cited by authors, without them from being unanimous, are age [26], gender [3,37,38] and ethnicity [3,37].

In sub-Saharan Africa, studies on the PP are rare. The only one, to our knowledge, that has addressed this issue has found no correlation at all between obesity and pulse pressure [39], reviving debate about the existence of this correlation and casting doubt on the existence of this association in Sub-Saharan Africa.

Therefore, this study aimed to assess whether the association between PP and the parameters defining obesity is modified by gender, age, sedentary and hypertension status in an apparently healthy Congolese Black Population.

Methods and Data Collection

This study is part of the MACRIS study. Data collection has been described elsewhere [40]. Pulse pressure was defined as the difference between SBP and DBP. Mean blood pressure was defined as the sum of diastolic blood pressure and the third of the pulse pressure. Waist Circumference (WC) and The Waist- Hip Ratio (WHR) were considered as parameters of abdominal obesity, while BMI was considered for general obesity. General obesity was defined as a body mass index (BMI) greater than or equal to 30 kg/m², BMI is the ratio of weight to height squared. Abdominal obesity (AO) has been defined by a waist circumference greater than or equal to 94 cm for men and greater than or equal to 80 cm for women.

Statistical Analysis

Continuous variables were presented as mean ± standard deviation (SD) or median (interquartile range) based on their distribution. Categorical variables were expressed as percentages.

Sociodemographic and clinical characteristics of the study population have been described for all subjects and by gender and quartiles of the PP (≤ 36 mmHg, 36<44 mmHg PP ≤ 44 <≤ 55 PP mmHg and >55 mmHg). Group means or medians were compared using Student t test, t test for unequal variances, oneway analysis of variance (ANOVA), Wilcoxon rank-sum test or Kruskal-Wallis rank test as appropriated. Categorical variables were compared using Pearson’s chi square or Chi-square for trend as appropriated. The homogeneity of variances was checked with Leven test.

Multiple linear regression models were developed to study the association between PP and parameters used to define obesity (WC, HC, WHR and BMI).

These models were adjusted for covariates age, sex, heart rate, diabetes mellitus, physical inactivity, smoking status and blood pressure. Biological parameters were not taken into account due to the importance of missing values.

In these models, interactions were tested to highlight the potential modifying effects respectively of age, gender, sedentary and hypertension status. In the presence of a significant interaction, models were built in the strata of the amending effect variable. These laminates models were adjusted for covariates listed above. Analysis was performed using the software STATA version 10.1 and statistical significance threshold for all the applied tests was 0.05.

Results

It was a young population (mean age 37 years), with only a quarter of the population over 55 years (97/397). The population was predominantly female. (Sex ratio: 1.7). Abdominal obesity (53.2%) and hypertension (40.8%) were the most prevalent cardiovascular risk factors in this population. The high rate of participants with abdominal obesity (53.2%) contrasts with the low overall obesity (14.9%). Only a small proportion of the population (4%) was sedentary.

Participants in the highest PP quartile (compared to the lower quartiles) were older, more often married, had more often average level of education, were more often smoking, mostly sedentary and tachycardia, had highest waist circumference, more often diabetic and more often hypertensive (Table 1).

Table 1 Sociodemographic and clinical characteristics of the population as a whole and according to gender.

Gender did not modify the correlation between PP and parameters of obesity (Table 2).

Table 2 Sociodemographic and clinical characteristics of subjects according to quartiles of pulse pressure.

Table 3 shows that waist circumference and hip circumference are associated with PP only in hypertensive participants. This association was not observed in non-hypertensive. BMI and TT/TH are not associated with pulse pressure. Covariates: age, gender, heart rate, diabetes mellitus, sedentary, cigarette smoking (Table 3).

Table 3 Associations between WC, BMI, WHR and pulse pressure, stratified by hypertension status and adjusted for covariates.

Associations PP versus TT, TH, IMC et rapport TT/TH

Associations between WC, BMI, WHR and PP, stratified by the age and adjusted for the covariables (Table 4).

Table 4 Associations between WC, BMI, WHR and PP, stratified by the age and adjusted for the covariables.

Associations between WC, BMI, WHR and PP, stratified by the variable sedentary and adjusted for the covariables (Table 5).

Table 5 Associations between WC, BMI, WHR and PP, stratified by the variable sedentary and adjusted for the covariables.

Discussion

This population-based study employs a representative sample of apparently healthy adult population of a Congolese southwest port city, in Sub-Saharan Africa. Three key messages emerged from this study: First, visceral obesity but not general obesity is correlated with pulse pressure. Second, age, sedentary and hypertension status but not gender nor diabetes, are the modifying factors of the relation between visceral obesity and pulse pressure.

Considering PP as a marker of cardiovascular risk, this study joins many previous studies for plebisciting measure of abdominal obesity as a better predictor of cardiovascular risk, compared to that of overall obesity. There are strong pathophysiological arguments to support this observation. Indeed, while BMI is widely used to monitor the prevalence of obesity, it provides no information about the distribution of body fat. Physiological characteristics of abdominal adipose tissues such as adipocyte size and number, lipolytic responsiveness, lipid storage capacity, and inflammatory cytokine production are significant correlates and even possible determinants of the increased cardiometabolic risk associated with visceral obesity [41].

The increase in pulse pressure with age is a well-known phenomenon. It is related to arterial aging. It has also been widely demonstrated that obesity was a protective factor in elderly patients. The finding in this study of a positive association between parameters of abdominal obesity and pulse pressure, in other words, between parameters of abdominal obesity and cardiovascular risk, which does not appear in older agrees with what the so called "obesity paradox". This is the fact that obese patients, especially elderly, may demonstrate lower all-cause and cardiovascular mortality compared with patients of normal weight [42].

Sedentary behavior appears to be linked to weight gain, both directly because it corresponds to low energy expenditure, but also indirectly by its association with other health behaviors, especially food intake. The association between physical activity and health was recognized as early as the fifth century BC by the Greek physician Hippocrates, who wrote the following: “All parts of the body, if used in moderation and exercised in labors to which each is accustomed, become thereby healthy and well developed and age slowly; but if they are unused and left idle, they become liable to disease, defective in growth and age quickly” [43]. The deleterious effects of physical inactivity are not exclusively due to its link with obesity. Sedentary behavior induces metabolic dysfunction, characterized by increased plasma triglyceride levels, decreased levels of high-density lipoprotein (HDL) cholesterol, and decreased insulin sensitivity [44]. It has been demonstrated that physical activity lowers PP and cardiovascular risk [45]. The beneficial effects of physical activity on cardiovascular risk occur even in the absence of weight loss. Other mechanisms by which physical activity reduces cardiovascular risk include, among others, an improve in lipid and inflammatory/hemostatic profile, and blood pressure lowering that have been observed with increased physical activity patterns or structured exercise programs [46]. The above mentioned physical inactivity induced metabolic dysfunction could potentialise the obesity related cardiovascular risk. This would be the explanation of the result of this study showing that abdominal obesity is correlated with pulse pressure in sedentary.

This study also showed that the cardiovascular risk of obese was increased in the presence of hypertension. High blood pressure is a well-known cardiovascular risk factor. The severity of hypertension in obese patients is also well known. This severity is due to its almost systematic association with a constellation of metabolic risk factors that interact among themselves to increase the overall cardiovascular risk.

Information obtained from this study is of great importance from an epidemiological point of view. This study indicates the groups to which the abdominal obesity management should be applied in a particular way to prevent the increase of cardiovascular risk, i.e., although it is worth recommending lifestyle changes for weight management across the population, more attention should be paid to young (<55 years), to hypertensive and to sedentary groups in which a positive and significant association between abdominal obesity parameters and PP is established in this study.

Limitations and Strengths

Because it was a cross-sectional study, no information on causality was obtained. The strengths of our investigation include a representative population so that the results could be extrapolated to the all the population of Matadi city.

Acknowledgement

Design and concept of study: Kianu Phanzu Bernard. Acquisition of data: Mpembele Mabaka. Data Analysis and interpretation: Mbutiwi Ikwa Ndol. Manuscripti draft: Kianu Phanzu Bernard. Statistical expertise: Mbutiwi Ikwa Ndol. Acquisition of Funding: Mpembele Mabaka and Kianu Phanzu Bernard. Administrative, technical, or material assistance: Mpembele Mabaka. Supervision: Kintoki Vita Eleuthère, M’buyamba-Kabangu Jean-Réné, Longo- Mbenza Benjamin. All the authors reviewed and approved the final manuscript.

Disclosure

The authors have no financial disclosures to report or any affiliations that may bias this work.

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