Obesity and hypertension are currently two of the most prevalent diseases. The National Health and Nutrition Examination Surveys indicated that the prevalence of obesity has increased dramatically in all race/sex groups. Longitudinal studies have shown that obesity is a risk factor for the development of hypertension.1) Obesity with its increasing prevalence, and as a consequence of its associated co-morbidities, is rapidly becoming the leading global cause for cardiovascular morbidity and mortality.2, 3) In several studies, patterns of blood pressure variability (BPV) over time have been used to evaluate the precise risk of current and long-term complications.4) Increased BPV may be an independent risk factor for cardiovascular events in elderly hypertensive patients.5) In particular, nighttime BPV is a strong predictor for cardiovascular events in patients with type 2 diabetes.6) Several factors are associated with BPV. The known mechanisms facilitating BPV are arterial stiffness,7) baro reflex regulation of BP,8) inflammation,9) and heart rate variability.10) Bonilla et al.11) reported that compared with non-obese adolescents, obese adolescents show greater changes in BPV over period of 24 hours. Lim et al.12) reported because of increase in children's obesity, use of ambulatory blood pressure monitoring (ABPM) is necessary for evaluating their risk of hypertension. Since, the influence of obesity on BPV in adults has not yet been studied, we investigated the effect of obesity on BPV in adults and its circadian variation.

The clinical characteristics of the study population are summarized in Table 1. The obese group had significant correlation with age (p < 0.001), sex (p = 0.011), history of hypertension (p < 0.001), and use of calcium channel blockers (p = 0.010), angiotensin-converting enzyme inhibitors and statins (p = 0.010 and p = 0.019, respectively).

Table 1 Comparison of baseline characteristics between the non obese and obese groups Click for larger image

In the univariate model, both daytime and nighttime systolic BP (SBP) and diastolic BP (DBP) averages were significantly higher in the obese group, (p < 0.001) (Table 2). In univariate regression analysis of the SD values of BP, there was no significant difference in BPV during daytime (SBP variability: 20.7 vs. 21.7, p = 0.511; DBP variability: 16.8 vs. 17.5, p = 0.539). However, both SBP variability (13.8 vs. 17.6, p = 0.009) and DBP variability (11.7 vs. 14.3, p = 0.042) during nighttime were significantly affected by BMI (Table 2). The univariate model showed that BMI caused no significant difference in average HR during daytime and nighttime between the 2 groups (Table 3). After adjusting other compounding variables (age > 60 years, current smoking habit, hypertension, diabetes mellitus, and use of calcium channel blockers or renin-angiotensin-aldosterone system blockers), multivariate analysis showed that BMI was an independent factor for increasing BPV during nighttime (SBP variability, p = 0.039; DBP variability, p = 0.034) (Figs. 1, 2).

Fig. 1 Comparison of changes in brachial artery flow-mediated dilatation during the 6-month follow-up between the pioglitazone and control groups. Click for larger image

Fig. 2 Multivariate regression analyses for diastolic blood pressure variability during nighttime. Click for larger image

Table 2 Comparison of average BP and standard deviation of BP between the non obese and obese groups during daytime and nighttime Click for larger image

Table 3 Comparison of average HR and standard deviation of HR between the non obese and obese groups during daytime and nighttime Click for larger image

Hypertension is an important cause of cardiovascular disease (CVD).1) Both SBP and DBP are significantly correlated with BMI.14) Because of the increasing prevalence of obesity and metabolic syndrome, and aging population worldwide, the global burden of hypertension is gradually rising. Therefore, the clinical management of hypertension is important for the prevention of CVD. Despite intensive efforts to prevent and treat hypertension, only less than one third of patients whose hypertension is assumed to be well-controlled by standard medication are protected from the risk of stroke, myocardial infarction, or heart failure.15) BPV is one of the reasons why hypertension cannot be successfully prevented or controlled.16) In several studies, BPV patterns have been used to evaluate the precise risk of the current and long-term complications.4) Asymptomatic (disease-free) overweight or obese adults with pre-diabetes (American Diabetes Association criteria: impaired fasting glucose and/or impaired glucose tolerance) may also have an increased risk of developing CVD.17) Pre-diabetes is associated with abnormal circadian BPV,18) and an exacerbated pro-inflammatory milieu in obese individuals is associated with pre-diabetes and pre-hypertension.19) Twenty-four-hour ABPM has been used to predict target-organ disease and clinical outcome in patients with hypertension.20) More recently, elevations in nighttime BP have been shown to precede diabetic nephropathy in hypertensive patients with Type 2 diabetes melliuts.21) Our study showed that obesity (BMI ≥ 25) increases both SBP and DBP variability, especially during the night (Figs. 1, 2). The mechanism underlying this finding is not clear, but we assumed that autonomic dysfunction and systemic inflammation played a role in this variability. The sympathoadrenal system is widely assumed to play a major role in the pathophysiology of obesity because of the regulation of energy expenditure.22) Our study suggested that obesity may disturb the autonomic nervous regulation, especially during the night (Table. 3). A dysregulated pro-inflammatory: anti-inflammatory balance and increased serum high-sensitivity C-reactive protein (hs-CRP) are associated with increased CVD.23) Using hs-CRP, a marker of inflammation, we showed that obesity increases the severity of systemic inflammation. However, the difference was not statistically significant (1.1 mg/L in the non-obese group vs. 2.6 mg/L in the obese group) (Table 1). Our study has several limitations. Several parameters can be used as an index of short-term BPV. We used SD as an index of BPV. However, because SD is defined as simple dispersion of values around the mean and does not reflect the order in which BP is acquired, SD is not a perfect index of BPV.24, 25) Therefore, average real variability (ARV) was proposed as an alternative index of BPV. This index is based on the total variability concept of real analysis in mathematics and is sensitive to the order of each BP measurement.24, 25) However, because of lack of ARV data in KorABP, we used SD as an index of BPV. The other limitation of this study is that it is a retrospective observational study. Therefore, further evaluation is necessary to study the effect of weight reduction on improvement in BPV. In addition, we did not define the mechanism underlying the relationship between the autonomic system and increased nighttime BPV in obesity. In summary, obesity increases BPV during the night. It is important to control the nighttime BPV in obese patients, and more studies are required to obtain a better understanding of the mechanism underlying this phenomenon.