Key result
Obese premenopausal women presented significantly higher office-based systolic blood pressure (124.7 vs 108.6 mm Hg) and 24-hour ambulatory systolic blood pressure compared to lean women.
Why the study?
Obesity is frequently an independent risk factor for high blood pressure, but the comparisons of office and 24 h blood pressure patterns and their correlations with insulin resistance and subclinical inflammation markers between lean and obese women required study.
Does obesity affect blood pressure, its circadian pattern, and correlate with insulin resistance and subclinical inflammation in premenopausal women?
Cross-Sectional (n=195)
No
Does obesity affect blood pressure, its circadian pattern, and correlate with insulin resistance and subclinical inflammation in premenopausal women?
Absolute Event Rate: 124.7% vs 108.6%
p-value: p=<0.001
Obese premenopausal women have higher blood pressure and more non-dipping patterns than lean women, with anthropometrics and insulin resistance being key determinants of blood pressure in obesity.
May support closer BP monitoring in obese premenopausal women; hypothesis-generating for anthropometric and insulin resistance determinants.
Background. Obesity is frequently referred to as an independent risk factor for high blood pressure and hypertension is very prevalent among obese people. The aims of this study were: to compare office-based and 24 h blood pressure (BP) and its circadian pattern between lean and obese women; to study correlations between BP, insulin resistance (IR) and markers of subclinical inflammation/early atherosclerosis. Material and methods. Eighty-eight lean and 107 otherwise healthy obese women were characterized for anthropometrics, BP (office-based determinations and 24 h ABPM) and for glucose, insulin, triglycerides, inteleukin 6 (IL-6), tumor necrosis factor alpha (TNF-a), high-sensitivity C reactive protein (hs-CRP), retinol-binding protein 4 (RBP-4), leptin, adiponectin, resistin, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1 (ICAM-1), and vascular-cellular adhesion molecule 1 (VCAM-1). Insulin resistance was determined by homeostasis model assessment of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), and McAuley indexes (also Matsuda in obese). Results. Obese group presented higher office-based systolic/diastolic BP, systolic ambulatory blood pressure monitoring (ABPM), and more non-dippers. HOMA-IR and body fat was correlated to systolic (r2 = 0.176) and glucose to diastolic (p = 0.008; r = 0.256) ABPM. Age, QUICKI, and TNF-a was correlated with dipping (r2 = 0.172); adiponectin, age, BMI, and glucose to systolic (r2 = 0.226) and diastolic (r2 = 0.215) office-based BP. Concerning lean women, MCP-1 was associated with diastolic ABPM (p = 0.013; r = 0.267). Systolic office-based BP was associated with waist-to-hip ratio (p = 0.01; r = 0.273); this and RBP-4 was correlated with office-based diastolic BP (r2 = 0.12). Conclusion. Although relatively healthy, obese women present higher BP than lean. Anthropometrics, IR, and fasting glucose all influence BP in obesity; additionally, IR is involved in non-dipping. No strong correlation exists between BP/dipping and subclinical inflammation in either group of women.
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Silva‐Nunes et al. (2020) conducted a cross-sectional in Obesity and Blood Pressure (n=195). Obesity vs. Lean (normal weight) was evaluated on Office systolic blood pressure (mm Hg) (p=<0.001). Obese premenopausal women presented significantly higher office-based systolic blood pressure (124.7 vs 108.6 mm Hg) and 24-hour ambulatory systolic blood pressure compared to lean women.
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