Abstract

Elevated short-term (24 hour) blood pressure variability (BPV) is associated with subclinical target organ damage and cardiovascular disease (CVD) among middle-aged/older (MA/O) adults with hypertension and obesity. Circulating total cholesterol (TC), low-density cholesterol (LDL-C) and triglycerides (TGs) increase with human obesity and are independent risk factors for CVD. In addition, BPV is increased in mouse models of hyperlipidemia and is normalized with statins. However, whether higher circulating lipoproteins independently contribute to greater short-term BPV among adults with obesity remains unclear. We hypothesized that higher LDL-C, TGs and lower high-density lipoprotein (HDL-C) would be associated with greater short-term BPV among individuals with obesity. Fasting plasma lipids and 24 hour ambulatory BP monitoring were assessed in fifty-six MA/O adults with obesity defined as body mass index (BMI) ≥ 30 kg/m 2 (56% F; age 54±7 yrs; BMI, 38.2±5.6 kg/m 2 ) and at least one other CVD risk factor. There was a significant relation between 24 hour systolic BPV and TC (r=0.30, P=0.03), TGs (r=0.34, P=0.01) and LDL-C (r=0.25, P=0.059), but not HDL-C (r=-0.07, P=0.61). Interestingly, these findings remained significant after adjusting for age, sex, BMI and 24 hour systolic BP (TC: r=0.34, P=0.01; TGs: r=0.39, P<0.01; LDL-C: r=0.31, P=0.03) but HDL-C remained non-significant (r=-0.16, P=0.27). In contrast, other cardiometabolic risk factors such as fasting glucose, insulin, c-reactive protein concentrations, carotid-femoral pulse wave velocity and HOMA-IR were not associated with 24 hour systolic BPV. In a multiple linear regression model that included age, sex, BMI, 24 hour systolic BP, TGs and LDL-C, only fasting TGs (β=0.02 ± 0.01, P=0.02) were a significant correlate of 24 hour systolic BPV (Model R 2 =0.24, P=0.03). Results were the same if TC was substituted for LDL-C in the model. In conclusion, higher plasma TC, LDL-C and TGs are associated with greater 24 hour BPV among MA/O adults with obesity with only TGs being independently associated with BPV. These data suggest that greater variability in BP among MA/O adults with obesity is mediated in part through circulating TGs suggesting that TGs may be a therapeutic target to modify short-term BPV.

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