Abstract
Inflammatory markers are susceptible to changes over time. Thus, we observed changes in inflammatory markers correlating with age-related increases in blood pressure (BP) through a prospective study. The aim of this study was to investigate changes in inflammatory markers that correlate with age-related increases in BP. The study included 1,500 nondiabetic and normotensive healthy subjects at baseline. Of these, 121 individuals who developed hypertension (defined as systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg) after 2 years formed the hypertension group. For each incident hypertension case, 2 age- and sex-matched control subjects were selected among those who did not develop hypertension (control group, n = 242). After baseline adjustment, the hypertension group exhibited greater increases in body mass index (BMI), systolic and diastolic BP, triglyceride, total cholesterol, glucose, Lp-PLA2 activity, and urinary 8-epi-prostaglandin F2α (8-epi-PGF2α) levels compared to the control group. In the hypertension group, changes in (Δ) systolic BP correlated positively with Δ Lp-PLA2 activity, which correlated positively with Δ low-density lipoprotein (LDL−) cholesterol and Δ urinary 8-epi-PGF2α levels. Moreover, multiple linear regression revealed baseline systolic BP and Δ Lp-PLA2 activity to be independent predictors of Δ systolic BP in the hypertension group. Our results suggest that age-related increases in systolic BP may correlate strongly with elevated Lp-PLA2 activity and that Lp-PLA2 can be considered a biomarker for systolic BP elevation.
Highlights
Evidence has emerged to support that inflammation may contribute to hypertension development [1, 2]
After 2 years, the hypertension group showed significant increases in body mass index (BMI), systolic and diastolic blood pressure (BP), total and Lowdensity lipoprotein (LDL)-cholesterol levels, glucose levels, and Homeostatic model assessment (HOMA)-insulin resistance (IR) index; these increases were significantly greater than the increases observed in the controls after adjusting for baseline values
At the 2-year follow-up, higher systolic and diastolic BP, and IL-1β levels were found in the hypertension group compared to the controls after adjusting for follow-up BMI (Table 1)
Summary
Evidence has emerged to support that inflammation may contribute to hypertension development [1, 2]. Systemic inflammation is associated with the progression of endothelial dysfunction [3], resulting in changes in the structure and function of the endothelium that are often obvious during the early stage of hypertension development [4, 5]. According to prospective studies investigating inflammatory markers, high-sensitivity C-reactive protein (hs-CRP) is related to the risk of developing hypertension [8]. In a nested case-control study, interleukin (IL)-6 was less highly related to the risk of developing hypertension than hs-CRP [9]. The mechanisms by which inflammatory markers other than hs-CRP and IL-6 are related to hypertension risk remain unclear.
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