Independent association between inflammatory markers (C-reactive protein, interleukin-6, and TNF-α) and essential hypertension

Abstract

High blood pressure (HBP) has been associated with elevated C-reactive protein (CRP), a marker of chronic mild inflammation. However, the association between HBP and other inflammatory markers, particularly interleukin 6 (IL-6) and tumour necrosis alpha (TNF-a), has not been evaluated in well-controlled studies. We examined the cross-sectional relationship between IL-6, TNF-a, and CRP and HBP in a random sample of 196 healthy subjects. All markers were measured in duplicate with high-sensitivity ELISA tests. Three blood pressure (BP) measurments were averaged for the analysis, and subjects with systolic BP X140 and/or diastolic BP X90 mmHg were considered hypertensive. Log binomial regression was used to estimate multivariate-adjusted prevalence ratios (PR) of HBP. Of the subjects, 40% (79) were hypertensive (mean age: 44 years; range 30-64). After adjustment for age, sex, body mass index, family history of HBP, and the level of the other inflammatory markers, subjects in the second (PR: 3.10, P ¼ 0.003), third (PR: 2.32; P ¼ 0.031), and fourth quartiles (PR: 2.30; P ¼ 0.036) of IL-6 were more than twice as likely to be hypertensive than those in the first quartile. Corresponding PR estimates for TNF-a levels were 1.41 (P ¼ 0.014) for the second; 1.59 (P ¼ 0.001) for the third; and 1.61 (P ¼ 0.025) for the fourth quartile. The CRP-HBP association was not statistically significant. Our results suggest that TNF-a and IL-6 could be independent risk factors for HBP in apparently healthy subjects. Nevertheless, the temporal relationship between elevated inflammation markers and HBP should be ascertained in prospective cohort studies.

Hypertension as an autoimmune and inflammatory disease

“…In a cross-sectional survey of 8347 apparently healthy Korean individuals, Sung et al 1 found that the prevalence of hypertension was 1.267-, 1.253-and 1.451 times higher in subjects from the second, third and fourth quartiles of the C-reactive protein (CRP) distribution, respectively, compared with subjects in the first quartile, even after the adjustment for many confounders (CRP level ranges for the first and fourth quartiles were 0.1-0.3 and 1.2-11 mg l − 1 , respectively). Similarly, Bautista et al 2 showed that patients in the third and fourth quartiles of the interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) distribution were more likely to have hypertension compared with patients in the first quartile. These and other studies 3 recruited apparently healthy individuals and assessed inflammatory markers along with a number of laboratory, clinical and demographic features described as independent predictors of elevated blood pressure.…”

Downregulation of Peroxisome Proliferator‐activated Receptor‐γ Expression in Hypertensive Atrial Fibrillation

“…Pathophysiologic studies have shown that both are related to inflammation. 1,2 Investigations in this field and development of new effective treatment strategies are of great interest.…”

“…Many inflammatory markers, such as Creactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and white blood cell count were proved in association with hypertension and its complications. 1,2 More recently, increasing data show that inflammation may be related to AF. 3,4 Bruins et al 3 has reported that frequency of AF was increased after cardiac surgery, and changes in levels of CRP, complement-CRP complexes after surgery, and cardiopulmonary bypass (CPB) were responsible for the occurrence of postoperative AF.…”

Fatality of acute coronary events in relation to hypertension and low-grade inflammation: a population-based cohort study

“…[7][8][9][10] Raised concentrations of inflammatory markers have been associated with increased incidences of cardiovascular diseases. [10][11][12][13][14][15][16][17] Furthermore, men who have been exposed to elevated levels of inflammatory proteins many years earlier have higher fatality in future coronary events, with a higher proportion of CHD deaths and less non-fatal myocardial infarction (MI).…”