Abstract 14004: Role of Inflammation in the Pathogenesis of Hypertension a 9-year Repeated-measures Data Analysis in a Prospective Cohort Study

Abstract

Introduction: The underlying mechanisms of the association of inflammation with the development of hypertension has not been clarified. Hypothesis: Inflammation affect the development of hypertension via vascular and/or renal abnormalities. Methods: The association of inflammation with vascular and/or renal abnormalities, and the association of such abnormalities with elevation of the blood pressure were examined by analyzing longitudinal repeated-measures data using a linear mixed model (LMM) approach in a 9-year prospective observational study. 3908 middle-aged Japanese employees of the construction company (aged 41 ± 9 years old) without hypertension at the study baseline. The blood pressure, brachial-ankle pulse wave velocity (baPWV), radial augmentation index (rAI), estimated glomerular filtration rate (eGFR; based on the serum creatinine) and serum C-reactive protein (CRP) levels were measured annually in the subjects from year 2007 to year 2015. Results: During this study period, 520 subjects (13%) developed hypertension. LMM analysis of the obtained repeated-measures data after adjustments for covariates revealed the following: 1) At each annual measurement, higher annual values of the log-transformed CRP were associated with a higher annual increase of the baPWV (beta = 62.647 ± 26.017, p < 0.001), but not the annual increase of the rAI or annual decrease of the eGFR; 2) higher annual values of the baPWV were associated with a higher annual elevation of the blood pressure (beta = 0.032 ± 0.001, p < 0.001). Conclusions: In middle-aged Japanese subjects without hypertension at the study baseline, the presence of inflammation, as reflected by serum CRP levels, appears to be associated with the longitudinal increase of the arterial stiffness, but not with abnormal progression of the central hemodynamics or decline of the glomerular filtration rate. In turn, this longitudinal increase in the arterial stiffness appears to be associated with the longitudinal elevation of the blood pressure to hypertensive range. Thus, inflammation may play a role in the pathogenesis of hypertension via the accelerated progression of arterial stiffness.