Background: Blood pressure (BP) variability has been reported to be associated with hypertensive target organ damage and cardiovascular events. However, the exact mechanism linking BP variability and organ damage is uncertain. This study was designed to investigate the association between BP variability and inflammatory marker in hypertensive patients.
Methods and results: Fifty-two hypertensive patients (28 men, 55.9+/-1.5 years) completed 24-h ambulatory BP monitoring. Inflammatory markers were evaluated by measuring plasma levels of interleukin (IL)-6, tumor necrosis factor (TNF)-alpha by enzyme-linked immunosorbent assay and high sensitive C-reactive protein (hs-CRP) by particle-enhanced light-scattering immunoassay. BP variability was obtained by calculating within-subject standard deviation (SD) and coefficient of variation of BP. Subjects were grouped into tertiles according to IL-6, TNF-alpha, and hs-CRP levels. A significant association between ambulatory BP and TNF-alpha level was identified (P for trend =0.011). In contrast, no association was observed between BP and IL-6 level; however, BP variability index was linked to IL-6 level (P for trend =0.046). The association between inflammatory marker and pattern of diurnal variation was investigated. The hs-CRP concentration was significantly higher in the riser group compared with the dipper group. However, IL-6 and TNF-alpha levels did not differ among the different diurnal variation groups. Correlation analysis showed varying associations between IL-6 and TNF-alpha. TNF-alpha level correlated with the BP index; however, IL-6 level correlated with the BP variability index. Multiple linear regression models revealed that the SD of daytime systolic BP (beta=0.065, p=0.001) and age (beta=0.024, p=0.016) were all positively and significantly related to IL-6. In contrast, only daytime diastolic BP (beta=0.029, p=0.002) was independently related to TNF-alpha.
Conclusion: Inflammatory markers are associated with BP variability in hypertensive patients. This finding implies that inflammation may be a mediator for the link between BP variability and target organ damage.