Pulsatile stress, inflammation and change in arterial stiffness

Understanding factors that contribute to changes in arterial stiffness over time is important as this may lead to therapies that can abrogate cardiovascular risk. We compared the contribution of pulsatile stress and inflammation to changes in arterial stiffness in middle-aged men using a 1-year follow-up study design.

Arterial stiffness was derived from brachial-ankle pulse wave velocity (baPWV) in 107 men (mean age 53±6 yrs) on two separate occasions. The changes in outcome variables were calculated as the difference between the first and second examinations (mean interval 403±122 days). Pulsatile stress was calculated as the product of heart rate and brachial pulse pressure. C-reactive protein (CRP), white blood cell count (WBC) and fibrinogen were measured as inflammatory markers.

At baseline, baPWV was significantly correlated with pulsatile stress (r=0.37, p<0.01), WBC (r=0.19, p<0.05), HbA1c (r=0.39, p<0.01), HDL-C (r=.0.20, p<0.05), but not CRP (r= 0.06, p=0.56), or fibrinogen (r=0.12, p=0.21). The change in baPWV over 1 year was associated with the change in pulsatile stress (r=0.26, p<0.01) and HbA1c (r=0.19, p<0.05) over that same time period. Change in baPWV was not associated with the change in WBC (r=0.18, p=0.06) or CRP (r=0.05, p=0.62).

These results demonstrate that both pulsatile stress and inflammation may be associated with arterial stiffness at any given moment in time, but change in pulsatile stress is a better predictor of change in arterial stiffness over time.