ISSN 1671-5411 CN 11-5329/R
Hao XUE, Jun-Juan LI, Jian-Li WANG, Shuo-Hua CHEN, Jing-Sheng GAO, Yun-Dai CHEN, Shou-Ling WU. Changes in pulse pressure heart rate, hs-CRP, and arterial stiffness progression in the Chinese general population: a cohort study involving 3978 employees of the Kailuan Company. J Geriatr Cardiol 2019; 16(9): 710-716. doi: 10.11909/j.issn.1671-5411.2019.09.010
Citation: Hao XUE, Jun-Juan LI, Jian-Li WANG, Shuo-Hua CHEN, Jing-Sheng GAO, Yun-Dai CHEN, Shou-Ling WU. Changes in pulse pressure heart rate, hs-CRP, and arterial stiffness progression in the Chinese general population: a cohort study involving 3978 employees of the Kailuan Company. J Geriatr Cardiol 2019; 16(9): 710-716. doi: 10.11909/j.issn.1671-5411.2019.09.010

Changes in pulse pressure heart rate, hs-CRP, and arterial stiffness progression in the Chinese general population: a cohort study involving 3978 employees of the Kailuan Company

doi: 10.11909/j.issn.1671-5411.2019.09.010
Funds:

This work was supported by Na?tional Natural Science Foundation of China (No.81570383) and the Capital Public Health Cultivation Project (No. Z141100002114029).

  • Received Date: 2019-02-15
  • Rev Recd Date: 2019-04-30
  • Publish Date: 2019-09-28
  • Background Pulse wave velocity (PWV) is a marker of arterial stiffness, which represents sub-clinical atherosclerosis. Pulsatile stress and high-sensitivity C-reactive protein (hs-CRP) are associated with arteriosclerosis. However, there is no prospective data confirming whether changes in pulsatile stress and inflammatory markers affect the progression of arterial stiffness. The aim of this study was to investigate the relationships over time between the effects of changes in pulsatile stress and hs-CRP, and arterial stiffness progression during a 2-year follow-up. Methods We performed a longitudinal study involving 3978 participants. All participants underwent a physical examination in 2010–2011 and 2012–2013, during which we measured participants’ hs-CRP levels, brachial–ankle pulse wave velocity (baPWV), and pulsatile stress. Results Baseline hs-CRP was correlated with baPWV (r = 0.18, P = 0.000); however the correlation was weaker than that with systolic blood pressure (r = 0.65), pulsatile stress (r = 0.57), and rate-pressure product (r = 0.58). Multiple linear regression analysis demonstrated that changes in pulsatile stress, mean arterial pressure, and low-density lipoprotein-C (LDL-C) were positively correlated with changes in baPWV, with correlation coefficients of 0.27, 0.25, and 0.07, respectively, but not with changes in hs-CRP. Moreover, each 100-aU increase in pulsatile stress, 1 mmHg increase in mean blood pressure, and 1 mmol/L increase in LDL-C was associated with a 3 cm/s, 4.78 cm/s, and 17.37 cm/s increase in baPWV, respectively. Conclusions Pulsatile stress increases are associated with arterial stiffness progression, but that changes in hs-CRP had no effect on arterial stiffness progression. Hs-CRP may simply be a marker of inflammation in arterial stiffness and has no association with arterial stiffness progression.
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