Key result
High hs-CRP and low adiponectin levels additively increased aortic stiffness in essential hypertensive patients, with high hs-CRP increasing pulse wave velocity by 0.8 m/s (P<0.0001).
Why the study?
Do low-grade inflammation and hypoadiponectinaemia have an additive detrimental effect on aortic stiffness in untreated patients with essential hypertension?
Population
267 untreated patients with stage I-II essential hypertension
Comparison
High hs-C-reactive protein and/or… vs Low hs-C-reactive protein and/or high adiponectin
Design
Cross-sectional
Authors
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Hypothesis-generating in untreated hypertension; leaves open causality and need for prospective outcome trials.
Observational (n=267)
Do low-grade inflammation and hypoadiponectinaemia have an additive detrimental effect on aortic stiffness in untreated patients with essential hypertension?
p-value: p=<0.0001
In untreated essential hypertension, low-grade inflammation and low adiponectin levels independently and additively increase aortic stiffness.
Tsioufis et al. (2007) conducted an observational in stage I-II essential hypertension (n=267). High hs-C-reactive protein and hypoadiponectinaemia vs. Low hs-C-reactive protein and high adiponectin was evaluated on carotid-femoral pulse wave velocity (c-f PWV) (p=<0.0001). High hs-CRP and low adiponectin levels additively increased aortic stiffness in essential hypertensive patients, with high hs-CRP increasing pulse wave velocity by 0.8 m/s (P<0.0001).
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