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Association of nocturnal blood pressure patterns with inflammation and central and peripheral estimates of vascular health in rheumatoid arthritis.
Journal of Human Hypertension 2018 April
Predictors of adverse cardiovascular outcomes include elevated nighttime systolic blood pressure (SBP) and a non-dipping pattern. We investigated whether these factors correlate with systemic inflammation, cardiovascular risk, and markers of central and peripheral vascular damage in rheumatoid arthritis (RA), a disease characterized by excess cardiovascular risk. Twenty-four-hour ambulatory blood pressure monitoring was applied in patients and controls. Vascular assessments included measurement of arterial stiffness (pulse wave velocity) and carotid atherosclerosis (carotid intima-media thickness). Peripheral vascular resistance was estimated from impedance cardiography. Cardiovascular risk was calculated from the Framingham Heart Study. RA patients exhibited a higher prevalence of non-dipping pattern, elevated nighttime SBP and blunted dipping, compared to controls without cardiovascular comorbidities. Among RA patients, dipping levels correlated with arterial stiffness, and nighttime SBP with all vascular markers and cardiovascular risk. After adjustment for inflammation, the above associations with vascular measures were no longer significant. Plain categorization to dippers and non-dippers did not reveal any differences regarding inflammation, vascular measurements, and cardiovascular risk. However, the combination of a non-dipping profile with high nighttime SBP was accompanied by significantly higher levels of arterial stiffness and cardiovascular risk, compared to non-dippers with normal nighttime SBP; these parameters were similar between the latter group and dippers. Inflammation appears to mediate the observed associations of nighttime SBP and dipping levels with markers of subclinical vascular damage in RA patients. In these patients, the combination of a non-dipping profile with elevated nighttime SBP is accompanied by prominent subclinical vascular impairment and confers the highest cardiovascular risk.
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