Abstract
We aimed to explore the influence that the circadian blood pressure (BP) profile could exert on the correlation between some inflammatory markers and hypertension-mediated organ damage (HMOD). This was a cross-sectional study that included patients with primary arterial hypertension older than 18 years old. We included some parameters of 24 h ambulatory blood pressure monitoring collection and several inflammatory markers, as follows: platelet count (PTC), erythrocyte sedimentation rate (ESR), ultrasensitive C-reactive-protein, ferritin, fibrinogen, and uric acid. Myocardial hypertrophy, albuminuria, carotid intima-media thicknesses and ankle brachial index were assessed as HMOD presentations. Individuals were divided into two groups: patients with and without HMOD. We included 522 patients (47% women, mean age of 54 years). Multivariate logistic regression analysis showed that male patients older than 50 years old with uric acid levels above 7 mg/dL, ESR higher than 20 mm/h, fibrinogen greater than 320 mg/dL and PTC lower than 275 × 103/µL were associated with HMOD (p < 0.05). The circadian BP profile (dipper versus non-dipper pattern) did reach neither statistical significance nor influence the odds ratio of those inflammatory markers for HMOD. We found that differences in some inflammatory markers between patients with and without HMOD were not explained by a different circadian BP profile.
Highlights
Elevated blood pressure (BP) is a major global contributor to cardiovascular (CV) risk and premature death
The presence of hypertension-mediated organ damage (HMOD) as a surrogate marker of inadequate BP control is related to an increased CV risk and mortality, and its prevention should be a therapeutic target
Several studies revealed that the inflammatory status could play a role in abnormalities of BP circadian rhythm, while other studies suggest that BP circadian profile could be related to HMOD [5–7]
Summary
Elevated blood pressure (BP) is a major global contributor to cardiovascular (CV) risk and premature death. Both office and out-of-office BP have an independent relationship with the onset of several CV events [1,2]. The presence of hypertension-mediated organ damage (HMOD) as a surrogate marker of inadequate BP control is related to an increased CV risk and mortality, and its prevention should be a therapeutic target. Recent evidence suggests that inflammation, immunity and arterial hypertension (AHT) may be related to each other, triggering an unfavorable inflammatory status that might increase BP and lead to HMOD and CV disease. Several studies revealed that the inflammatory status could play a role in abnormalities of BP circadian rhythm, while other studies suggest that BP circadian profile could be related to HMOD [5–7]
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