Abstract

Objective The objective of this study was to compare the level of serum high-sensitivity C-reactive protein (hs-CRP) in hypertensive and normotensive individuals. Background Hs-CRP production is part of the nonspecific acute-phase response to most forms of inflammation, infection, and tissue damage. The association between hs-CRP and hypertension (HTN) could be related in part as follows: correlation between elevated CRP and arterial stiffness; association between CRP and metabolic syndrome, one of whose criteria is HTN and the possibility that CRP may directly contribute to reduced nitric oxide synthesis in endothelial cells, leading to increased vascular resistance. Patients and methods Our study comprised 80 patients, divided into two groups: the first group consisted of 55 patients with blood pressure more than140/90 mmHg recorded in at least two separate clinic-based measurements after ruling out secondary causes. The second group consisted of 25 normotensive individuals with a blood pressure of 100–120/60–80 mmHg as a control group. All individuals were subjected to full history taking, complete medical examination, 12-lead ECG, conventional echocardiography, routine laboratory investigations, and measurement of hs-CRP by CRP HS enzyme-linked immunosorbent assay. Results The study showed that the mean age of the studied group was 43.9 years; 58.8% were male individuals. Mean systolic and diastolic blood pressure was 146.4 and 91.5 mmHg, respectively. There were highly significant differences between the patient and control groups with regard to age, blood pressure, left ventricular mass, left ventricular mass index, lipid profile, and hs-CRP (higher in the patient group). The study showed also highly significant positive correlations between hs-CRP and age, blood pressure, left ventricular mass and left ventricular mass index. There was a significant positive correlation between hs-CRP and total cholesterol. Conclusion The levels of hs-CRP were elevated in hypertensive individuals, which suggests the possibility of an inflammatory pathogenesis in HTN.

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