C-reactive protein among community-dwelling hypertensives on single-agent antihypertensive treatment

C-reactive protein (CRP) is a predictor of adverse cardiovascular outcomes. The effect of antihypertensive therapy on CRP levels is largely unknown. We undertook a cross-sectional study of CRP levels among participants with primary hypertension on single-agent antihypertensive therapy in the community-based biracial Genetic Epidemiology Network of Arteriopathy cohort. Linear regression models were used to assess the association of antihypertensive medication class with log-transformed CRP after adjustment for age, gender, ethnicity, body mass index, smoking, diabetes, hydroxymethylglutaryl CoA reductase inhibitor use, achieved blood pressure control (<140/90 mm Hg), serum creatinine and urine albumin-to-creatinine ratios. There were 662 participants in the cohort taking single-agent therapy for hypertension. Median CRP levels differed across participants: 0.40 mg/dL for those on diuretics, 0.34 mg/dL on calcium-channel blockers, 0.25 mg/dL on beta-blockers and 0.27 mg/dL on renin-angiotensin-aldosterone system (RAAS) inhibitors (P < .001). With multivariable adjustment, the group on RAAS inhibitors had a 20% lower mean CRP on average than the group on diuretics (P = .044), differences between other medication classes were not apparent. Heart rate had a strong association with CRP (P < .001). Antihypertensive medication class may influence inflammation, particularly in patients on RAAS inhibitors.