C-reactive Protein among Community-Dwelling Hypertensives on Single-agent Antihypertensive Treatment

C-reactive protein is a predictor of adverse cardiovascular outcomes. The effect of antihypertensive therapy on C-reactive protein levels is largely unknown.

We undertook a cross-sectional study of CRP levels among participants with primary hypertension on single-agent anti-hypertensive therapy in the community-based biracial Genetic Epidemiology Network of Arteriopathy cohort. Linear regression models were used to assess the association of anti-hypertensive medication class with log-transformed C-reactive protein after adjustment for age, gender, ethnicity, body mass index, smoking, diabetes, HMG-Co-A reductase inhibitor use, achieved blood pressure control (<140/90 mmHg), serum creatinine and urine albumin-to-creatinine ratios.

There were 662 participants in the cohort taking single-agent therapy for hypertension. Median C-reactive protein 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 inhibitors (p<0.001). With multivariable adjustment, the group on renin-angiotensin-aldosterone system inhibitors had a 20% lower mean CRP on average than the group on diuretics (p=0.044), differences between other medication classes were not apparent. Heart rate had a strong association with C-reactive protein (p < 0.001).

Antihypertensive medication class may influence inflammation, particularly in patients on RAAS inhibitors.