Key result
Beta-blocker use was associated with lower mean serum CRP levels compared to non-use (2.13 vs 2.54 mg/L, P=0.002), a difference that persisted after multivariate adjustment.
Why the study?
Are different antihypertensive medication classes (such as beta-blockers, ACE inhibitors, or ARBs) associated with lower C-reactive protein levels compared to other classes or non-use in patients with treated hypertension?
Cross-Sectional (n=2,340)
Are different antihypertensive medication classes (such as beta-blockers, ACE inhibitors, or ARBs) associated with lower C-reactive protein levels compared to other classes or non-use in patients with treated hypertension?
Absolute Event Rate: 2.13% vs 2.54%
p-value: p=.002
Beta-blocker, ACE inhibitor, and ARB use are associated with lower CRP levels compared to diuretic use or non-use in hypertensive patients, suggesting potential anti-inflammatory differences among antihypertensive classes.
Beta-blocker use may link to lower CRP; hypothesis-generating and should not change practice without prospective trials.
BACKGROUND: The effects of different antihypertensive medication classes on C-reactive protein (CRP) levels are still not well characterized, and might be of relevance to treatment choices. METHODS: We studied the association between antihypertensive medication class and CRP levels among participants with treated hypertension in the Multi-Ethnic Study of Atherosclerosis. We performed a cross-sectional study of hypertensive participants free of clinical cardiovascular disease who were taking one or more of the following medication classes: beta-blockers, calcium channel blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors, or angiotensin II type I receptor blockers (ARB). RESULTS: Among 2340 participants taking one or more antihypertensive medications, the mean serum CRP level was lower among participants taking a beta-blocker than among those not taking a beta-blocker (2.13 v 2.54 mg/L, P = .002). This difference persisted after multivariate adjustment (P = .021). There were no other statistically significant differences in multivariate models. Among 1314 participants receiving monotherapy, the multivariate adjusted mean CRP level among participants taking a beta-blocker was lower (1.97 mg/L) than those taking a diuretic (2.72 mg/L, P < .001). In this monotherapy group, participants taking an ACE inhibitor or ARB also had a lower adjusted mean CRP (2.25 mg/L) than those taking a diuretic (P = .046). African-American race/ethnicity did not modify any of those relationships. CONCLUSIONS: The beta-blocker use was associated with lower CRP levels overall and among participants on monotherapy, whereas ACE inhibitor and ARB use was associated with lower CRP levels among participants on monotherapy. These findings warrant further evaluation in randomized trials.
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Palmas et al. (2007) conducted a cross-sectional in treated hypertension (n=2,340). Beta-blockers vs. Not taking a beta-blocker was evaluated on Mean serum C-reactive protein (CRP) level (p=.002). Beta-blocker use was associated with lower mean serum CRP levels compared to non-use (2.13 vs 2.54 mg/L, P=0.002), a difference that persisted after multivariate adjustment.
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