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Published on: January 28, 2020
Angiotensin receptor blockers are not associated with reduced inflammatory markers in the general population
Pedro Marques-Vidal1, Peter Vollenweider, Gérard Waeber
1Department of Internal Medicine, Internal Medicine, Lausanne University Hospital, Lausanne, Switzerland.
Insights
Angiotensin receptor blockers (ARBs) did not show a reduction in inflammatory markers like CRP or interleukins in a general population study. These findings suggest ARBs may not be effective for reducing inflammation in non-clinical settings.
Area of Science:
- Cardiovascular Research
- Inflammation Biology
- Pharmacology
Background:
- Randomized controlled trials suggest Angiotensin Receptor Blockers (ARBs) may possess anti-inflammatory properties.
- The association between ARBs and inflammatory markers in a general population remains underexplored.
Purpose of the Study:
- To investigate the association between Angiotensin Receptor Blockers (ARBs) and key inflammatory markers in a general population.
- To determine if ARBs reduce levels of C-reactive protein (CRP), interleukin-1β, interleukin-6, and tumor necrosis factor alpha (TNF-α).
Main Methods:
- Population-based prospective study in Lausanne, Switzerland, with baseline (2003-2006) and follow-up (2009-2012) data.
- Assessed inflammatory markers (CRP, IL-1β, IL-6, TNF-α) in 933 (baseline) and 1120 (follow-up) participants, with 424 and 572 on ARBs, respectively.
- Utilized multivariate adjustment and compared ARB users with non-users and users of other antihypertensives.
Main Results:
- No significant differences in baseline or follow-up inflammatory marker levels were observed between participants on ARBs and those not on ARBs.
- Multivariate analysis showed no association between ARB use and higher quartiles of CRP, IL-1β, IL-6, or TNF-α at baseline or follow-up.
- Comparison of long-term ARB users with users of other antihypertensives also revealed no significant effect on inflammatory markers.
Conclusions:
- Angiotensin Receptor Blockers (ARBs) are not associated with reduced levels of key inflammatory markers in the general population.
- The anti-inflammatory effects suggested by some trials may not translate to real-world, non-clinical settings.
- Further research may be needed to clarify the role of ARBs in inflammation.
Objective:
Angiotensin receptor blockers (ARBs) have been suggested to reduce inflammation in randomized controlled trials. We assessed the association between ARBs and inflammatory markers in a general population setting.
Methods:
This is a population-based prospective study conducted in Lausanne, Switzerland. Baseline data from 933 participants on antihypertensive drugs (424 on ARBs) was collected in 2003-2006. Follow-up data from 1120 participants (572 on ARBs) was collected in 2009-2012. C-reactive protein (CRP), interleukins 1β and 6 and tumor necrosis factor alpha (TNF-α) were assessed and categorized in quartiles.
Results:
At baseline, no differences were found between participants taking or not taking ARBs for all inflammatory markers studied, and this association persisted after multivariate adjustment: odds ratios (ORs) and (95% confidence interval) for being in the highest quartile of interleukin-1β, interleukin-6, TNF-α and CRP for participants on ARB compared to participants not on ARB were 1.23 (0.89-1.70), 1.26 (0.93-1.70), 1.14 (0.85-1.53) and 1.27 (0.96-1.69) respectively (P > 0.05). These findings were further replicated in the follow-up study: OR and (95% CI) of 1.10 (0.78-1.55), 0.87 (0.64-1.19), 0.83 (0.61-1.14) and 0.91 (0.68-1.22) for interleukin-1β, interleukin-6, TNF-α and CRP respectively (P > 0.05). Finally, no effect of ARBs was found when comparing participants who received ARBs throughout the 5.4-year follow-up with participants on other antihypertensive drugs: OR and (95% CI) of 0.93 (0.61-1.42), 0.80 (0.54-1.17), 0.86 (0.59-1.25) and 0.95 (0.67-1.35) for interleukin-1β, interleukin-6, TNF-α and CRP respectively (P > 0.05).
Conclusion:
ARBs are not associated with reduced levels of inflammatory markers in the general population.
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