Do beta blockers inhibit the anti-inflammatory effect of statins?

A new study in the American Journal of Cardiology raises the possibility that beta blockers might blunt the CRP-reducing effects of statins. Franz Messerli provided a comment on this provocative study to CardioBrief:

“Beta-blockers as a class have been under fire recently.  This is perhaps not surprising given that they have been inappropriately touted as being cardioprotective for many unsubstantiated indications such as hypertension, prevention of atrial fibrillation, perioperative patients, etc.  We also have become more aware of their metabolic adverse effects such as increasing insulin resistance, triglycerides, weight gain, fatigue and sexual dysfunction.  The study of Quinaglia e Silva documents that beta-blockade attenuates the statin induced fall in CRP.  The authors enthusiastically interpret this as meaning that the anti-inflammatory action of statins may be attenuated by beta-blockers.  Before we fully subscribe to this hypothesis we should remember that CRP is merely a marker of inflammation which, again as a surrogate endpoint, correlates to some extent with the real endpoint i.e., major cardiovascular events (MACE).  Beta-blockers, time and again, have been clearly beneficial in the post MI patient to reduce MACE.  Thus, when looking at the outcome data it doesn’t seem to matter much that CRP is not reduced when a statin is given.  In other words, in the post MI patient the benefits of beta-blockade seem to outweigh the mitigated decrease or the lack of decrease with CRP.  Could this be yet another situation in which markers and surrogate endpoint do not parallel major cardiovascular events?”

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