Pleiotropic Effect of Metoprolol: Different From other B-blockers

The clinical practice guidelines recommend the early use of endovenous B-blockers in patients undergoing acute myocardial MI, taking for granted that all B-blockers have a similar class effect. 

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This experimental study might show metoprolol has other benefits that could make it superior to the rest of the B-blocker family. 

Using an animal model with 45-minute ongoing ischemia, metoprolol, atenolol, or propranolol was administered at min 35.

Ten minutes after administering one of the three B-blockers (blindly and in a randomized fashion) reperfusion was carried out, and after 24 hours, the pathological anatomy test was carried out. 

Out of all B blockers tested, only metoprolol reduced the damage caused by injury/reperfusion and MI size compared against atenolol and propranolol (p<0.001).


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Neutrophil infiltration resulted significantly lower only with metoprolol. This was observed both in the MI injury/reperfusion model and in inflammation models such as thioglycolate-induced peritonitis, or lipopolysaccharide-induced acute lung injury. 

Cell migration studies confirmed this particular ability of metoprolol to attenuate neutrophil dynamics. 

There was also a change in B1 receptor conformational changes when bound to metoprolol (different from the other two β-blockers).

Conclusion

Metoprolol can limit neutrophil action, reducing inflammation and resulting in a smaller infarct size, something not observed with propranolol or atenolol. 

This differential effect of metoprolol compared against other drugs of the same family might be due to a different conformation of B1 receptor when bound to it. If more studies confirm this effect, metoprolol might become the B-blocker of choice for treating patients undergoing acute myocardial infarction. 

ehaa733free

Original Title: Metoprolol exerts a non-class effect against ischaemia–reperfusion injury by abrogating exacerbated inflammation.

Reference: Agustín Clemente-Moragón et al. European Heart Journal (2020) 41, 4425–4440. doi:10.1093/eurheartj/ehaa733.


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