Key result
Cardiomyocyte chymase mechanisms may explain residual CV risk despite conventional RAS blockade.
Chymase-mediated mechanisms may account for residual cardiovascular risk in patients treated with conventional renin-angiotensin system blockade.
Chymase pathways merit exploration to address residual CV risk after RAS blockade; leaves open whether targeted inhibition improves outcomes.
Chymase is the most efficient Ang II (angiotensin II)-forming enzyme in the human body and has been implicated in a wide variety of human diseases that also implicate its many other protease actions. Largely thought to be the product of mast cells, the identification of other cellular sources including cardiac fibroblasts and vascular endothelial cells demonstrates a more widely dispersed production and distribution system in various tissues. Furthermore, newly emerging evidence for its intracellular presence in cardiomyocytes and smooth muscle cells opens an entirely new compartment of chymase-mediated actions that were previously thought to be limited to the extracellular space. This review illustrates how these multiple chymase-mediated mechanisms of action can explain the residual risk in clinical trials of cardiovascular disease using conventional renin-angiotensin system blockade.
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Dell’Italia et al. (2018) conducted a review in Cardiovascular disease. Chymase was evaluated. Chymase-mediated mechanisms, including its intracellular presence in cardiomyocytes, may explain the residual risk in cardiovascular disease despite conventional renin-angiotensin system blockade.
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