Increase of chymase-dependent angiotensin II-forming activity in circulating mononuclear leukocytes after acute myocardial infarction chymase activity after acute myocardial infarction.

A previous clinical study revealed elevation of chymase- and cathepsin G-dependent angiotensin II-forming activity (AIIFA) in the myocardium after acute myocardial infarction (AMI). This study examined the time course of chymase- and cathepsin G-dependent AIIFA in circulating mononuclear leukocytes (CML) after AMI. Consecutive patients with AMI were recruited. Chymase- and cathepsin G-dependent AIIFA in CML were assayed using a modified angiotensin I substrate with Nma/Dnp fluorescence quenching. The changes of CML AIIFA were monitored over time in the patients. Fifteen consecutive AMI patients admitted to our hospital were recruited. At 1 day after the admission, CML chymase- and cathepsin G-dependent AIIFA were 2.9- and 1.7-fold higher than at discharge, respectively. The ratio of chymase-dependent AIIFA to total AIIFA was significantly increased. AIIFA gradually decreased over time after the admission. The peak value of chymase- and cathepsin G-dependent AIIFA was significantly correlated with the maximum levels of aspartate aminotransferase (r = 0.53, 0.64), lactate dehydrogenase (r = 0.57, 0.62), and creatine kinase (r = 0.60, 0.65). This is the first evidence that chymase- and cathepsin G-dependent AIIFA is elevated in CML after AMI. Our data suggested that chymase-dependent AIIFA is increased in CML as well as in the myocardium after AMI, and that the level of chymase-dependent AIIFA might reflect the severity of infarction.