Post-myocardial infarction hearts exhibited significantly higher cardiac total and chymase-dependent angiotensin-II-forming activities in both infarcted and non-infarcted myocardium versus controls.
Observational (n=17)
The aims of this study were to compare human cardiac angiotensin-II-forming activity (AIIFA) between the intact area of control autopsy hearts without cardiac disease (n = 10) and the infarcted or non-infarcted area of autopsy hearts with myocardial infarction (MI, n = 7) and to determine responsible angiotensin-II-forming enzymes. Cardiac total and chymase-dependent AIIFAs were significantly higher in the infarcted and non-infarcted myocardium than those in non-MI heart, while angiotensin-converting enzyme-dependent AIIFA increased only in the infarcted myocardium. The density of chymase antibody-positive mast cells in the non-infarcted area of MI heart correlated positively with total or chymase-dependent AIIFA. Augmented AIIFA was also detected in the left atrium of post-MI hearts. Our results indicated that cardiac angiotensin II formation could be activated in the infarcted as well as in non-infarcted myocardium of the post-MI human heart.
Ihara et al. (Sat,) conducted a observational in Myocardial infarction (n=17). Post-myocardial infarction state vs. Control autopsy hearts without cardiac disease was evaluated on Cardiac angiotensin-II-forming activity (AIIFA). Post-myocardial infarction hearts exhibited significantly higher cardiac total and chymase-dependent angiotensin-II-forming activities in both infarcted and non-infarcted myocardium versus controls.
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