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  • Title: Increased angiotensin converting enzyme activity in left ventricular aneurysm of patients after myocardial infarction.
    Author: Hokimoto S, Yasue H, Fujimoto K, Sakata R, Miyamoto E.
    Journal: Cardiovasc Res; 1995 May; 29(5):664-9. PubMed ID: 7606755.
    Abstract:
    OBJECTIVE: Angiotensin converting enzyme (ACE) inhibitors have been shown to improve left ventricular dysfunction and survival in patients with chronic myocardial infarction. The aim of this study was to examine the ACE activity in infarcted tissues in such patients in comparison with non-diseased tissues from control subjects obtained at necropsy. METHODS: ACE activity was measured in the left ventricles and right atrial auricles of patients (n = 9) with chronic myocardial infarction obtained at left ventricular aneurysmectomy, and in the hearts of control subjects at necropsy (n = 10). RESULTS: In non-diseased hearts, the ACE activity was highest in right atria and auricles [2.4(SEM 0.2), 2.2(0.3) nmol.mg-1 protein.min-1, NS, respectively], followed by left atria [1.7(0.2)], left auricles [1.5(0.1)], right ventricles [1.0(0.2)], and left ventricles [0.5(0.1)]. The ACE activity was significantly increased in aneurysmal tissues of patients with chronic myocardial infarction relative to left ventricles of control subjects [4.2(0.4) v 0.5(0.1) nmol.mg-1 protein.min-1, P < 0.01]. There was, however, no difference in the ACE activity of right atrial auricles between patients with chronic myocardial infarction and control subjects [2.8(0.5) v 2.2(0.3), NS]. In patients with chronic myocardial infarction, the ACE activity was higher in left ventricles than in right auricles (P < 0.01). The ACE activities in the infarcted and control ventricles were negatively correlated with the membrane protein content (r = -0.77, P < 0.01). CONCLUSIONS: In non-diseased human hearts, the ACE activity is higher in atria than in ventricles and higher in the right than in the left ventricle. Furthermore, the ACE activity in aneurysmal left ventricular tissue after myocardial infarction is higher than in non-diseased left ventricular myocardium. These results suggest that the local ACE in the human heart may play an important role in the pathophysiological state after myocardial infarction.
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