INCREASED ANGIOTENSIN-CONVERTING ENZYME-ACTIVITY IN LEFT-VENTRICULAR ANEURYSM OF PATIENTS AFTER MYOCARDIAL-INFARCTION

Objective: Angiotensin converting enzyme (ACE) inhibitors have been sh own to improve left ventricular a dysfunction and survival in patients with chronic myocardial infarction. The aim of this study was to exam ine the ACE activity in infarcted tissues in such patients in comparis on with non-diseased tissues from control subjects obtained at necrops y. Methods: ACE activity was measured in the left ventricles and right atrial auricles of patients (n = 9) with chronic myocardial infarctio n obtained at left ventricular aneurysmectomy, and in the hearts of co ntrol 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], followe d 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 sign ificantly increased in aneurysmal tissues of patients with chronic myo cardial infarction relative to left ventricles of control subjects [4. 2(0.4) v 0.5(0.1) nmol . mg(-1 v protein . min?(-1), P < 0.01]. There was, however, no difference in the ACE activity of right atrial auricl es between patients with chronic myocardial infarction and control sub jects [2.8(0.5) v 2.2(0.3), NS]. In patients with chronic myocardial i nfarction, the ACE activity was higher in left ventricles than in righ t auricles (P < 0.01). The ACE activities in the infarcted and control ventricles were negatively correlated with the membrane protein conte nt (r=-0.77, P < 0.001). Conclusions: In nondiseased 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 ane urysmal left ventricular tissue after myocardial infarction is higher than in non-diseased left ventricular myocardium. These results sugges t that the local ACE in the human heart may play an important role in the pathophysiological state after myocardial infarction.