S. Hokimoto et al., INCREASED ANGIOTENSIN-CONVERTING ENZYME-ACTIVITY IN LEFT-VENTRICULAR ANEURYSM OF PATIENTS AFTER MYOCARDIAL-INFARCTION, Cardiovascular Research, 29(5), 1995, pp. 664-669
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.