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Circulation. 1996;94:1513-1518

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(Circulation. 1996;94:1513-1518.)
© 1996 American Heart Association, Inc.


Articles

Expression of Angiotensin-Converting Enzyme in Remaining Viable Myocytes of Human Ventricles After Myocardial Infarction

Seiji Hokimoto, MD; Hirofumi Yasue, MD; Kazuteru Fujimoto, MD; Hideyuki Yamamoto, MD; Koichi Nakao, MD; Koichi Kaikita, MD; Ryuzo Sakata, MD; Eishichi Miyamoto, MD

the Division of Cardiology (S.H., H.Yasue, K.F., K.N., K.K.) and the Department of Pharmacology (H.Yamamoto, E.M.), Kumamoto University School of Medicine, and the Division of Cardiovascular Surgery, Kumamoto Chuo Hospital (R.S.), Kumamoto, Japan.

Correspondence to Hirofumi Yasue, MD, Division of Cardiology, Kumamoto University School of Medicine, 1-1-1, Honjo, Kumamoto City, Kumamoto 860, Japan.

Background Local ACE in the heart may be important in the pathophysiological state after myocardial infarction (MI). It is unknown, however, whether ACE is expressed in myocytes of the human heart.

Methods and Results Using a newly generated polyclonal antibody to a synthetic peptide corresponding to part of the human endothelial ACE sequence, we examined the localization of ACE in left ventricles of patients (n=10) with MI obtained at left ventricular aneurysmectomy or autopsy and in the hearts of control subjects at autopsy (n=10). The avidin–biotinylated peroxidase complex method was used for the immunohistochemical staining for ACE. In the left ventricles, positively stained myocytes for ACE were found in 8 of the 10 patients with MI. ACE immunoreactivity was seen in the remaining viable myocytes located near the infarct scar of the aneurysmal left ventricle and in nonmyocytes such as fibroblasts, macrophages, vascular smooth muscle cells, and endothelial cells within the scarred tissue. On the other hand, no immunoreactivity for ACE was detected in the ventricular myocytes of all control hearts obtained at autopsy.

Conclusions We observe immunohistochemical staining for ACE in the left ventricular myocytes of the region adjacent to the infarct scar and in nonmyocytes. These results indicate that ACE is markedly increased on the edge of the infarct scar and suggest that local ACE may be important in the ventricular remodeling after MI.


Key Words: angiotensin • myocardial infarction • aneurysm • immunohistochemistry




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