Balance between angiotensin converting enzyme and angiotensin converting enzyme 2 in patients with chronic heart failure. (September 2015)

• Record Type: Journal Article
• Authors: Wang, Jiang; Li, Nan; Gao, Feng; Song, Rong; Zhu, Shanjun; Geng, Zhaohua
• Is Part Of: Journal of the renin-angiotensin-aldosterone system. Volume 16:Number 3(2015:Sep.)
• Page Start: 553
• Page End: 558
• Publication Date: 2015-09
• Subjects: Chronic heart failure -- angiotensin converting enzyme -- angiotensin converting enzyme 2 -- renin–angiotensin–aldosterone system -- angiotensin II; Renin-angiotensin system -- Periodicals; 616.132
• DOI: 10.1177/1470320315576257
• Languages: English
• ISSNs: 1470-3203

Abstract

Aim: It has been reported that angiotensin converting enzyme 2 (ACE2) is an endogenous counter-regulator of the renin–angiotensin–aldosterone system. However, angiotensin converting enzyme (ACE)/ACE2 balance in the development of human heart failure is not well established. Methods: Here we evaluated the expression of ACE and ACE2 at the mRNA and protein levels in the myocardium of 78 patients with mild or moderate to severe heart failure and in 13 cases with normal myocardium. Results: In the myocardium of patients with dilated or ischemic cardiomyopathy, ACE and ACE2 expression at the mRNA and protein levels was significantly increased compared with those in normal myocardium ( P <0.01, P <0.01, respectively). The ratios of ACE/ACE2 mRNA and ACE/ACE2 were lower in the myocardium of patients with mild heart failure than those in normal myocardium but higher than those in patients with moderate to severe heart failure. Conclusions: ACE and ACE2 expression at the mRNA and protein levels are significantly increased in the myocardium of patients with heart failure. The compensatory mechanism of patients with mild heart may cause the decreased ACE/ACE2 ratio. However, increased ACE/ACE2 ratios may induce angiotensin II over-activation and accelerate cardiac remodeling in patients with moderate to severe heart failure.