Abstract
Objective: Elucidation of the role of angiotensin-converting enzyme (ACE) 2 (ACE2)/angiotensin (Ang)-(1-7)/Mas receptor axis in heart failure is necessary. No previous study has reported serial changes in ACE2 and Ang-(1-7) concentrations after optimal therapy (OT) in acute heart failure (AHF) patients. We aimed to investigate serial changes in serum ACE2 and Ang-(1-7) concentrations after OT in AHF patients with reduced ejection fraction (EF).Methods: ACE2 and Ang-(1-7) concentrations were measured in 68 AHF patients with reduced EF immediately after admission and 1 and 3 months after OT. These parameters were compared with the healthy individuals at three time points.Results: In the acute phase, Ang-(1-7) and ACE2 concentrations was statistically significantly lower and higher in AHF patients than the healthy individuals (2.40 ± 1.11 vs. 3.1 ± 1.1 ng/ml, P<0.005 and 7.45 ± 3.13 vs. 4.84 ± 2.25 ng/ml, P<0.005), respectively. At 1 month after OT, Ang-(1-7) concentration remained lower in AHF patients than the healthy individuals (2.37 ± 1.63 vs. 3.1 ± 1.1 ng/ml, P<0.05); however, there was no statistically significant difference in ACE2 concentration between AHF patients and the healthy individuals. At 3 months after OT, there were no statistically significant differences in Ang-(1-7) and ACE2 concentrations between AHF patients and the healthy individuals.Conclusion: ACE2 concentration was equivalent between AHF patients and the healthy individuals at 1 and 3 months after OT, and Ang-(1-7) concentration was equivalent at 3 months after OT.
Highlights
Studies have shown that the renin–angiotensin system (RAS) is associated with worsening of hypertension and various types of organopathies via the angiotensin-converting enzyme (ACE)/angiotensin (Ang) angiotensin II (II) (Ang II)/Ang II type 1 receptor axis [1,2]
We previously reported that acute heart failure (AHF) patients requiring hospitalization had higher serum ACE2 and lower Ang-(1-7) concentrations in the acute phase when compared with the concentrations in healthy volunteers [13]
The present study did not elucidate the mechanisms of the changes in ACE2 and Ang-(1-7) concentrations, it showed that the serum ACE2 concentration declined and the Ang-(1-7) concentration increased by optimal therapy (OT) in compensated heart failure cases, and as a result, both concentrations were equivalent to the healthy individuals
Summary
Studies have shown that the renin–angiotensin system (RAS) is associated with worsening of hypertension and various types of organopathies via the angiotensin-converting enzyme (ACE)/angiotensin (Ang) II (Ang II)/Ang II type 1 receptor axis [1,2]. Long-term activation of the neurohormonal response, especially of the sympathetic nervous system and the renin–angiotensin–aldosterone system, is a major molecular hallmark of adverse LV remodeling. The levels of both plasma catecholamines and aldosterone are important predictors of cardiovascular mortality in post-MI patients [3,4]. Recent studies have established the existence of a new cascade in the RAS called the ACE2/Ang-(1-7)/Mas receptor axis [5,6]. Ang-(1-7) is a degradation product of Ang I and Ang II associated with ACE2. Studies in mice have reported that Ang-(1-7) stimulates the Mas receptor and induces
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