After Cox multivariable adjustment, log ACE2 activity remained an independent predictor of MACE (hazard ratio (HR) 2.4, 95% confidence interval (CI) 1.24-4.72, p = 0.009) and HF hospitalisation (HR: 4.03, 95% CI: 1.42-11.5, p = 0.009).
We would like to comment on the article entitled "Prognostic and diagnostic significance of copeptin in acute exacerbation of chronic obstructive pulmonary disease and acute heart failure: data from ACE 2 study" by Jacob A. Winther and colleagues, in the light of the results of a multicentric study published in 2014 by Vetrone F. et al., in which 336 patients with dyspnea were enrolled in the Emergency Departments of three University Hospitals in Italy.These two studies confirm the prognostic role of copeptin in patients with dyspnea due to heart failure but, while Winther et al. performed the copeptin measurements only at admission, Vetrone et al. evaluated the time-course of copeptin plasma concentration from the admission to the hospital discharge.
However, increased ACE/ACE2 ratios may induce angiotensin II over-activation and accelerate cardiac remodeling in patients with moderate to severe heart failure.
There are 10 studies to date that have measured circulating ACE2 activity in humans, including in healthy subjects and those with heart failure, Type 1 diabetes, implantable cardioverter/defibrillator, elderly subjects undergoing emergency orthopaedic surgery and kidney transplant patients.
This report describes the effects of ACE2 and Ang-(1-7) that appear to be relevant in cardiac remodeling and heart failure and explores potential therapeutic strategies designed to increase ACE2 activity and Ang-(1-7) levels to treat these conditions.
In the cardiovascular system, the ACE2/angiotensin 1 - 7/Mas axis, mainly through the inhibition of fibrosis, inflammation, thrombosis and cell proliferation, modulates RAS activity with significant pathophysiological implications in clinical conditions such as hypertension, myocardial ischemia and heart failure.
Compared with double noncarriers (angiotensinogen -20aa and ACE II), double heterozygotes (ac-I/D genotype), and double homozygotes (cc-DD) had hazard ratios for atrial fibrillation of 1.2(0.9-1.6; P=0.06) and 2.4(1.4-4.1; P=0.001). a-20c cc homozygotes above 70 years of age who were overweight, severely hypertensive, and had heart failure, had an absolute 10-year risk of atrial fibrillation of 61%.
A novel human homologue of the angiotensin-converting enzyme (ACE), named ACE2, has been described but its role in human heart failure (HF) has not been elucidated.
These data suggest that ACE2 is up-regulated in human IDC and ICM and are consistent with the hypothesis that differential regulation of this enzyme may have important functional consequences in heart failure.
ACE2, the first known human homologue of angiotensin-converting enzyme (ACE), was identified from 5' sequencing of a human heart failure ventricle cDNA library.