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[56] In a cross-sectional cohort study in subjects suspected of heart failure (n?=?221),[39] serum ACE2 activity strongly correlated with a clinical diagnosis click here of heart failure, left ventricular ejection fraction (LVEF) and increasing B-type natriuretic (BNP) peptide levels. Higher serum ACE2 activity also reflected the severity of heart failure according to the New York Heart Association function classification. Serum ACE2 activity was increased in heart failure of both ischaemic and non-ischaemic origin, as well as in those with heart failure and preserved LVEF. In a separate cohort of 113 patients with stable chronic systolic heart failure, those with a lower LVEF had higher ACE2 activity, and levels were correlated with higher plasma N-terminal (NT)-proBNP.[40] Plasma ACE2 activity predicted the combined clinical end-point (occurred in 29%) of all-cause mortality, heart transplantation and heart failure hospitalization independent of LVEF and NT-proBNP levels.[40] Similar results have been reported for patients with Chagas disease, a leading cause of heart disease in Central and South America.[41] Plasma ACE2 activity was significantly higher in those with Chagas disease and heart failure compared with healthy controls and was predictive of cardiac death and heart transplantation.[41] As mentioned earlier, in the MI rat this website model of heart failure, increased cardiac ACE2 is reflected by increased plasma ACE2 activity.[36] The results of increased circulating ACE2 in human heart failure are also consistent with our own study that reported ACE2 immunoreactivity is increased in explanted ischaemic failing human heart tissue.[21] Others have shown that the ACE2 gene is upregulated in human idiopathic Adenosine and ischaemic cardiomyopathy,[58] and in myocardial biopsies from subjects with heart failure.[22] Increased plasma BNP and NT-proBNP levels are powerful independent predictors of morbidity and mortality in heart failure.[59] The current ACE2 activity studies in heart failure subjects suggest a significant positive correlation between circulating ACE2 activity and BNP levels.[39-41] Epelman et?al.[40] reported that, in 113 heart failure subjects, ACE2 activity levels above the ROC-derived value of 28.3?ng/mL in combination with NT-proBNP levels above the median value of 1240?pg/mL (AUC?=?0.78; P?
