Key result
Ang-(1-7)-forming activity from Ang II was increased in failing left ventricles of idiopathic dilated cardiomyopathy compared to nonfailing hearts (139.7 vs 32.89 fmol/min/mg; P<0.001).
Population
Left and right ventricular membranes from 14 idiopathic dilated cardiomyopathy, 8 primary pulmonary…
Comparison
Measurement of angiotensinase activity using… vs Nonfailing human heart ventricles.
Design
Preclinical
Authors
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May indicate compensatory Ang-(1-7) upregulation in failing hearts; leaves open whether targeting this pathway benefits patients with dilated cardiomyopathy.
Observational (n=35)
Absolute Event Rate: 139.7% vs 32.89%
p-value: p=<0.001
Angiotensin-(1-7)-forming activity is increased in failing human heart ventricles, mediated by NEP-like and ACE2 enzymes.
Zisman et al. (2003) conducted an observational in Idiopathic dilated cardiomyopathy and primary pulmonary hypertension (n=35). Failing human heart ventricles (IDC and PPH) vs. Nonfailing human hearts was evaluated on Ang-(1-7)-forming activity with 125I-Ang II as substrate in left ventricles (fmol/min/mg) (p=<0.001). Ang-(1-7)-forming activity from Ang II was increased in failing left ventricles of idiopathic dilated cardiomyopathy compared to nonfailing hearts (139.7 vs 32.89 fmol/min/mg; P<0.001).
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