Monoamine oxidase is overactivated in the human left and right ventricles from ischemic hearts: an intriguing therapeutic target.

The present study was aimed at investigating: a) the activity of total MAO activity in non-failing human (NF) and end-stage failing hearts with ischemic (IHD) and non-ischemic etiology; b) the activity of MAO isoforms in the left (LV) and in the right ventricle (RV) of NF and failing IHD hearts; c) the activity of two enzymes linked to MAO catalysis: catalase (CAT) and aldehyde dehydrogenase-2 (ALDH2); c) the oxidative stress markers , malonildialdehyde (MDA) and protein carbonyls; d) the oxidation index of myofibrillar proteins critical for contractile impairment; e) the possible correlation between MAO-A activity, oxdation index and functional parameters: pulmonary capillary wedge pressure (PCWP) and pulmonary artery pressure (PAP)