Catecholamine metabolism via monoamine oxidase (MAO) contributes to cardiac injury in models of ischemia and diabetes, but the pathogenic mechanisms involved are unclear. MAO deaminates norepinephrine (NE) and dopamine (DA) to produce H2O2 and highly reactive ‘catecholaldehydes,’ which may be toxic to mitochondria due to the localization of MAO to the outer mitochondrial membrane. We performed a comprehensive analysis of catecholamine metabolism and its impact on mitochondrial energetics in atrial myocardium obtained from patients with and without type 2 diabetes. This data set contains a list of human cardiac mitochondrial proteins that were isolated following aminophenylboronic acid (APBA) column chromatography, which allows for selective purification of catechol-modified proteins. Samples of human heart mitochondria were prepared from discarded atrial appendage biopsies taken during elective cardiac surgery. Following extraction via APBA, bands were excised from a gel and subjected to proteomics analysis.