As deficits in NADH-dependent mitochondrial complex I activity and oxidative phosphorylation are a feature of human systolic heart failure and most studies of PDH function in heart failure have examined animal models [15], the aims of this study were to measure PDH activity, protein complex subunit expression, and the protein expression of PDH regulatory kinases and phosphatases in left ventricular biopsies from adult human end-stage systolic heart failure and nonfailing donor hearts. This evidence concerns the gene PDP1 and heart failure.