PDP1 and myocardial infarction: This is evidenced by a study using hyperpolarized carbon-13 (13C) magnetic resonance spectroscopy to show that the activity of PDH diminished accordingly with the progression of cardiac dysfunction after myocardial infarction (MI) surgery in rats.96 Similar results were also shown in rapid pacing-induced heart failure in pigs, where the flux of PDH was reduced as evidenced by a 67% reduction in the [13C] bicarbonate/[1-13C] pyruvate ratio.94 Of importance, this suppression of cardiac glucose oxidation rates can, at least in part, contribute to the pathogenesis of HFrEF.