Cardiac PDH E1a deficiency caused a large myocardial infarct area and increased macrophage infiltration in the heart, while PDH activated by dichloroacetate in WT hearts during ischemia/reperfusion increased glucose oxidation and reduced myocardial infarct size.221 Moreover, in an IDH2-deficient mouse model, mitochondrial dysfunction and cardiac hypertrophy were promoted by PDH activation.222 Mitochondrial long-chain fatty acid (LCFA) oxidation, the main FAO pathway involved in myocardial energy supply, was also inhibited due to the reduced activity of the rate-limiting enzyme CPT1. Here, CPT2 is linked to cardiac hypertrophy.