Therefore, by modifying the rate of degradation of acetylcholine release into the heart, during and post-MI, PYR enhanced the bioavailability of ACh in the neural junction of the sinus and atrioventricular nodes and increased the activity of muscarinic receptors, suppress the augmented sympathetic drive to the heart (i.e., lower sympathetic tone and LH/HF ratio). This evidence concerns the gene PLOD1 and myocardial infarction.