Acute myocardial infarction is associated with high levels of cardiac sympathetic stimulation [1], which is strongly related to poor outcome [2]. Prolongation of this sympathetic drive leads to the release of the co-transmitter neuropeptide-Y (NPY) with a relatively long half-life, abundant in the peripheral nervous system [3]. NPY is released from cardiac sympathetic nerve endings in collaboration with the main neurotransmitter norepinephrine, where it can act as a potent vasoconstrictor in a variety of vascular beds [4].
