Published: 29 March 2024
Author(s): Christina Tiller, Martin Reindl, Magdalena Holzknecht, Ivan Lechner, Felix Troger, Fritz Oberhollenzer, Sebastian von der Emde, Thomas Kremser, Agnes Mayr, Axel Bauer, Bernhard Metzler, Sebastian J Reinstadler
Issue: June 2024
Section: Original Article

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].

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