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Its rapid onset, shorter half-life, and selective action on depolarized ischemic fibers allow prompt suppression of ectopic foci with minimal negative inotropy, making it particularly useful immediately after coronary reperfusion

Stenson, B

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However, under pro-inflammatory conditions, some of the major NAD + consumers, such as PARPs, become highly activated, tilting the scales of NAD + homeostasis toward excessive consumption, quickly depleting intracellular NAD + stores, and leading to mitochondrial dysfunction and impaired energy metabolism (16, 17, 18, 20, 21, 22)