Abstract
To the Editor: We have read with interest the article by Ejiri and colleagues1 about the possible role of brain-derived neurotrophic factor (BDNF) in the pathogenesis of coronary artery disease, which suggests that BDNF might contribute to plaque instability in coronary artery disease because of enhanced local nicotinamide adenine dinucleotide (phosphate) oxidase activity and superoxide production. On the basis of increased BDNF concentrations in EDTA-containing plasma in the coronary sinus (compared with concentrations measured in the aortic root) and several histological studies in patients with acute coronary syndrome, the authors assume that BDNF is derived mainly from diseased coronary arteries.1 We would like to suggest an alternative interpretation. It has been well established that BDNF is one of the major mediators stored in human platelets. Human platelets contain large amounts of BDNF (&100 pg/106 platelets) that is released …
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