Abstract

We read with interest the recent article by Manni et al. [1] in which reduced levels of both nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) were described in patients with acute coronary syndromes (ACS) compared with healthy controls. BDNF has attracted considerable research interest in recent years, and this neurotropin has been implicated in the pathophysiology of numerous disparate disease states. Although, as stated by the authors, BDNF may indeed be involved in maintaining cardiac homeostasis and have a role in the pathogenesis of human coronary atherosclerosis, the reduced plasma levels of BDNF and NGF reported by Manni et al. may be explained by the stress and hypercortisolaemia associated with ACS. As the authors themselves acknowledge, stress can alter BDNF and NGF expression [1]. This is supported by a wealth of preclinical data which has shown that exogenous corticosteroid administration or stress-induced hypercortisolaemia can cause acute downregulation of BDNF and NGF expression, an effect which is rapidly reversible following removal of the stressor [2]. Both coronary artery disease [3] and myocardial infarction [4] are associated with activation of the hypothalamic–pituitary–adrenal (HPA) axis and raised cortisol levels for at least 24 h post infarction. Given that

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