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Beta-blockers (BB) are the only anti-arrhythmic drugs that improve mortality in patients with ischaemic heart disease, but a significant risk of arrhythmia remains. During high-level sympathetic drive, such as during myocardial infarction, co-transmitters including neuropeptide Y (NPY) can be released with norepinephrine. NPY is a potent vasoconstrictor that can also alter cardiac electrophysiology. We hypothesised that ventricular fibrillation threshold (VFT) would still be reduced following high-level sympathetic stimulation even in the presence of a BB. We also investigated whether NPY is independently pro-arrhythmic and decreases VFT, and if this mechanism is mediated by the Y1 receptor.

Original publication




Journal article



Publication Date



16 Suppl 3