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T he relationship between the heart and the brain is complex and integral in the maintenance of normal cardiovascular function. Certain pathological conditions can interfere with the normal brain-heart regulatory mechanisms and result in impaired cardiovascular function. Although significant clinical overlap exists in those presenting with stress-associated cardiomyopathy, it is unclear whether myocardial adrenergic hyperstimulation is the only pathophysiological mechanism responsible for these syndromes (Tables
Bybee et al. (Mon,) studied this question.