| Summary: | The maintenance of cardiovascular and cerebrovascular health is based on a complex relationship between the heart and the brain. While some responses to stress are vital for survival, mental stress has also been claimed to cause cardiovascular disease. The Japanese observation from the early 1990s of a reversible stress-induced cardiomyopathy, the takotsubo cardiomyopathy (TC), a peculiar type of left ventricular (LV) dysfunction triggered by an acute strong emotional or physical stressor, supports this notion. The syndrome, mostly affecting postmenopausal women, presents signs and symptoms of acute coronary syndrome without evidence of obstructive coronary artery disease. Though the definite pathophysiology of TC remains to be identified, a catecholamine overstimulation of the myocardium is thought to underlie the pathogenesis and forms the basis for treatment of this medical entity.Direct recordings of multiunit efferent postganglionic muscle sympathetic nerve activity (MSNA) were obtained from 12 female patients, 5 in the acute (24–48 hours) and 7 in the recovery phase (1–6 months), with apical ballooning pattern and 12 healthy matched controls. MSNA was expressed as burst frequency (BF), burst incidence (BI) and relative median burst amplitude (RMBA%). All patients were investigated with ongoing medication.MSNA was lower in patients with TC as compared to matched controls, but did not differ between the acute and recovery phase of TC. RMBA%, blood pressure and heart rate did not differ between the groups.MSNA is shown to be lower in patients with TC compared to healthy controls, suggesting that sympathetic neuronal outflow is rapidly reduced following the initial phase of TC. A distension of the ventricular myocardium, due to excessive catecholamine release over the heart in the acute phase may increase the firing rate of unmyelinated cardiac c-fibre afferents resulting in widespread sympathetic inhibition. Such a mechanism may underlie the lower MSNA reported in our patients.
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