Research Article

Clinical Autonomic Research

, Volume 22, Issue 6, pp 259-264

Open Access This content is freely available online to anyone, anywhere at any time.

Sympathetic nerve activity in stress-induced cardiomyopathy

  • Yrsa Bergmann SverrisdóttirAffiliated withDepartment of Clinical Neurophysiology, Institute of Neuroscience and PhysiologyDepartment of Physiology, Anatomy and Genetics, University of OxfordNuffield Department of Surgical Sciences, John Radcliffe Hospital Headington Email author 
  • , Tomas SchultzAffiliated withDepartment of Molecular and Clinical Medicine, Sahlgrenska University Hospital
  • , Elmir OmerovicAffiliated withDepartment of Molecular and Clinical Medicine, Sahlgrenska University Hospital
  • , Mikael ElamAffiliated withDepartment of Clinical Neurophysiology, Institute of Neuroscience and Physiology

Abstract

Purpose

To evaluate directly recorded efferent sympathetic nerve traffic in patients with stress-induced cardiomyopathy (SIC).

Background

SIC is a syndrome affecting mostly postmenopausal women following severe emotional stress. Though the precise pathophysiology is not well understood, a catecholamine overstimulation of the myocardium is thought to underlie the pathogenesis.

Methods

Direct recordings of multiunit efferent postganglionic muscle sympathetic nerve activity (MSNA) were obtained from 12 female patients, 5 in the acute (24–48 h) 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 %). One of the twelve patients in this study was on beta blockade treatment due to a different illness, at time of onset of SIC. All patients were investigated with ongoing medication.

Results

MSNA was lower in patients with SIC as compared to matched controls, but did not differ between the acute and recovery phase of SIC. RMBA %, blood pressure and heart rate did not differ between the groups.

Conclusion

MSNA is shown to be lower in patients with SIC compared to healthy controls, suggesting that sympathetic neuronal outflow is rapidly reduced following the initial phase of SIC. 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.

Keywords

Sympathetic nervous system Cardiomyopathy Stress Women