Sympathetic nerve activity in stress-induced cardiomyopathy.

Department of Clinical Neurophysiology, Institute of Neuroscience and Physiology, Gothenburg, Sweden, .
Clinical Autonomic Research (Impact Factor: 1.86). 04/2012; DOI: 10.1007/s10286-012-0162-x
Source: PubMed

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.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Integrating into the clinical practice of medicine the recent evidence that psychiatric illness and mental stress contributes to the development of cardiovascular disease has not been a seamless process. The evidence for such a link, in fact, had been slow in materializing. The importance of acute mental stress as a trigger for cardiac catastrophes (acute myocardial infarction, sudden death) and of depressive illness as a cause of coronary heart disease, however, is now firmly established. But the spectre of workplace litigation still does hang over the field, clouding the arguments and polarizing medical opinion. Now that a consensus finally seems to have been reached that mental stress, including in the workplace, is an important cause of coronary heart disease and hypertension, it is hoped that the primary outcome will be the implementation of preventive measures to reduce stress in the workplace, such as worker empowerment to end the very adverse high demand/low job control scenario, rather than a rash of lawsuits. Copyright © 2008 John Wiley & Sons, Ltd.
    Stress and Health 07/2008; 24(3):175 - 180. · 1.34 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Five patients with typical myocardial stunning were presented. They had chest pain and had electrocardiographic abnormalities matching the symptoms of acute myocardial infarction (AMI) but had no coronary artery stenoses on angiogram (CAG). The prevalence of cases with these clinical manifestations was 1.2% among 415 consecutive AMI patients who were examined invasively. The electrocardiographic abnormalities varied; ST elevations were observed in 4 patients, R waves decreased transiently in one, and Q waves developed in one patient. Typical left ventriculogram (LVG) was akinesis in the apical, diaphragmatic and/or anterolateral segments, but hyperkinesis in the basal segments. This akinesis was transient and resolved in 7 days. CAG revealed diffuse multi-vessel spasms in 2 patients, which were also observed in additional 2 patients after ergonovine administration. The intracoronary administration of nitroglycerin disclosed no coronary artery stenoses in any of the patients.
    Journal of Cardiology 02/1991; 21(2):203-14. · 2.57 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To determine the clinical features of a novel heart syndrome with transient left ventricular (LV) apical ballooning, but without coronary artery stenosis, that mimics acute myocardial infarction, we performed a multicenter retrospective enrollment study. Only several case presentations have been reported with regard to this syndrome. We analyzed 88 patients (12 men and 76 women), aged 67 +/- 13 years, who fulfilled the following criteria: 1) transient LV apical ballooning, 2) no significant angiographic stenosis, and 3) no known cardiomyopathies. Thirt-eight (43%) patients had preceding aggravation of underlying disorders (cerebrovascular accident [n = 3], epilepsy [n = 3], exacerbated bronchial asthma [n = 3], acute abdomen [n = 7]) and noncardiac surgery or medical procedure (n = 11) at the onset. Twenty-four (27%) patients had emotional and physical problems (sudden accident [n = 2], death/funeral of a family member [n = 7], inexperience with exercise [n = 6], quarreling or excessive alcohol consumption [n = 5] and vigorous excitation [n = 4]). Chest symptoms (67%), electrocardiographic changes (ST elevation [90%], Q-wave formation [27%] and T-wave inversion [97%]) and elevated creatine kinase (56%) were found. After treatment of pulmonary edema (22%), cardiogenic shock (15%) and ventricular tachycardia/fibrillation (9%), 85 patients had class I New York Heart Association function on discharge. The LV ejection fraction improved from 41 +/- 11% to 64 +/- 10%. Transient intraventricular pressure gradient and provocative vasospasm were documented in 13/72 (18%) and 10/48 (21%) of the patients, respectively. During follow-up for 13 +/- 14 months, two patients showed recurrence, and one died suddenly. A novel cardiomyopathy with transient apical ballooning was reported. Emotional or physical stress might play a key role in this cardiomyopathy, but the precise etiologic basis still remains unclear.
    Journal of the American College of Cardiology 08/2001; 38(1):11-8. · 15.34 Impact Factor

Full-text (2 Sources)

Available from
May 27, 2014

Similar Publications