Article

Sympathetic nerve activity in stress-induced cardiomyopathy

Department of Clinical Neurophysiology, Institute of Neuroscience and Physiology, Gothenburg, Sweden, .
Clinical Autonomic Research (Impact Factor: 1.49). 04/2012; 22(6). 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.

Download full-text

Full-text

Available from: Elmir Omerovic
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes (T1D), which without treatment leads to death. Fulminant type 1 diabetes (FT1D) is a subtype characterised by a markedly rapid and almost complete destruction of pancreatic β-cells, with acute onset leading to severe metabolic derangement and commonly ICU admission. We present a case of an 18-year-old male presenting with FT1D with two rare complications of pneumomediastinum and stress-induced cardiomyopathy (SIC) with significant myocardial necrosis. We also discuss the aetiology of the pneumomediastinum; the latest thoughts on SIC: moving beyond the simple description of ‘Takotsubo cardiomyopathy’; the role of troponins in critical illness; and genetic predisposition for DKA due to FT1D.
    Preview · Article · Feb 2014 · Journal of the Intensive Care Society
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This concept-based review provides historical perspectives and updates about sympathetic noradrenergic and sympathetic adrenergic responses to mental stress. The topic of this review has incited perennial debate, because of disagreements over definitions, controversial inferences, and limited availability of relevant measurement tools. The discussion begins appropriately with Cannon's "homeostasis" and his pioneering work in the area. This is followed by mental stress as a scientific idea and the relatively new notions of allostasis and allostatic load. Experimental models of mental stress in rodents and humans are discussed, with particular attention to ethical constraints in humans. Sections follow on sympathoneural responses to mental stress, reactivity of catecholamine systems, clinical pathophysiologic states, and the cardiovascular reactivity hypothesis. Future advancement of the field will require integrative approaches and coordinated efforts between physiologists and psychologists on this interdisciplinary topic. © 2015 American Physiological Society. Compr Physiol 5: 119-146, 2015.
    Full-text · Article · Jan 2015 · Comprehensive Physiology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Takotsubo syndrome is an acute cardiac syndrome first described in 1990 and characterized by transient left ventricular dysfunction affecting more than one coronary artery territory, often in a circumferential apical, mid-ventricular, or basal distribution. Several pathophysiological explanations have been proposed for this syndrome and its intriguing appearance, and awareness is growing that these explanations might not be mutually exclusive. The reversible apical myocardial dysfunction observed might result from more than one pathophysiological phenomenon. The pathophysiology of Takotsubo syndrome is complex and integrates neuroendocrine physiology, potentially involving the cognitive centres of the brain, and including the hypothalamic–pituitary–adrenal axis. Cardiovascular responses are caused by the sudden sympathetic activation and surge in concentrations of circulating catecholamines. The multiple morphological changes seen in the myocardium match those seen after catecholamine-induced cardiotoxicity. The acute prognosis and recurrence rate are now known to be worse than initially thought, and much still needs to be learned about the epidemiology and the underlying pathophysiology of this fascinating condition in order to improve diagnostic and treatment pathways.
    No preview · Article · Apr 2015 · Nature Reviews Cardiology
Show more