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Cardiovascular Research 2006 70(3):434-445; doi:10.1016/j.cardiores.2006.01.013
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Copyright © 2006, European Society of Cardiology

Autonomic imbalance and immune activation in chronic heart failure – Pathophysiological links

Ewa A. Jankowskaa,b,c,*, Piotr Ponikowskia, Massimo F. Piepolib,d, Waldemar Banasiaka, Stefan D. Ankerb,e and Philip A. Poole-Wilsonb

aCardiology Department, Military Hospital, Wroclaw, Poland
bNational Heart and Lung Institute, Imperial College London, Clinical Cardiology, Royal Brompton Hospital, London, United Kingdom
cInstitute of Anthropology, Polish Academy of Sciences, Wroclaw, Poland
dHeart Failure Unit, Cardiac Department, G. da Saliceto Polichirurgico Hospital, Piacenza, Italy
eDivision of Applied Cachexia Research, Department of Cardiology, Charite, Berlin, Germany

* Corresponding author. Cardiology Department, Military Hospital, ul. Weigla 5; 50–981 Wroclaw; Poland. Tel./fax: +48 71 7660 250. Email address: Ewa.Jankowska{at}antro.pan.wroc.pl

Activation of the immune system and derangement of cardiorespiratory neural control are established elements of the complex pathophysiology of chronic heart failure (CHF). The magnitude of these abnormalities relates to disease progression and mortality. Less clear is the origin of these derangements and the sequence of triggering mechanisms in the course of the natural history of CHF. To date, immune activation and autonomic imbalance have been considered independently; we hypothesise they are closely related. Damaged heart muscle through autonomic afferents triggers functional and structural changes in the central nervous system, in part related to inflammatory processes. The altered function of the autonomic centres is expressed as a reduction of central parasympathetic tone. Diminished cholinergic signalling (mainly nicotinergic) activates inflammation and stimulates immune response. These two phenomena predict prognosis and represent therapeutic targets in the syndrome of CHF.

KEYWORDS Immune activation; Autonomic imbalance; Parasympathetic depletion; Nicotinergic signalling; Chronic heart failure

Time for primary review 18 days


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