The emerging role of the gut in chronic heart failure.
OBJECTIVE
Chronic heart failure is a multisystem disease with increased sympathetic tone, an anabolic/catabolic dysbalance, and chronic inflammation. Recent studies suggest an altered morphology, permeability, and absorption of the digestive tract in chronic heart failure. Due to nonocclusive mesenterial ischaemia and disturbed intestinal microcirculation, bacterial endotoxin is thought to enter the bloodstream through the hypoperfused, oedematous gut wall, thereby triggering an inflammatory response. Circulating cytokines act as cardiosuppressors. Their plasma levels predict increased mortality in chronic heart failure.


RESULTS
The present article focuses on specific alterations of the gastric, small intestinal, and large intestinal region in chronic heart failure. It describes the leaky intestinal barrier with an augmented bacterial biofilm that may contribute to chronic inflammation and malnutrition. Furthermore, we review methods for bowel perfusion measurement and potential therapeutic approaches.


CONCLUSIONS
It remains unclear whether increased adherent bacteria in patients with chronic heart failure are a primary or secondary event and whether they contribute to systemic inflammation. Both lack of mucosal integrity with consecutive local and systemic inflammation and dysfunction of transport proteins may worsen the clinical symptoms of chronic heart failure. Therefore, future studies need to address the pathophysiology of the intestinal barrier whose reactivity seems to be crucial for heart function.
Sandek
Anja
A
Applied Cachexia Research, Department of Cardiology, Campus Virchow-Klinikum, Charité, Berlin, Germany.
Rauchhaus
Mathias
M
Anker
Stefan D
SD
von Haehling
Stephan
S
D002908:Chronic Disease; D004435:Eating; D005215:Fasting; D005767:Gastrointestinal Diseases / Q000150:complications*; D006333:Heart Failure / Q000209:etiology*; D006801:Humans; D007249:Inflammation / Q000150:complications* / Q000382:microbiology; D007413:Intestinal Mucosa / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D007422:Intestines / Q000098:blood supply / Q000382:microbiology; D007511:Ischemia / Q000503:physiopathology; D013152:Splanchnic Circulation / Q000502:physiology