Chronic heart failure (CHF) is a multi-organ disease with increasing evidence for the involvement of the gastrointestinal (GI) system in this syndrome. In recent research, the gut has received very little attention from cardiologists as its role in the pathogenesis of cardiovascular disease is poorly understood. Intestinal ischaemia may play an important role in bacterial translocation by increasing bowel permeability. Decreased cardiac function can reduce bowel perfusion and so clearly impairs the function of the intestinal barrier. There is an increasing evidence to suggest that a 'leaky' bowel wall may lead to translocation of bacteria and/or endotoxin, which may be an important stimulus for inflammatory cytokine activation in CHF. Impaired functioning of the GI system may also contribute to malnutrition and cachexia in CHF. It is hoped that by improving our understanding of the role of the gut in cardiac disease will lead to the development of novel therapeutic strategies in the future.

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The treatment of CTOs with a paclitaxel-eluting stent drastically reduces MACE and restenosis, and almost eliminates re-occlusion, which is typically frequent with BMS in CTOs. Chronic total coronary occlusion should be a preferred indication for drug-eluting stents.

Aims: The aim of this study was to investigate mesenteric ischaemia by determining intragastric PCO (iPCO ) with gastric 2 2 tonometry during rest and exercise stress testing in patients with chronic heart failure (CHF). In CHF inflammatory immune activation is hypothesized to result from a chronic endotoxin challenge due to bacterial translocation of hypoperfused intestinal mucosa. Methods and Results: In 10 patients with CHF and ten healthy controls a tonometry catheter was inserted into the stomach. IPCO was measured at rest and during bicycle exercise every 5 min. At rest arterial pCO (aPCO ), intragastric pCO 12"2% vs. 1"0.4%, P-0.001). In CHF, iPCO during peak exercise was 25"3% higher than at rest, compared to controls 2 (increase 2"1, P-0.0001). Conclusions: Patients with CHF already at low level exercise develop an increase in iPCO . This is 2 likely to reflect hypoperfusion of the intestinal mucosa, which may contribute to the development of bacterial translocation.