Ann Thorac Surg 2006;82:700-701
© 2006 The Society of Thoracic Surgeons
Original article: Cardiovascular
Invited commentary
Markus K. Heinemann, MD, PhD
Cardiac, Thoracic and Vascular Surgery, Mainz University Hospital, Langenbeckstr 1, 505, Mainz, 55131 Germany
(Email: heinemann{at}uni-mainz.de).
In this study the authors [1] have looked in great detail into the potential pathophysiology of abnormal enteric protein loss (AEPL), also known as protein-losing enteropathy after Fontan-type operations. Designed as a cross-sectional study during outpatient visits, mesenteric and celiac artery blood flows were measured by ultrasound and markers for inflammation, liver function, coagulopathy, and glycosylation defects, as well as neurohormonal levels were determined, thereby covering the current pathophysiologic theories.
In concurrence with their previous work, a significantly lower mesenteric-to-celiac artery flow ratio was found in the patients afflicted, with mesenteric vascular resistance indices being elevated in all patients. This supports the theory that the Fontan circulation is a state of more or less evidently diminished cardiac output, which combined with elevated central venous pressure leads to marked changes in organ perfusion profiles. In addition, inflammatory markers were elevated in many patients, although there was no significant correlation with AEPL. The authors also found changes in the levels of several neuro-hormones and coagulation factors.
Great care was taken in analyzing and discussing the various mechanisms believed to be responsible for this dreadful illness. The measured targets were selected accordingly and were put into the proper perspective. By doing this the authors have succeeded in providing both original new data as well as a thorough overview concerning our current knowledge. The only thing lacking is a valid hemodynamic study complementing the noninvasive findings. This would have been of particular interest in the 2 patients with "asymptomatic" AEPL. Although coming from a large institution, the numbers were relatively small, which is fortunate for the Fontan patients. The resulting need for true multi-institutional studies is emphasized. The confusing and sometimes seemingly contradictory findings encountered in this devastating disease demand the analysis of as many data as there are available, and the Philadelphia group should be supported in their continued efforts. It is surely not an enviable task to investigate the downsides of success. Nevertheless only relentless expert research will one day find a solution for this vexing enigma.
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References
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- Ostrow AM, Freeze H, Rychik J. Protein-losing enteropathy after Fontan operationinvestigations into possible pathophysiologic mechanisms. Ann Thorac Surg 2006;82:695-701.[Abstract/Free Full Text]