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Updated in 1/17/2017 5:40:56 PM      Viewed: 1178 times      (Journal Article)
Journal of the American College of Cardiology 65 (4): 378-88 (2015)

The pathophysiological role of interstitial sodium in heart failure.

Petra Nijst , Frederik H Verbrugge , Lars Grieten , Matthias Dupont , Paul Steels , W H Wilson Tang , Wilfried Mullens
The current understanding of heart failure (HF) does not fully explain the spectrum of HF symptoms. Most HF hospitalizations are related to sodium (Na(+)) and fluid retention resulting from neurohumoral up-regulation. Recent insights suggest that Na(+) is not distributed in the body solely as a free cation, but that it is also bound to large interstitial glycosaminoglycan (GAG) networks in different tissues, which have an important regulatory function. In HF, high Na(+) intake and neurohumoral alterations disrupt GAG structure, leading to loss of the interstitial buffer capacity and disproportionate interstitial fluid accumulation. Moreover, a diminished endothelial GAG network (the endothelial glycocalyx) results in increased vascular resistance and disturbed endothelial nitric oxide production. New imaging modalities can help evaluate interstitial Na(+) and endothelial glycocalyx integrity. Furthermore, several therapies have been proven to stabilize interstitial GAG networks. Hence, a better appreciation of this new Na(+) "compartment" might improve current management of HF.
DOI: 10.1016/j.jacc.2014.11.025      ISSN: 0735-1097