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The article focuses on a study that proves that the endothelium is responsible for the paradoxical acetylcholine induced vasodilation via nitric oxide release as denudation of the endothelium resulted in vasoconstriction when acetylcholine is applied. Increased circulating endothelial cells (CECs) are detached, probably dysfunctional cells, and imply that parts of the endothelium are denuded while flow mediated dilatation is a physiological measure of endothelial function. Researchers studied 30 patients with chronic congestive heart failure in sinus rhythm with ejection fraction <40% and compared with 20 healthy controls CECs were captured by immunomagnetic separation and counted under fluorescent microscopy.

This article focuses on a study related to relationship of angiopoietin-1 (Ang-1) and a Ang-2 to endothelial damage in congestive heart failure (CHF). Ang-1 and Ang-2 are angiogenic markers that modulate the function of vascular endothelial growth factor. Ang-1 is recognized to be a potent anti-apoptotic factor. The ret increase in Ang-2 over Ang-1 in CHF and the relationship to vWf supports our hypothesis that the imbalance between Ang-1 and Ang-2 levels in CHF may be exacerbating endothelial damage.