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Nat Clin Pract Cardiovasc Med. 2008 Dec;5(12):811-20. doi: 10.1038/ncpcardio1364. Epub 2008 Oct 28.

Circulating white blood cells and platelets amplify oxidative stress in heart failure.

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  • 1Department of Cardiology, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands.



Mitochondria of circulating white blood cells (WBC) and platelets sense oxidative stress during capillary passage and react by producing reactive oxygen species (ROS). Although evidence indicates that congestive heart failure (CHF) is associated with oxidative stress, the role of WBC and platelets as mediators in CHF has not been investigated.


Patients with CHF (n = 15) and healthy volunteers (n = 9) were enrolled between 2006 and 2007 into this observational study. Arterial and venous blood samples from participants were incubated with probes to detect cytosolic and mitochondrial ROS. Fluorescence-activated cell sorting was used to measure the degree of fluorescence in WBC and platelets.


Patients with CHF had a higher proportion of ROS-positive arterial WBC and platelets than did controls (67% +/- 47% versus 16% +/- 9%; P <0.005), as well as venous WBC and platelets (77% +/- 43% versus 38% +/- 13%; P <0.01). In the control group, the proportion of cytosolic ROS-positive arterial WBC and platelets was lower than that for ROS-positive venous WBC and platelets (16% +/- 9% versus 38% +/- 13%; P <0.005). CHF patients had a higher proportion of mitochondrial ROS-positive arterial and venous WBC and platelets than did controls.


In CHF, the proportion of WBC and platelets that are ROS-positive is raised, possibly because cytosolic ROS-positive WBC and platelets are normally cleared in the lungs; this function is deficient in CHF while mitochondrial ROS production is increased. The raised numbers of circulating ROS-positive WBC and platelets amplify oxidative stress in CHF.

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