| ||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2004;110:3503.)
© 2004 American Heart Association, Inc.
Issue Highlights
CONTROL OF PLASMA NITRIC OXIDE BIOACTIVITY BY PERFLUOROCARBONS: PHYSIOLOGICAL MECHANISMS AND CLINICAL IMPLICATIONS, by Rafikova et al.The development of blood substitutes originally focused on heme-based compounds; however, this class of agents was problematic, in part because of their tendency to degrade nitric oxide (NO), an important endothelial product that prevents vasospasm and thrombosis. In the search for blood substitutes, perfluorocarbons recently have emerged as a promising class of compounds, largely as a result of their transport capacity for both oxygen and carbon dioxide. Rafikova and colleagues report in this issue of Circulation that perfluorocarbons offer the additional advantage of transporting NO and preserving its actions in the bloodstream. In this regard, perfluorocarbons more closely mimic whole blood. These data also highlight the role of NO in preserving vascular homeostasis. See p 3573.
FACTOR VLEIDEN INHIBITS FIBRINOLYSIS IN VIVO, by Parker et al.
Disruption in the normal balance between procoagulant and anticoagulant mechanisms can result in bleeding or thrombosis. Factor V normally contributes to the prothrombinase complex, but a mutation in this factor (factor V Leiden) results in an inability to turn off factor V and predisposes individuals to thrombosis. The in vivo effects of this mutation and how the mutation leads to enhanced thrombosis are unclear. Parker and colleagues studied the lysis of clots in mice with or without the factor V Leiden mutation. They found that clot lysis was significantly reduced in mice with the mutation as compared with normal mice. These studies suggest that the common factor V Leiden mutation, associated with enhanced thrombosis, also leads to impaired fibrinolysis. See p 3594.
BRACHIAL ARTERY VASODILATOR FUNCTION AND SYSTEMIC INFLAMMATION IN THE FRAMINGHAM OFFSPRING STUDY, by Vita et al.
Although inflammatory markers have attracted a lot of attention, their true role as risk predictors compared with traditional risk factors remains controversial. In their study in this issue, Vita et al have used the Framingham Offspring Study to assemble a cohort in which they measured flow-mediated vasodilation, an index of endothelial dysfunction as a marker of vascular disease. They then analyzed inflammatory markers as well as traditional risk factors with regard to their relation to endothelial dysfunction. They found that there were modest unadjusted inverse relations between flow-mediated dilation and C-reactive protein, interleukin-6, and soluble intracellular adhesion molecule-1 that, however, were rendered nonsignificant when traditional risk factors were taken into account. In contrast, reactive hyperemia was inversely related to markers of inflammation, and an attenuated but still significant relation remained even after accounting for traditional risk factors. Thus, it is likely that risk factors do induce a state of inflammation that impairs vascular function and that inflammatory markers are an intermediate between traditional risk factors and vascular dysfunction. See p 3604.
Visit www.circ.ahajournals.org:
Clinician Update
Clinical Decision Making for Endovascular Repair of Abdominal Aortic Aneurysm. See p e517.
Images in Cardiovascular Medicine
Rare Form of Right Ventricular Outflow Tract Obstruction. See p e524.
Endocardial Implantation of a Cardioverter-Defibrillator in a 13-Month-Old Child Affected by Long-QT Syndrome and Syndactyly. See p e525.
|
Related Articles:
Circulation 2004 110: 3594-3598.
Circulation 2004 110: 3573-3580.
Circulation 2004 110: 3604-3609.
Circulation 2004 110: e517-e523.
Circulation 2004 110: e524.
Circulation 2004 110: e525-e527.
| ||||||||||||||||||||||||||||||||||||||||||||||||||