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(Circulation. 2004;110:3289.)
© 2004 American Heart Association, Inc.
Issue Highlights |
EPICARDIAL MAPPING OF CHRONIC ATRIAL FIBRILLATION IN PATIENTS: PRELIMINARY OBSERVATIONS, by Sahadevan et al.
Hypothesized mechanisms of chronic atrial fibrillation include multiple reentry wavefronts and rapid activation from areas of automaticity or relatively fixed sites of reentry that function as "drivers." Evidence supporting either mechanism in humans is limited. In 9 patients, extensive epicardial mapping at the time of cardiac surgery often identified areas of regular activation that was faster than in other atrial regions, consistent with a driver causing fibrillatory conduction to the rest of the atrium. These findings further suggest the potential existence of regions that are drivers for atrial fibrillation and might be targeted for ablation in some patients. Other mechanisms or drivers not detectable from the epicardium might be present in other patients. See p 3293.
SIMVASTATIN PREVENTS VASCULAR HYPOREACTIVITY DURING INFLAMMATION, by Pleiner et al.
Inflammation is a recognized event in the pathophysiology of atherosclerosis and coronary artery disease in particular. Statins have been shown to reduce C-reactive protein, a marker of inflammation; however, the underlying mechanisms by which statins exert antiinflammatory effects are not fully clarified. In this study, healthy subjects were exposed to lipopolysaccharide to induce an inflammatory state. The treatment of these subjects with simvastatin prevented endothelial dysfunction, reduced contractility to norepinephrine, fever, increased oxidative bursts from neutrophils, as well as increases in plasma levels of tumor necrosis factor-
. Thus, this study demonstrates important antiinflammatory activity of statins that might be relevant for patients with coronary heart disease. See p 3349.
DIRECTED VASCULAR EXPRESSION OF HUMAN CYSTEINYL LEUKOTRIENE 2 RECEPTOR MODULATES ENDOTHELIAL PERMEABILITY AND SYSTEMIC BLOOD PRESSURE, by Hui et al.
Cysteinyl leukotrienes are inflammatory mediators that, via activation of the cysteinyl leukotriene 1 receptor (CysLT1R), promote bronchial vascular smooth muscle constriction, enhanced vascular permeability, and recruitment of eosinophils. The cysteinyl leukotriene 2 receptor (CysLT2R) is expressed in the heart and coronary vessels. In vitro studies have shown that human umbilical vein endothelial cells express CysLT2R but not CysLT1R, which suggests that CysLT2R may be important for endothelial function. To date, there have been no adequate models to evaluate vascular CysLT2R function in vivo. In this issue of Circulation, Hui et al report that they have constructed a transgenic mouse model that overexpresses human CysLT2R in the endothelium. Using this model, these authors have examined the vascular consequences of CysLT2R activation. See p 3360.
Visit www.circ.ahajournals.org:
Clinician Update
Prognostic Impact of Early ST-Segment Resolution in Acute ST-Elevation Myocardial Infarction. See p e506.
Images in Cardiovascular Medicine
Anomalous Origin of the Left Coronary Artery From the Main Pulmonary Artery in Adults: Coronary Collateralization at Its Best. See p e511.
In-Stent Neointimal Hyperplasia With 16-Row Multislice Computed Tomography Coronary Angiography. See p e514. 
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Related Articles:
Circulation 2004 110: 3349-3354.
Circulation 2004 110: 3360-3366.
Circulation 2004 110: 3293-3299.
Circulation 2004 110: e506-e510.
Circulation 2004 110: e511-e513.
Circulation 2004 110: e514.
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