(Circulation. 2005;112:935.)
© 2005 American Heart Association, Inc.
Issue Highlights
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REAL-TIME THREE-DIMENSIONAL ECHOCARDIOGRAPHY: A NOVEL TECHNIQUE TO QUANTIFY GLOBAL LEFT VENTRICULAR MECHANICAL DYSSYNCHRONY, by Kapetanakis et al. |
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Left ventricular (LV) dyssynchrony is recognized as being an important contributor to LV dysfunction in patients with wide QRS complexes. Optimal evaluation of patients with dyssynchrony is uncertain, and various techniques have been described to identify appropriate candidates for cardiac resynchronization therapy (CRT) and to optimize settings after implantation. Kapetanakis et al describe a real-time 3-dimensional echocardiography technique in which global and regional volume and function are assessed in 89 healthy volunteers and 174 patients with and without LV dysfunction. A dyssynchrony index of the entire LV is derived that increases with worsening LV function irrespective of QRS duration. In 26 patients treated with CRT, the dyssynchrony index improves, and this correlates with reverse remodeling. This real-time, 3-dimensional, echo technique may help to quantify objectively the degree of dyssynchrony, direct CRT settings, and identify a larger group of patients with dyssynchrony in the absence of increased QRS duration. See p 992.
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CONTRIBUTION OF CYCLOOXYGENASE-2 TO ELEVATED BIOSYNTHESIS OF THROMBOXANE A2 AND PROSTACYCLIN IN CIGARETTE SMOKERS, by McAdam et al. |
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TopREAL-TIME THREE-DIMENSIONAL...CONTRIBUTION OF CYCLOOXYGENASE-2...BILIRUBIN: A NATURAL INHIBITOR...Visit... |
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In recent months, we have experienced an intense and fierce debate about the cardiovascular safety of COX-2 inhibitors. One of the issues in this context is their effects on the biosynthesis of prostaglandins. In this issue of Circulation, McAdam et al report on the effects of rofecoxib at a high dose on the biosynthesis of thromboxane A2 and prostacyclin in smokers and nonsmokers. Prostacyclin metabolites were increased in smokers and were reduced by rofecoxib; this also occurred to some degree in nonsmokers. Furthermore, the metabolites of thromboxane were increased in smokers and reduced by rofecoxib in smokers but not in nonsmokers. In contrast to the urinary excretion of thromboxane B2, plasma levels of thromboxane did not differ in smokers and nonsmokers and were unaffected by rofecoxib. This study demonstrates that, particularly in smokers, the increase in the biosynthesis of prostacyclin is largely derived from cyclooxygenase-2. Inhibition of this most likely compensatory mechanism in this group of patients at high risk for cardiovascular effects by COX-2 inhibitors may be disadvantageous in this context and potentially may facilitate thrombus formation in smokers. See p 1024.
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BILIRUBIN: A NATURAL INHIBITOR OF VASCULAR SMOOTH MUSCLE CELL PROLIFERATION, by Öllinger et al. |
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Atherosclerosis is a disorder associated with vascular stress response, and heme oxygenase induction is one component of vascular stress. Considerable data demonstrate that induction of heme oxygenase ameliorates many features of vascular disease. The mechanism(s) responsible for such observations, however, have been unclear. In this issue, Öllinger and colleagues have examined the biological activity of a heme oxygenase product, bilirubin, with regard to vascular injury and smooth muscle cell proliferation. This study increases our understanding of how heme oxygenase induction may limit the vascular injury response. See p 1030.
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Clinician Update
Should Aspirin Be Discontinued Before Coronary Artery Bypass Surgery? See p e85.
Images in Cardiovascular Medicine
Prinzmetal Angina in an Adolescent: Adjunctive Role of Tissue Synchronization Imaging. See p e91.
Visualization of Regional Left Ventricular Mechanical Delay by Tissue Synchronization Imaging in Heart Failure Patients With Wide and Narrow QRS Complexes Undergoing Cardiac Resynchronization Therapy. See p e93.
Adult Patient With Isolated Noncompaction of Ventricular Myocardium. See p e96.
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Book Review
Inside the FDA: The Business and Politics Behind the Drugs We Take and the Food We Eat. See p e98.
Correspondence
See p e99.
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