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HomeCirculationVol. 111, No. 25Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published28 Jun 2005https://doi.org/10.1161/circ.111.25.3341Circulation. 2005;111:3341IS OBESITY A RISK FACTOR FOR MORTALITY IN CORONARY ARTERY BYPASS SURGERY? by Jin et al.This article investigates the role of body size on operative mortality after isolated coronary artery bypass graft surgery in 16 218 patients. Prior reports on body size (body mass index) have resulted in conflicting results. Body mass index in a logistic regression model was not found to be a statistically significant risk factor for mortality. The lowest mortality was observed in the high, normal, and overweight subgroups as compared with obese and underweight subgroups. However, obesity does remain a risk factor for sternal wound complications and negatively impacts late cardiovascular health. A little fat may be protective to get you through surgery, and being underweight increases the operative risk. See p 3359.EFFECTS OF EXERCISE AND ISCHEMIA ON MOBILIZATION AND FUNCTIONAL ACTIVATION OF BLOOD-DERIVED PROGENITOR CELLS IN PATIENTS WITH ISCHEMIC SYNDROMES: RESULTS OF 3 RANDOMIZED STUDIES, by Sandri et al.Exercise training reduces myocardial ischemia in patients with coronary artery disease and lower-limb ischemia in patients with peripheral arterial disease. Several mechanisms may account for these findings, including an improvement in regional perfusion. Previous studies have demonstrated that exercise training induces changes in vascular endothelial function and leads to enhanced vasodilation in local vascular beds. In this provocative study, Sandri and colleagues evaluated whether regular exercise may induce a regeneration of diseased endothelium by circulating progenitor cells or circulating progenitor cell-derived vasculogenesis, and whether ischemic stimuli are required to effect such changes. Their findings provide important new insights into this complex process. See p 3391.IMPROVED MYOCARDIAL β-ADRENERGIC RESPONSIVENESS AND SIGNALING WITH EXERCISE TRAINING IN HYPERTENSION, by MacDonnell et al.Myocardial β-adrenergic receptor responsiveness is depressed in pressure overload-induced cardiac hypertrophy, in association with multiple alterations in the signaling pathway that couples the β-adrenergic receptor to calcium handling and myocyte function. Exercise training is known to improve myocardial β-adrenergic responsiveness in this setting. MacDonnell et al examined the mechanism of this beneficial effect of exercise in spontaneously hypertensive rats. They found that levels of GRK2, a protein that desensitizes the β-adrenergic receptor, were reduced by exercise, in association with increased phosphorylation of two targets of β-adrenergic receptor-mediated phosphorylation, the ryanodine receptor and phospholamban. These findings suggest that biochemical alterations in the β-adrenergic receptor signaling cascade can have important functional consequences in both the pathophysiology of cardiac dysfunction and the response to therapeutic interventions such as exercise training. See p 3420.Visit http://www.circ.ahajournals.org:Images in Cardiovascular MedicineVentricular Septum Rupture After Myocardial Infarction Demonstrated by Multislice Computed Tomography. See p e449.Right Ventricular Lead Perforation Presenting as Left Chest Wall Muscle Stimulation. See p e451. Download figureDownload PowerPointPosterior Descending Artery Milking-Like Effect Caused by Ventricle Pseudoaneurysm Compression. See p e453.CorrespondenceSee p e455. Previous Back to top Next FiguresReferencesRelatedDetails June 28, 2005Vol 111, Issue 25 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.111.25.3341 Originally publishedJune 28, 2005 PDF download Advertisement