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HomeCirculationVol. 112, No. 2Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published12 Jul 2005https://doi.org/10.1161/circ.112.2.147Circulation. 2005;112:147EFFECT OF PRAVASTATIN ON RATE OF KIDNEY FUNCTION LOSS IN PEOPLE WITH OR AT RISK FOR CORONARY DISEASE, by Tonelli et al.Renal dysfunction is an independent risk factor for cardiovascular disease and its associated complications. Prior studies have suggested that lipid-lowering medications may reduce the rate of loss of renal function. A group of investigators from three large pravastatin studies (CARE, LIPID, and WOSCOPS) combined their data from more than 18 thousand patients, followed up for 5 years, either with previous coronary events or at high risk of cardiovascular disease. In patients with moderate chronic kidney disease, pravastatin reduced the rate of loss of renal function by about 8% and also reduced the risk of acute renal failure. The mechanisms of benefit are unknown but may include the antiinflammatory effects of statins or reduction in renal atherosclerosis. Further studies will be needed to determine the effect of statins in patients with more severe renal dysfunction. See p 171.HEREDITARY HEMOCHROMATOSIS AND RISK OF ISCHEMIC HEART DISEASE: A PROSPECTIVE STUDY AND A CASE-CONTROL STUDY, by Ellervik et al.The potential link between iron levels and the risk of coronary artery disease has been termed the “iron hypothesis.” Some have speculated that the oxidation of iron produces free hydroxyl radicals, leading to more oxidized LDL particles and subsequent atherosclerosis. These investigators use hereditary hemochromatosis to study the effect of iron overload on risk of ischemic heart disease. They conducted a prospective study with long follow-up and a case-control study to investigate the association of specific hereditary hemochromatosis genotypes with the risk of ischemic heart disease. They also examined the relationship of these genotypes with oxidized LDL, transferrin saturation, and ferritin levels. Thus, the study provides insight about the overall association and whether it is mediated through oxidized LDL. See p 185.ALLOGENEIC MESENCHYMAL STEM CELL TRANSPLANTATION IN POSTINFARCTED RAT MYOCARDIUM: SHORT- AND LONG-TERM EFFECTS, by Dai et al.Although prior studies have demonstrated that the injection of stem cells results in improvement in global myocardial function after myocardial infarction, the mechanism for this beneficial effect remains elusive. In rat hearts in which mesenchymal stem cells were injected into the scar one week after myocardial infarction, Dai et al compared the time courses for the improvement in cardiac function and the expression of muscle-specific markers. Cardiac function was improved one month after injection, at a time when mesenchymal stem cells did not express muscle-specific markers. In contrast, after 6 months, muscle-specific markers were expressed, but cardiac function was no longer improved. This study raises the possibility that improved cardiac function in this setting is not related to contractile properties of the implanted cells but rather may relate to a paracrine action on preexisting myocytes. See p 214.Visit http://www.circ.ahajournals.org:Clinician UpdateManagement of Massive Pulmonary Embolism. See p e28.Images in Cardiovascular MedicineTransient Occlusion of the Middle Cerebral Artery by Macroembolism During Carotid Stenting for Traumatic Dissection of the Common Carotid Artery. See p e33.Download figureDownload PowerPointIntegration of 3-Dimensional Cardiac Computed Tomography Images With Real-Time Electroanatomic Mapping to Guide Catheter Ablation of Atrial Fibrillation. See p e35.CorrespondenceSee p e37. Previous Back to top Next FiguresReferencesRelatedDetailsCited By Boink G, Seppen J, de Bakker J and Tan H (2006) Gene therapy to create biological pacemakers, Medical & Biological Engineering & Computing, 10.1007/s11517-006-0112-7, 45:2, (167-176), Online publication date: 1-Feb-2007. Boink G, Seppen J, de Bakker J and Tan H (2007) Gene Therapy to Create Biological Pacemakers Biopacemaking, 10.1007/978-3-540-72110-9_6, (79-93), . July 12, 2005Vol 112, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.112.2.147 Originally publishedJuly 12, 2005 PDF download Advertisement