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HomeCirculationVol. 110, No. 24Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published14 Dec 2004https://doi.org/10.1161/circ.110.24.3617Circulation. 2004;110:3617CHRONIC KIDNEY DISEASE, CARDIOVASCULAR RISK, AND RESPONSE TO ANGIOTENSIN-CONVERTING ENZYME INHIBITION AFTER MYOCARDIAL INFARCTION: THE SURVIVAL AND VENTRICULAR ENLARGEMENT (SAVE) STUDY, by Tokmakova et al.It is well known that kidney disease portends increased cardiovascular mortality. This increased risk is likely to be largely due to hypertension, dyslipidemia, and anemia associated with kidney disease, but unknown factors contributing to plaque rupture also may play a role. ACE inhibitors have been shown to reduce the risk of myocardial infarction and death in patients with chronic kidney disease but often are not prescribed because of concerns about deterioration in kidney function. The SAVE investigators report, from their randomized study of captopril versus placebo in 2000 patients with ejection fractions <40% after acute myocardial infarction, that heightened cardiovascular risk occurred at a threshold of an estimated glomerular filtration rate (GFR) of 60 mL · min−1 · 1.73 m−2. Captopril tended to have a larger relative treatment effect and a greater absolute benefit in reducing the risk of cardiovascular events, including myocardial infarction, in patients with lower GFRs. Only 9 patients with GFRs <60 mL · min−1 · 1.73 m−2 needed to be treated for 31/2 years to reduce 1 cardiovascular event. See p 3667.IMPAIRED l-ARGININE TRANSPORT AND ENDOTHELIAL FUNCTION IN HYPERTENSIVE AND GENETICALLY PREDISPOSED NORMOTENSIVE SUBJECTS, by Schlaich et al.Prior studies have demonstrated dysfunction of the vascular endothelium in patients with hypertension, but the underlying mechanisms remain incompletely defined. In this regard, experimental studies have implicated impaired transport of l-arginine into endothelial cells, leading to an intracellular deficiency of the substrate for synthesis of nitric oxide. In this issue of Circulation, Schlaich and colleagues demonstrate impaired uptake of l-arginine in the forearm and into isolated blood monocytes in patients with hypertension. Interestingly, the results were similar in normotensive individuals with a family history of hypertension. The mechanisms accounting for impaired l-arginine transport were not determined in this human study and will require further study; however, these findings provide further evidence that loss of endothelium-derived nitric oxide precedes the development of hypertension and thus may contribute to the underlying pathogenesis of the disease in some individuals. See p 3680.GENOME-WIDE SCAN FOR JAPANESE FAMILIAL INTRACRANIAL ANEURYSMS: LINKAGE TO SEVERAL CHROMOSOMAL REGIONS, by Yamada et al.According to the American Stroke Association (http://www.americanheart.org/presenter.jhtml?identifier=3018827) it is estimated that about 3 to 5 million people in the United States have cerebral aneurysms, the vast majority of which are asymptomatic. However, bleeding occurs in approximately 0.5% to 3% of intracranial aneurysms, leading to major morbidity and mortality. Family history of aneurysm is known to be a risk factor, with first-degree relatives having a 4-fold increased risk of intracranial aneurysms. In this issue of Circulation, Yamada, Utsunomiya, and colleagues describe 29 Japanese intracranial aneurysm families with at least 3 affected relatives. They performed a genome-wide linkage scan and found several areas of suggestive linkage on chromosomes 17 and 19 and the X chromosome. The investigators examined polymorphisms in 4 potential, attractive candidate genes but found no evidence of association. The study describes attractive regions for further investigation of genetic susceptibility for intracranial aneurysms but underscores the difficulty in pinpointing the genetic determinants of complex diseases. See p 3727.Visit www.circ.ahajournals.org:Images In Cardiovascular MedicineEsophageal Migration During Left Atrial Catheter Ablation for Atrial Fibrillation. See p e528.Cardiac Sarcoidosis in a Patient With Hypertrophic Cardiomyopathy Demonstrated by Magnetic Resonance Imaging and Single Photon Emission Computed Tomography Dual-Isotope Scintigraphy. See p e529.CorrespondenceLetter Regarding Article by Ridker et al, “Should C-Reactive Protein Be Added to Metabolic Syndrome and to Assessment of Global Cardiovascular Risk?” See p e532.Download figureDownload PowerPoint Previous Back to top Next FiguresReferencesRelatedDetails December 14, 2004Vol 110, Issue 24 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.110.24.3617 Originally publishedDecember 14, 2004 PDF download Advertisement