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HomeCirculationVol. 113, No. 23Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published13 Jun 2006https://doi.org/10.1161/circ.113.23.2675Circulation. 2006;113:2675SINGLE-GENE MUTATIONS AND INCREASED LEFT VENTRICULAR WALL THICKNESS IN THE COMMUNITY: THE FRAMINGHAM HEART STUDY, by Morita et al.Left ventricular hypertrophy (LVH) is associated with stroke, coronary heart disease, heart failure, and cardiovascular and all-cause mortality. LVH results from increases in LV wall thickness (LVWT), LV mass, and LV volume. Unexplained increases in LVWT (LVWT 13mm) contribute to LVH in 3% of the general population over the age of 45. Mutations in sarcomere protein, PRKAG2, LAMP2, α-galactosidase A (GLA), and several mitochondrial genes are associated with rare familial cardiomyopathies; their contribution to LVH in the community is unknown, however. Morita et al identified the prevalence and clinical features of single-gene mutations in adults in the community with increased LVWT in the absence of obvious secondary forms of hypertrophy. Among 1862 Framingham Heart Study participants, 50 had unexplained increased LVWT. Eight subjects (16%) had sarcomere protein gene mutations and one (2%) had a GLA mutation. Therefore, approximately 0.5% of the general population over age 45 has increased unexplained LVWT and a single-gene mutation that probably accounts for their hypertrophy. Increased LVWT in the community is a heterogeneous condition, and additional investigation of the prevalence and clinical features of single-gene mutations in other community-based cohorts will help improve our understanding of the broad spectrum of genetic causes of increased LVWT. See p 2697.AEROBIC CAPACITY IN PATIENTS ENTERING CARDIAC REHABILITATION, by Ades et al.Exercise training is a key component of comprehensive cardiac rehabilitation/secondary prevention programs and generally yields marked improvements in exercise capacity, particularly among those with the lowest initial fitness levels. In this issue of Circulation, Ades et al provide normative values for exercise capacity relative to age, gender, and diagnosis among patients entering cardiac rehabilitation that are derived from 2896 patients. The nomograms provided in this paper will serve to assist the clinician in comparing patient status relative to program peers and established norms, motivating the patient, and setting exercise training goals. Incorporation of this important information into the initial patient assessment should serve to enhance the treatment of patients as they enter cardiac rehabilitation programs. See p 2706.HEMOGLOBIN LEVEL, CHRONIC KIDNEY DISEASE, AND THE RISKS OF DEATH AND HOSPITALIZATION IN ADULTS WITH CHRONIC HEART FAILURE: THE ANEMIA IN CHRONIC HEART FAILURE: OUTCOMES AND RESOURCE UTILIZATION (ANCHOR) STUDY, by Go et al.Although several retrospective studies have suggested a link between anemia and adverse events in patients with heart failure, the roles of renal insufficiency, treatment differences, and comorbidities in leading to this relationship have not been clear. Go et al examined longitudinal outpatient hemoglobin and creatinine levels in 59 722 adults with heart failure in an integrated healthcare system. Decreasing hemoglobin and calculated glomerular filtration rate were both associated with increased mortality, and these associations were independent of whether heart failure was due to systolic or diastolic ventricular dysfunction. These results from a large outpatient population support the thesis that anemia and renal dysfunction are independent predictors of adverse outcomes in patients with heart failure. See p 2713.Visit http://circ.ahajournals.org:Images in Cardiovascular MedicineLarge Renal Artery Aneurysm Treated With Stent Graft. See p e848.Severe Endothelial Dysfunction After Sirolimus-Eluting Stent Implantation. See p e850.A 54-Year-Old Female With Chest Pain, Dyspnea, and Inferior Injury on Electrocardiography. See p e852. Download figureDownload PowerPointBook ReviewMolecular Mechanisms of Cardiac Hypertrophy and Failure. See p e853.CorrespondenceSee p e854. Previous Back to top Next FiguresReferencesRelatedDetails June 13, 2006Vol 113, Issue 23 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.113.23.2675 Originally publishedJune 13, 2006 PDF download Advertisement