HomeCirculationVol. 114, No. 3Issue Highlights Free AccessIn BriefPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessIn BriefPDF/EPUBIssue Highlights Originally published18 Jul 2006https://doi.org/10.1161/circ.114.3.183Circulation. 2006;114:183PLASMA PHOSPHOLIPIDTRANSFATTY ACIDS, FATAL ISCHEMIC HEART DISEASE, AND SUDDEN CARDIAC DEATH IN OLDER ADULTS: THE CARDIOVASCULAR HEALTH STUDY, by Lemaitre et al.Higher dietary consumption of trans fatty acids has been associated with elevated risk of coronary heart disease. Data are limited, however, regarding variation in coronary risk according to the type of trans fatty acid, eg, trans-isomers of oleic acid (trans-18:1) versus trans-isomers of linoleic acid (trans-18:2). In this issue of Circulation, Lemaitre and colleagues conducted a nested case-control study using data from elderly participants in the Cardiovascular Health Study. The investigators compared plasma trans-18:1 and trans-18:2 levels (collected 3 years before occurrence of events) in 214 individuals (cases) with fatal coronary heart disease with plasma levels of these trans fatty acids in 214 matched controls. They report that higher plasma trans-18:2 levels were associated with greater risk of fatal ischemic heart disease and sudden cardiac death in multivariable analyses that adjusted for clinical and lifestyle risk factors including plasma levels of n-3 polyunsaturated fatty acids. In contrast, higher levels of trans-18:1 were associated with lower risk. These observations suggest that different types of trans-isomers in the diet may influence coronary risk differentially. If confirmed, these findings suggest that current efforts at decreasing trans fatty acid intake in foods should take into consideration their trans-18:2 content. See p 209.PREVALENCE, CLINICAL PROFILE, AND SIGNIFICANCE OF LEFT VENTRICULAR REMODELING IN THE END-STAGE PHASE OF HYPERTROPHIC CARDIOMYOPATHY, by Harris et al.A minority of patients with hypertrophic cardiomyopathy (HCM) enter a phase known as “end-stage,” thought to be represented by systolic dysfunction, left ventricular dilation, and thinning of previously hypertrophied walls. In this issue of Circulation, Harris and colleagues provide results of the largest group of end-stage patients reported to date, culled from a large multicenter cohort of over 1200 HCM patients. These data demonstrate a far more diverse pattern of left ventricular (LV) remodeling than has been appreciated—including a significant number of patients who, despite an abnormal ejection fraction, still maintain normal LV cavity size and/or persistently hypertrophied LV walls. Furthermore, the clinical course appears largely unfavorable, with a substantial number of sudden arrhythmic deaths as well as heart failure events or transplantations occurring over a short period following clinical recognition. This study provides broader insight into the prevalence, morphology, and clinical course of this unique subset of HCM patients, with the hope of earlier disease recognition and with implications for aggressive treatment interventions. See p 216.ANGIOTENSIN II TYPE I RECEPTOR BLOCKADE PREVENTS ALCOHOLIC CARDIOMYOPATHY, by Cheng et al.The mechanism responsible for alcoholic cardiomyopathy is not known. Cheng et al caused myocardial dysfunction in dogs by feeding them alcohol once daily accounting for 33% of daily calorie intake. Alcohol caused activation of the renin-angiotensin system (RAS) at virtually all levels, including increased plasma angiotensin, renin activity, myocardial angiotensin-converting-enzyme activity and cardiac myocyte angiotensin II type 1 receptor expression. Alcohol was also associated with abnormalities in myocardial contractility, and at the isolated myocyte level, with reduced shortening, prolonged relaxation, and decreased calcium transient amplitude. Treatment with the angiotensin receptor blocker ibresartan reduced the activation of the RAS and corrected the functional abnormalities at the myocardial and isolated myocyte levels. These observations thus implicate the RAS in the pathophysiology of alcoholic myocardial dysfunction, and suggest a potentially useful therapeutic role for the angiotensin receptor blocker. See p 226.Visit http://circ.ahajournals.org:Clinician UpdateAcute Pulmonary Embolism: Part II: Treatment and Prophylaxis. See p e42.Images in Cardiovascular MedicineHereditary Hemorrhagic Telangiectasia With Pulmonary Arteriovenous Fistulas. See p e48.Iatrogenic Left Ventricle-to-Coronary Venous Fistula. See p e50.Epicardial Radiofrequency Catheter Ablation of Ventricular Tachycardia in the Vicinity of Coronary Arteries Is Facilitated by Fusion of 3-Dimensional Electroanatomical Mapping With Multislice Computed Tomography. See p e51. Download figureDownload PowerPointCorrespondenceSee p e53. Previous Back to top Next FiguresReferencesRelatedDetails July 18, 2006Vol 114, Issue 3 Advertisement Article InformationMetrics https://doi.org/10.1161/circ.114.3.183 Originally publishedJuly 18, 2006 PDF download Advertisement SubjectsHeart Failure
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