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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/?rss=yes"><title>Journal of the American College of Cardiology</title><description>Journal of the American College of Cardiology RSS feed: Current Issue. 
 As the leader in its field,  JACC  publishes original peer-reviewed clinical and experimental reports 
on all aspects of cardiovascular disease. Topics covered include coronary artery and valve disease, congenital heart defects, vascular 
surgery, cardiomyopathy, drug treatment, new diagnostic techniques, findings from the laboratory, and large multicenter studies of new 
therapies.  JACC  also publishes abstracts of papers presented at the annual scientific sessions of the American College of Cardiology 
and the reports and recommendations of the Bethesda Conferences on current topics in cardiovascular disease.</description><link>http://www.journals.elsevierhealth.com/periodicals/jac/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:issn>0735-1097</prism:issn><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:publicationDate>24 November 2009</prism:publicationDate><prism:copyright> © 2009 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029283/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029222/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970902926X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031969/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970903201X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029246/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029192/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029295/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031453/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031465/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970903143X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031477/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029350/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031441/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031489/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029751/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029763/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970902974X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709022475/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709023857/abstract?rss=yes"/><rdf:li rdf:resource="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709035463/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029283/abstract?rss=yes"><title>Appropriate Evaluation and Treatment of Heart Failure Patients After Implantable Cardioverter-Defibrillator Discharge: Time to Go Beyond the Initial Shock</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029283/abstract?rss=yes</link><description>Multiple clinical trials support the use of implantable cardioverter-defibrillators (ICDs) for prevention of sudden cardiac death in patients with heart failure (HF). Unfortunately, several complicating issues have arisen from the universal use of ICDs in HF patients. An estimated 20% to 35% of HF patients who receive an ICD for primary prevention will experience an appropriate shock within 1 to 3 years of implant, and one-third of patients will experience an inappropriate shock. An ICD shock is associated with a 2- to 5-fold increase in mortality, with the most common cause being progressive HF. The median time from initial ICD shock to death ranges from 168 to 294 days depending on HF etiology and the appropriateness of the ICD therapy. Despite this prognosis, current guidelines do not provide a clear stepwise approach to managing these high-risk patients. An ICD shock increases HF event risk and should trigger a thorough evaluation to determine the etiology of the shock and guide subsequent therapeutic interventions. Several combinations of pharmacologic and device-based interventions such as adding amiodarone to baseline beta-blocker therapy, adjusting ICD sensitivity, and employing antitachycardia pacing may reduce future appropriate and inappropriate shocks. Aggressive HF surveillance and management is required after an ICD shock, as the risk of sudden cardiac death is transformed to an increased HF event risk.</description><dc:title>Appropriate Evaluation and Treatment of Heart Failure Patients After Implantable Cardioverter-Defibrillator Discharge: Time to Go Beyond the Initial Shock</dc:title><dc:creator>Joseph D. Mishkin, Sherry J. Saxonhouse, Gregory W. Woo, Thomas A. Burkart, William M. Miles, Jamie B. Conti, Richard S. Schofield, Samuel F. Sears, Juan M. Aranda</dc:creator><dc:identifier>10.1016/j.jacc.2009.07.039</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>State-of-the-Art Paper</prism:section><prism:startingPage>1993</prism:startingPage><prism:endingPage>2000</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029222/abstract?rss=yes"><title>Implantable Cardioverter-Defibrillator Therapy After Acute Myocardial Infarction: The Results Are Not Shocking</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029222/abstract?rss=yes</link><description>The risk of sudden death is highest early after myocardial infarction (MI) and progressively declines over the ensuing 6 to 12 months. Nevertheless, several randomized clinical trials have failed to show a survival benefit for implantable cardioverter-defibrillators when implanted early after MI in high-risk patients. The etiology of this acute MI–sudden cardiac death paradox is unclear, but may be related to the changing nature of the substrate over the several month period after acute MI. Further investigation is needed to delineate the actual causes of death in the early post-MI period and which interventions can be implemented to reduce the increased rate of sudden death that is observed.</description><dc:title>Implantable Cardioverter-Defibrillator Therapy After Acute Myocardial Infarction: The Results Are Not Shocking</dc:title><dc:creator>Jeffrey J. Goldberger, Rod Passman</dc:creator><dc:identifier>10.1016/j.jacc.2009.08.018</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Viewpoint</prism:section><prism:startingPage>2001</prism:startingPage><prism:endingPage>2005</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970902926X/abstract?rss=yes"><title>Women Have a Lower Prevalence of Structural Heart Disease as a Precursor to Sudden Cardiac Arrest: The Ore-SUDS (Oregon Sudden Unexpected Death Study)</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970902926X/abstract?rss=yes</link><description>Objectives: Our aim was to utilize a community-based approach to identify sex-related differences in risk factors for sudden cardiac arrest (SCA).Background: There are significant sex-based differences in prevalence and manifestation of SCA. Any differences related to predictors of SCA in women versus men are likely to have implications for risk stratification and prevention.Methods: The Ore-SUDS (Oregon Sudden Unexpected Death Study) is an ongoing prospective investigation of SCA in the Portland, Oregon, metropolitan area (population approximately 1 million). All cases meeting criteria for SCA were ascertained using multiple sources. Medical records were reviewed to identify clinical conditions that may contribute to SCA risk, and comparisons were made between male and female SCA cases using Pearson's chi-square tests for categorical variables, t tests for continuous variables, and multivariate logistic regression analysis.Results: During 2002 to 2007, 1,568 adult SCA cases were identified (women 36% vs. men 64%; p &lt; 0.0001) and women were older (mean age 71 ± 14 years vs. 65 ± 14 years, p &lt; 0.0001). There were no significant sex differences in prevalence of obesity, dyslipidemia, history of chronic obstructive pulmonary disease/asthma, left ventricular (LV) hypertrophy, or history of myocardial infarction. In multivariate analysis, women were significantly less likely to have severe LV dysfunction (odds ratio: 0.51; 95% confidence interval: 0.31 to 0.84) or previously recognized coronary artery disease (odds ratio: 0.34; 95% confidence interval: 0.20 to 0.60) compared with men.Conclusions: Women were significantly less likely than men to have a diagnosis of structural heart disease (LV dysfunction or coronary artery disease) before SCA. These findings suggest that fewer women may be eligible for prophylactic implantable cardioverter-defibrillator placement based on current guidelines and therefore may not have equal opportunity for prevention. Enhancement of SCA risk stratification may have even higher importance for women.</description><dc:title>Women Have a Lower Prevalence of Structural Heart Disease as a Precursor to Sudden Cardiac Arrest: The Ore-SUDS (Oregon Sudden Unexpected Death Study)</dc:title><dc:creator>Sumeet S. Chugh, Audrey Uy-Evanado, Carmen Teodorescu, Kyndaron Reinier, Ronald Mariani, Karen Gunson, Jonathan Jui</dc:creator><dc:identifier>10.1016/j.jacc.2009.07.038</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Clinical Research</prism:section><prism:startingPage>2006</prism:startingPage><prism:endingPage>2011</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031969/abstract?rss=yes"><title>Clinical Benefits of Remote Versus Transtelephonic Monitoring of Implanted Pacemakers</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031969/abstract?rss=yes</link><description>Objectives: The purpose of this study was to evaluate remote pacemaker interrogation for the earlier diagnosis of clinically actionable events compared with traditional transtelephonic monitoring and routine in-person evaluation.Background: Pacemaker patient follow-up procedures have evolved from evaluating devices with little programmability and diagnostic information solely in person to transtelephonic rhythm strip recordings that allow monitoring of basic device function. More recently developed remote monitoring technology leverages expanded device capabilities, augmenting traditional transtelephonic monitoring to evaluate patients via full device interrogation.Methods: The time to first diagnosis of a clinically actionable event was compared in patients who were followed by remote interrogation (Remote) and those who were followed per standard of care with office visits augmented by transtelephonic monitoring (Control). Patients were randomized 2:1. Remote arm patients transmitted pacemaker information at 3-month intervals. Control arm patients with a single-chamber pacemaker transmitted at 2-month intervals. Control arm patients with dual-chamber devices transmitted at 2-month intervals with an office visit at 6 months. All patients were seen in office at 12 months.Results: The mean time to first diagnosis of clinically actionable events was earlier in the Remote arm (5.7 months) than in the Control arm (7.7 months). Three (2%) of the 190 events in the Control arm and 446 (66%) of 676 events in the Remote arm were identified remotely.Conclusions: The strategic use of remote pacemaker interrogation follow-up detects actionable events that are potentially important more quickly and more frequently than transtelephonic rhythm strip recordings. The use of transtelephonic rhythm strips for pacemaker follow-up is of little value except for battery status determinations. (PREFER [Pacemaker Remote Follow-up Evaluation and Review]; NCT00294645)</description><dc:title>Clinical Benefits of Remote Versus Transtelephonic Monitoring of Implanted Pacemakers</dc:title><dc:creator>George H. Crossley, Jane Chen, Wassim Choucair, Todd J. Cohen, Douglas C. Gohn, W. Ben Johnson, Eleanor E. Kennedy, Luc R. Mongeon, Gerald A. Serwer, Hongyan Qiao, Bruce L. Wilkoff, PREFER Study Investigators</dc:creator><dc:identifier>10.1016/j.jacc.2009.10.001</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2012</prism:startingPage><prism:endingPage>2019</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970903201X/abstract?rss=yes"><title>Transtelephonic Versus Remote Monitoring of Cardiovascular Implantable Electronic Devices: Is One Approach to Be Preferred?⁎</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970903201X/abstract?rss=yes</link><description>Intracardiac pacemaker implantation was first described a half century ago; the same authors first reported on transtelephonic monitoring (TTM) of such devices a dozen years later (). Follow-up of the pacemaker patient was recognized as critical, particularly in view of the uncertain reliability associated with leads and generators. Tracking device longevity and function have remained an important problem (), compounded by the development of more widespread indications for pacemakers (), increasingly complex devices, and mounting advisories that attest to an ever-present threat of premature device failure (). Ironically, the population at risk of device malfunction has expanded due to medical and technological advances resulting in greater patient and pacemaker longevity. Device follow-up technology has also evolved, inevitably raising the question “how are pacemaker patients and their devices best monitored?”</description><dc:title>Transtelephonic Versus Remote Monitoring of Cardiovascular Implantable Electronic Devices: Is One Approach to Be Preferred?⁎</dc:title><dc:creator>Mark H. Schoenfeld</dc:creator><dc:identifier>10.1016/j.jacc.2009.09.019</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Editorial Comment</prism:section><prism:startingPage>2020</prism:startingPage><prism:endingPage>2022</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029246/abstract?rss=yes"><title>Atrial Fibrillation at Baseline and During Follow-Up in ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial)</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029246/abstract?rss=yes</link><description>Objectives: The ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial) determined that treatment with amlodipine, lisinopril, or doxazosin was not superior to thiazide-like diuretic (chlorthalidone) in preventing coronary heart disease (CHD) or other cardiovascular events. This subanalysis examines baseline prevalence and in-trial incidence of new-onset atrial fibrillation (AF) or atrial flutter (AFL) and their influence on clinical outcomes.Background: Limited information is available on whether atrial fibrillation incidence is affected differentially by different classes of antihypertensive medications or treatment with statins.Methods: AF/AFL was identified from baseline and follow-up electrocardiograms performed biannually. Analyses were performed to identify characteristics associated with baseline AF/AFL and its subsequent incidence.Results: AF/AFL was present at baseline in 423 participants (1.1%), more frequent in men (odds ratio: 1.72; 95% confidence interval [CI]: 1.37 to 2.17) and nonblacks (odds ratio: 2.09; 95% CI: 1.58 to 2.75). Its prevalence increased with age (p &lt; 0.001) and was associated with CHD, cardiovascular disease, obesity, and high-density lipoprotein cholesterol &lt;35 mg/dl. New-onset AF/AFL was associated with the same baseline risk factors plus electrocardiogram left ventricular hypertrophy. It occurred in 641 participants (2.0%) and, excluding doxazosin, did not differ by antihypertensive treatment group or, in a subset of participants, by pravastatin versus usual care. Baseline AF/AFL was associated with increased mortality (hazard ratio [HR]: 2.82; 95% CI: 2.36 to 3.37; p &lt; 0.001), stroke (HR: 3.63; 95% CI: 2.72 to 4.86; p &lt; 0.001), heart failure (HR: 3.17; 95% CI: 2.38 to 4.25; p &lt; 0.001), and fatal CHD or nonfatal myocardial infarction (HR: 1.64; 95% CI: 1.22 to 2.21; p &lt; 0.01). There was a nearly 2.5-fold increase in mortality risk when AF/AFL was present at baseline or developed during the trial (HR: 2.42; 95% CI: 2.11 to 2.77; p &lt; 0.001).Conclusions: In this high-risk hypertensive population, pre-existing and new-onset AF/AFL were associated with increased mortality. Excluding doxazosin, treatment assignment to either antihypertensive drugs or pravastatin versus usual care did not affect AF/AFL incidence. (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [ALLHAT]; NCT00000542)</description><dc:title>Atrial Fibrillation at Baseline and During Follow-Up in ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial)</dc:title><dc:creator>L. Julian Haywood, Charles E. Ford, Richard S. Crow, Barry R. Davis, Barry M. Massie, Paula T. Einhorn, Angela Williard, ALLHAT Collaborative Research Group</dc:creator><dc:identifier>10.1016/j.jacc.2009.08.020</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2023</prism:startingPage><prism:endingPage>2031</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029192/abstract?rss=yes"><title>Role of the CHADS2 Score in the Evaluation of Thromboembolic Risk in Patients With Atrial Fibrillation Undergoing Transesophageal Echocardiography Before Pulmonary Vein Isolation</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029192/abstract?rss=yes</link><description>Objectives: The goals of this study were to determine: 1) if low-risk patients assessed by a CHADS2 score, a clinical scoring system quantifying a risk of stroke in patients with atrial fibrillation (AF), require a routine screening transesophageal echocardiogram (TEE) before pulmonary vein isolation (PVI); and 2) the relationship of a CHADS2 score with left atrial (LA)/left atrial appendage (LAA) spontaneous echo contrast, sludge, and thrombus.Background: There is no clear consensus of whether a screening TEE before catheter ablation of AF should be performed in every patient.Methods: Initial TEEs for pre-PVI of 1,058 AF patients (age 57 ± 11 years, 80% men) were reviewed and compared with a CHADS2 score.Results: CHADS2 scores of 0, 1, 2, 3, 4, 5, and 6 were present in 47%, 33%, 14%, 5%, 1%, 0.3%, and 0% of patients, respectively. The prevalence of LA/LAA thrombus, sludge, and spontaneous echo contrast were present in 0.6%, 1.5%, and 35%. The prevalence of LA/LAA thrombus/sludge increased with ascending CHADS2 score (scores 0 [0%], 1 [2%], 2 [5%], 3 [9%], and 4 to 6 [11%], p &lt; 0.01). No patient with a CHADS2 score of 0 had LA/LAA sludge/thrombus. In a multivariate model, history of congestive heart failure and left ventricular ejection fraction &lt;35% were significantly associated with sludge/thrombus.Conclusions: The prevalence of LA/LAA sludge/thrombus in patients with AF undergoing a pre-PVI screening TEE is very low (&lt;2%) and increases significantly with higher CHADS2 scores. This suggests that a screening TEE before PVI should be performed in patients with a CHADS2 score of ≥1, and in patients with a CHADS2 score of 0 when the AF is persistent and therapeutic anticoagulation has not been maintained for 4 weeks before the procedure.</description><dc:title>Role of the CHADS2 Score in the Evaluation of Thromboembolic Risk in Patients With Atrial Fibrillation Undergoing Transesophageal Echocardiography Before Pulmonary Vein Isolation</dc:title><dc:creator>Sarinya Puwanant, Brandon C. Varr, Kevin Shrestha, Sarah K. Hussain, W.H. Wilson Tang, Ruvin S. Gabriel, Oussama M. Wazni, Mandeep Bhargava, Walid I. Saliba, James D. Thomas, Bruce D. Lindsay, Allan L. Klein</dc:creator><dc:identifier>10.1016/j.jacc.2009.07.037</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2032</prism:startingPage><prism:endingPage>2039</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029295/abstract?rss=yes"><title>Transesophageal Echocardiography Before Atrial Fibrillation Ablation: Looking Before Cooking⁎</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029295/abstract?rss=yes</link><description>In many electrophysiology laboratories, atrial fibrillation (AF) is becoming the most common heart rhythm disorder being treated with catheter ablation. Reasons for this include the large numbers of patients with AF, the poor quality of life commonly associated with AF, the limitations of drug therapy, advances in ablation tools and methods, and the increasing number of electrophysiologists trained in the technique. Catheter ablation is now recognized as a legitimate option for patients with symptomatic AF who have failed antiarrhythmic drug therapy ().</description><dc:title>Transesophageal Echocardiography Before Atrial Fibrillation Ablation: Looking Before Cooking⁎</dc:title><dc:creator>Bradley P. Knight</dc:creator><dc:identifier>10.1016/j.jacc.2009.07.040</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Editorial Comment</prism:section><prism:startingPage>2040</prism:startingPage><prism:endingPage>2042</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031453/abstract?rss=yes"><title>A Comparison of Atrial Arrhythmias After Heart or Double-Lung Transplantation at a Single Center: Insights Into the Mechanism of Post-Operative Atrial Fibrillation</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031453/abstract?rss=yes</link><description>Objectives: We compared the incidence of atrial arrhythmias in double-lung transplant patients versus heart transplant patients to gain insight into factors that contribute to post-operative atrial fibrillation (AF).Background: Atrial fibrillation is a common complication after thoracic surgery. Pulmonary vein isolation is an effective treatment for AF. Heart or double-lung transplantation surgery both involve pulmonary vein isolation because of suture lines.Methods: We reviewed the records of 174 consecutive heart transplant patients and 122 double-lung transplant patients at the Columbia Presbyterian Medical Center between January 2005 and June 2008. Electrocardiograms during atrial arrhythmia episodes were reviewed by an electrophysiologist. Clinical variables, biopsy results, immunosuppressive regimens, and echocardiographic measurements were collected from the perioperative time period and at the time of arrhythmia occurrence.Results: In the heart transplant group, 8 (4.6%) patients had AF (group A). In the lung transplant group, 23 (18.9%) patients had AF (group B; p &lt; 0.001). The incidence of AF in a comparison group of 131 patients with normal left ventricular function who underwent coronary artery bypass graft surgery was 19.8%. Immunosuppressive regimens and clinical variables were similar for both groups. Echocardiographic data revealed no significant cardiac abnormalities in 74% of group B compared with 25% of group A (p &lt; 0.05), and 78% of biopsy results in group B were normal, whereas only 25% of group A results were normal (p &lt; 0.05).Conclusions: In heart transplant recipients, AF is uncommon and occurs in the setting of myocardial dysfunction and graft rejection. In contrast, AF is more common after lung transplantation despite the absence of graft rejection and cardiac dysfunction. Pulmonary vein isolation alone cannot explain the discrepancy in AF incidence between heart transplant recipients and double-lung transplant recipients. Cardiac autonomic denervation may have a protective effect for heart transplant patients in the post-operative setting.</description><dc:title>A Comparison of Atrial Arrhythmias After Heart or Double-Lung Transplantation at a Single Center: Insights Into the Mechanism of Post-Operative Atrial Fibrillation</dc:title><dc:creator>José Dizon, Kimberly Chen, Matthew Bacchetta, Michael Argenziano, Donna Mancini, Angelo Biviano, Joshua Sonett, Hasan Garan</dc:creator><dc:identifier>10.1016/j.jacc.2009.08.029</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2043</prism:startingPage><prism:endingPage>2048</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031465/abstract?rss=yes"><title>Atrial Fibrillation After Major Thoracic Surgery: New Insights Into Underlying Mechanisms⁎</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031465/abstract?rss=yes</link><description>Atrial fibrillation (AF) is a common complication in patients undergoing major thoracic surgery (). It is most frequently observed acutely after valve surgery and/or coronary artery bypass graft surgery (CABG), but it can also manifest after lung and heart transplantation procedures (). Although mechanisms underlying this unique form of AF have not been adequately elucidated, it is likely that these involve a combination of pericardial inflammation, myocardial ischemia, catecholamine surge, autonomic imbalance, interstitial fluid mobilization, tissue rejection, and so forth (). It is interesting to note that AF is observed significantly less often after cardiac transplantation than after valve surgery and/or CABG (). This relative protection from AF after cardiac transplantation has been attributed to factors unique to this procedure, including the accomplishment of pulmonary vein (PV) isolation (because the technique involves implanting all 4 of the recipient's PVs along with the adjacent atrial cuff into the donor's left atrium), reduction in the arrhythmogenic substrate due to inadvertent left atrium “debulking,” autonomic denervation, and so forth (). However, because of the lack of any representative animal model and/or comparative clinical outcomes, these postulations have up until now largely remained speculative. In response to this lacuna, the study by Dizon et al. () in this issue of the Journal provides us with some additional insights into the mechanisms that may underlie the development of AF in patients undergoing major thoracic surgery.</description><dc:title>Atrial Fibrillation After Major Thoracic Surgery: New Insights Into Underlying Mechanisms⁎</dc:title><dc:creator>Sanjay Dixit</dc:creator><dc:identifier>10.1016/j.jacc.2009.09.015</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Editorial Comment</prism:section><prism:startingPage>2049</prism:startingPage><prism:endingPage>2051</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970903143X/abstract?rss=yes"><title>Genotype-Phenotype Aspects of Type 2 Long QT Syndrome</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970903143X/abstract?rss=yes</link><description>Objectives: The purpose of this study was to investigate the effect of location, coding type, and topology of KCNH2(hERG) mutations on clinical phenotype in type 2 long QT syndrome (LQTS).Background: Previous studies were limited by population size in their ability to examine phenotypic effect of location, type, and topology.Methods: Study subjects included 858 type 2 LQTS patients with 162 different KCNH2 mutations in 213 proband-identified families. The Cox proportional-hazards survivorship model was used to evaluate independent contributions of clinical and genetic factors to the first cardiac events.Results: For patients with missense mutations, the transmembrane pore (S5-loop-S6) and N-terminus regions were a significantly greater risk than the C-terminus region (hazard ratio [HR]: 2.87 and 1.86, respectively), but the transmembrane nonpore (S1–S4) region was not (HR: 1.19). Additionally, the transmembrane pore region was significantly riskier than the N-terminus or transmembrane nonpore regions (HR: 1.54 and 2.42, respectively). However, for nonmissense mutations, these other regions were no longer riskier than the C-terminus (HR: 1.13, 0.77, and 0.46, respectively). Likewise, subjects with nonmissense mutations were at significantly higher risk than were subjects with missense mutations in the C-terminus region (HR: 2.00), but that was not the case in other regions. This mutation location–type interaction was significant (p = 0.008). A significantly higher risk was found in subjects with mutations located in α-helical domains than in subjects with mutations in β-sheet domains or other locations (HR: 1.74 and 1.33, respectively). Time-dependent β-blocker use was associated with a significant 63% reduction in the risk of first cardiac events (p &lt; 0.001).Conclusions: The KCNH2 missense mutations located in the transmembrane S5-loop-S6 region are associated with the greatest risk.</description><dc:title>Genotype-Phenotype Aspects of Type 2 Long QT Syndrome</dc:title><dc:creator>Wataru Shimizu, Arthur J. Moss, Arthur A.M. Wilde, Jeffrey A. Towbin, Michael J. Ackerman, Craig T. January, David J. Tester, Wojciech Zareba, Jennifer L. Robinson, Ming Qi, G. Michael Vincent, Elizabeth S. Kaufman, Nynke Hofman, Takashi Noda, Shiro Kamakura, Yoshihiro Miyamoto, Samit Shah, Vinit Amin, Ilan Goldenberg, Mark L. Andrews, Scott McNitt</dc:creator><dc:identifier>10.1016/j.jacc.2009.08.028</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2052</prism:startingPage><prism:endingPage>2062</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031477/abstract?rss=yes"><title>Genotype–Phenotype Relationship in the Long QT Syndrome: Brimming With Knowledge but Thirsting for a Therapeutic Solution⁎</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031477/abstract?rss=yes</link><description>Since it was first reported 50 years ago, the long QT syndrome (LQTS) is now recognized as a genetic disease caused by mutations of ion channel genes encoding a cardiac channel essential for the control of ventricular repolarization (). The LQTS is not only the most common and extensively researched genetic cardiac arrhythmia (), it has also attracted premier scientists and scholars in single-cell electrophysiology and molecular genetics. In turn, they have produced seminal discoveries that shaped our understanding of the syndrome. The mutated genes in LQTS patients cause delayed repolarization and, in turn, prolong the QT interval on the surface electrocardiogram; these abnormalities are associated with torsade de pointes and/or ventricular fibrillation, resulting in the clinical manifestation of syncope and/or sudden death ().</description><dc:title>Genotype–Phenotype Relationship in the Long QT Syndrome: Brimming With Knowledge but Thirsting for a Therapeutic Solution⁎</dc:title><dc:creator>Koonlawee Nademanee</dc:creator><dc:identifier>10.1016/j.jacc.2009.09.016</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Editorial Comment</prism:section><prism:startingPage>2063</prism:startingPage><prism:endingPage>2064</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029350/abstract?rss=yes"><title>The RYR2-Encoded Ryanodine Receptor/Calcium Release Channel in Patients Diagnosed Previously With Either Catecholaminergic Polymorphic Ventricular Tachycardia or Genotype Negative, Exercise-Induced Long QT Syndrome: A Comprehensive Open Reading Frame Mutational Analysis</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029350/abstract?rss=yes</link><description>Objectives: This study was undertaken to determine the spectrum and prevalence of mutations in the RYR2-encoded cardiac ryanodine receptor in cases with exertional syncope and normal corrected QT interval (QTc).Background: Mutations in RYR2 cause type 1 catecholaminergic polymorphic ventricular tachycardia (CPVT1), a cardiac channelopathy with increased propensity for lethal ventricular dysrhythmias. Most RYR2 mutational analyses target 3 canonical domains encoded by &lt;40% of the translated exons. The extent of CPVT1-associated mutations localizing outside of these domains remains unknown as RYR2 has not been examined comprehensively in most patient cohorts.Methods: Mutational analysis of all RYR2 exons was performed using polymerase chain reaction, high-performance liquid chromatography, and deoxyribonucleic acid sequencing on 155 unrelated patients (49% females, 96% Caucasian, age at diagnosis 20 ± 15 years, mean QTc 428 ± 29 ms), with either clinical diagnosis of CPVT (n = 110) or an initial diagnosis of exercise-induced long QT syndrome but with QTc &lt;480 ms and a subsequent negative long QT syndrome genetic test (n = 45).Results: Sixty-three (34 novel) possible CPVT1-associated mutations, absent in 400 reference alleles, were detected in 73 unrelated patients (47%). Thirteen new mutation-containing exons were identified. Two-thirds of the CPVT1-positive patients had mutations that localized to 1 of 16 exons.Conclusions: Possible CPVT1 mutations in RYR2 were identified in nearly one-half of this cohort; 45 of the 105 translated exons are now known to host possible mutations. Considering that ≈65% of CPVT1-positive cases would be discovered by selective analysis of 16 exons, a tiered targeting strategy for CPVT genetic testing should be considered.</description><dc:title>The RYR2-Encoded Ryanodine Receptor/Calcium Release Channel in Patients Diagnosed Previously With Either Catecholaminergic Polymorphic Ventricular Tachycardia or Genotype Negative, Exercise-Induced Long QT Syndrome: A Comprehensive Open Reading Frame Mutational Analysis</dc:title><dc:creator>Argelia Medeiros-Domingo, Zahurul A. Bhuiyan, David J. Tester, Nynke Hofman, Hennie Bikker, J. Peter van Tintelen, Marcel M.A.M. Mannens, Arthur A.M. Wilde, Michael J. Ackerman</dc:creator><dc:identifier>10.1016/j.jacc.2009.08.022</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2065</prism:startingPage><prism:endingPage>2074</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031441/abstract?rss=yes"><title>The Role of Ganglionated Plexi in Apnea-Related Atrial Fibrillation</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031441/abstract?rss=yes</link><description>Objectives: This study was conducted to simulate sleep apnea-induced atrial fibrillation (AF) in an experimental model and to determine whether neural ablation will prevent AF.Background: An increasing number of clinical reports have associated sleep apnea and AF, and many possible mechanisms responsible for this relationship have been proposed.Methods: Thirty dogs anesthetized with Na-pentobarbital were ventilated by a positive pressure respirator. Protocol 1 (n = 14): After a right thoracotomy, atrial and pulmonary vein programmed pacing at 2× and 4× threshold determined the shortest atrial refractory period. Obstructive apnea was induced by turning off the respirator during end expiration for 2 min. During apnea, programmed pacing was performed with S1-S2 = 5 to 10 ms earlier than the atrial refractory period. Neural activity was monitored from the ganglionated plexi (GP) adjacent to the right pulmonary veins. Protocol 2 (n = 16): Electrical stimulation identified the GP at the right pulmonary artery (RPA). Programmed pacing was again instituted, below atrial refractory period, during 2 min of apnea. After radiofrequency ablation of the RPA GP, continuous programmed pacing was again repeated during 2 min of apnea. In 5 dogs, blood gases were determined at baseline and at 2 min of apnea.Results: Protocol 1: During apnea, S1-S2 induced AF within 85 ± 38 s (9 of 10). In 1 case, AF occurred spontaneously at 1 min 36 s of apnea. Recorded GP neural activity progressively increased before AF onset. Systolic but not diastolic blood pressure rose significantly before AF (149 ± 26 mm Hg to 193 ± 38 mm Hg, p &lt; 0.05). In 4 dogs, autonomic blockade prevented apnea-induced AF. Protocol 2: AF induced by pacing occurred in 8 of 11 dogs within the 2-min period of apnea, before neural ablation. After ablation, 0 of 6 showed AF during 2 min of apnea (p = 0.009).Conclusions: This experimental model of apnea shows a reproducible incidence of AF. After neural ablation of the RPA GP or autonomic blockade, AF inducibility was significantly inhibited.</description><dc:title>The Role of Ganglionated Plexi in Apnea-Related Atrial Fibrillation</dc:title><dc:creator>Muhammad Ghias, Benjamin J. Scherlag, Zhibing Lu, Guodong Niu, Annerie Moers, Warren M. Jackman, Ralph Lazzara, Sunny S. Po</dc:creator><dc:identifier>10.1016/j.jacc.2009.09.014</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>QUARTERLY FOCUS ISSUE: HEART RHYTHM DISORDERS</prism:section><prism:startingPage>2075</prism:startingPage><prism:endingPage>2083</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031489/abstract?rss=yes"><title>Sleep Apnea and Atrial Fibrillation: The Autonomic Link⁎</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709031489/abstract?rss=yes</link><description>The intuitive and postulated links () between the established association of obstructive sleep apnea with atrial fibrillation (AF) are hypertension, diastolic dysfunction, and the resultant long-term atrial remodeling (). However, studies suggest that the relationship between sleep apnea and AF is independent of hypertension, cardiac function, or body mass index. Further, untreated sleep apnea doubles the risk of AF recurrence within 12 months of cardioversion independent of other risk factors (). Thus, is the relationship between sleep apnea and AF an epiphenomenon, or is it truly causative and the linking mechanism is simply not yet explained?</description><dc:title>Sleep Apnea and Atrial Fibrillation: The Autonomic Link⁎</dc:title><dc:creator>Samuel J. Asirvatham, Suraj Kapa</dc:creator><dc:identifier>10.1016/j.jacc.2009.09.017</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Editorial Comment</prism:section><prism:startingPage>2084</prism:startingPage><prism:endingPage>2086</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029751/abstract?rss=yes"><title>A Meta-Analysis of the Mechanism of Blood Pressure Change With Aging</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029751/abstract?rss=yes</link><description>Objectives: We undertook a meta-analysis to determine whether changes in wave reflection substantiate the consensus explanation of why blood pressure (BP) changes with aging.Background: Consensus documents attribute the aging changes in BP to wave reflection moving progressively from diastole into systole. However, the extensive quantitative data on this phenomenon have never been systematically reviewed. Individual studies have been small, and limited to a narrow age range.Methods: Using PubMed, Cochrane, and Web of Science databases, we identified 64 studies (including 13,770 subjects, age range 4 to 91 years) reporting the timing of wave reflection, defined as the time from the onset (foot) of the pressure waveform to the shoulder point (anachrotic notch).Results: In subjects of all ages, reflection times were well within systole. There was a small tendency for younger subjects to have later reflection, but this was only 0.7 ms per year, whereas the weighted mean reflection time was 136 ms (99% confidence interval: 130 to 141 ms) and the mean duration of systole was 328 ms (99% confidence interval: 310 to 347 ms). At this rate of change with age, arrival of wave reflection would only be construed to be in diastole at an extrapolated age of −221 years.Conclusions: These findings challenge the current consensus view that a shift in timing of wave reflection significantly contributes to the changes in the BP waveform with aging. We should re-evaluate the mechanisms of BP elevation in aging.</description><dc:title>A Meta-Analysis of the Mechanism of Blood Pressure Change With Aging</dc:title><dc:creator>Arun J. Baksi, Thomas A. Treibel, Justin E. Davies, Nearchos Hadjiloizou, Rodney A. Foale, Kim H. Parker, Darrel P. Francis, Jamil Mayet, Alun D. Hughes</dc:creator><dc:identifier>10.1016/j.jacc.2009.06.049</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>HYPERTENSION</prism:section><prism:startingPage>2087</prism:startingPage><prism:endingPage>2092</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029763/abstract?rss=yes"><title>Anemia in Adults With Congenital Heart Disease Relates to Adverse Outcome</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709029763/abstract?rss=yes</link><description>Objectives: To assess the relation of anemia in noncyanotic adults with congenital heart disease (ACHD) to functional capacity and mortality.Background: Anemia is common in acquired heart failure and affects prognosis. The presence of anemia and its relation to outcome in ACHD remain unknown.Methods: Data were collected on consecutive noncyanotic ACHD patients attending our tertiary center between 2001 and 2006 in whom hemoglobin concentration was measured. Anemia was defined as hemoglobin concentration &lt;13 g/dl in males and &lt;12 g/dl in females. Cyanotic patients were excluded to avoid confounding from secondary erythrocytosis.Results: Overall, 830 noncyanotic ACHD patients (age 36.5 ± 15.0 years, 49.6% male) fulfilled the inclusion criteria. The prevalence of anemia was 13.1% and was highest in patients with congenitally corrected transposition of great arteries and Ebstein anomaly of the tricuspid valve. Anemic patients were more likely to be receiving diuretics (p &lt; 0.0001) and have a lower mean corpuscular volume (p = 0.0001), with a trend toward a higher New York Heart Association functional class (p = 0.06). During a median follow-up of 47 months, 55 patients died. Anemic patients had a 3-fold higher mortality risk compared with nonanemic patients, even after propensity score adjustment for clinical variables such as systemic ventricular function, renal impairment, and diuretic therapy (adjusted hazard ratio: 3.00; 95% confidence interval: 1.46 to 6.13).Conclusions: Anemia is not uncommon in ACHD patients attending tertiary services and is associated with a 3-fold increased risk of death. Screening for anemia should be part of the routine assessment of ACHD patients for risk stratification and treatment when correctable causes are identified.</description><dc:title>Anemia in Adults With Congenital Heart Disease Relates to Adverse Outcome</dc:title><dc:creator>Konstantinos Dimopoulos, Gerhard-Paul Diller, Georgios Giannakoulas, Ricardo Petraco, Aikaterini Chamaidi, Evaggelia Karaoli, Michael Mullen, Lorna Swan, Massimo F. Piepoli, Philip A. Poole-Wilson, Darrel P. Francis, Michael A. Gatzoulis</dc:creator><dc:identifier>10.1016/j.jacc.2009.06.050</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>CONGENITAL HEART DISEASE</prism:section><prism:startingPage>2093</prism:startingPage><prism:endingPage>2100</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970902974X/abstract?rss=yes"><title>Coronary Artery Aneurysm Formation Within New-Generation Bare-Metal Stents: Not Just Due to Drug Elution!</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS073510970902974X/abstract?rss=yes</link><description>A 57-year-old woman with chronic stable angina underwent uncomplicated stenting in the left anterior descending artery (LAD) and right coronary artery (RCA) (A) with excellent results in the target vessel. Coronary angiogram repeated for atypical chest pain 6 months later demonstrated coronary artery aneurysm (CAA) (arrowheads) within the segments stented with a bare-metal stent (BMS) in both arteries (B), confirmed on intravascular ultrasound examination (C). Arrows show the extent of the aneurysm as seen on the intravascular ultrasound images. The RCA segment stented with the everolimus-eluting stent Xience (Abbott Laboratories, Abbott Park, Illinois) was free of aneurysm. History did not suggest any predisposition to aneurysm formation, and systemic arteritis was excluded. The patient was treated conservatively with life-long dual antiplatelet therapy to avoid compromising flow in branches arising from the aneurysmal segments. She remains well currently. Repeat angiogram (D and E) shows a partial regression of the aneurysms (arrowheads).</description><dc:title>Coronary Artery Aneurysm Formation Within New-Generation Bare-Metal Stents: Not Just Due to Drug Elution!</dc:title><dc:creator>Sudipta Chattopadhyay, Timothy Kinnaird, Richard A. Anderson</dc:creator><dc:identifier>10.1016/j.jacc.2009.04.099</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>IMAGES IN CARDIOLOGY</prism:section><prism:startingPage>2101</prism:startingPage><prism:endingPage>2101</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709022475/abstract?rss=yes"><title>2009 ACCF/AHA Focused Update on Perioperative Beta Blockade</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709022475/abstract?rss=yes</link><description>Lee A. Fleisher, MD, FACC, FAHA, Chair   Joshua A. Beckman, MD, FACC</description><dc:title>2009 ACCF/AHA Focused Update on Perioperative Beta Blockade</dc:title><dc:creator>Kirsten E. Fleischmann, Joshua A. Beckman, Christopher E. Buller, Hugh Calkins, Lee A. Fleisher, William K. Freeman, James B. Froehlich, Edward K. Kasper, Judy R. Kersten, John F. Robb, R. James Valentine, American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine, Society for Vascular Surgery</dc:creator><dc:identifier>10.1016/j.jacc.2009.07.004</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>ACCF/AHA PRACTICE GUIDELINES: FOCUSED UPDATE</prism:section><prism:startingPage>2102</prism:startingPage><prism:endingPage>2128</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709023857/abstract?rss=yes"><title>2009 ACCF/AHA Focused Update on Perioperative Beta Blockade Incorporated Into the ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709023857/abstract?rss=yes</link><description>Kirsten E. Fleischmann, MD, MPH, FACC, Chair   Joshua A. Beckman, MD, FACC</description><dc:title>2009 ACCF/AHA Focused Update on Perioperative Beta Blockade Incorporated Into the ACC/AHA 2007 Guidelines on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery</dc:title><dc:creator>Lee A. Fleisher, Joshua A. Beckman, Kenneth A. Brown, Hugh Calkins, Elliot L. Chaikof, Kirsten E. Fleischmann, William K. Freeman, James B. Froehlich, Edward K. Kasper, Judy R. Kersten, Barbara Riegel, John F. Robb, American College of Cardiology Foundation, American Heart Association Task Force on Practice Guidelines, American Society of Echocardiography, American Society of Nuclear Cardiology, Heart Rhythm Society, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine, Society for Vascular Surgery</dc:creator><dc:identifier>10.1016/j.jacc.2009.07.010</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>ACCF/AHA PRACTICE GUIDELINES: FULL TEXT</prism:section><prism:startingPage>e13</prism:startingPage><prism:endingPage>e118</prism:endingPage></item><item rdf:about="http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709035463/abstract?rss=yes"><title>Inside This Issue</title><link>http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109709035463/abstract?rss=yes</link><description>1993   Joseph D. Mishkin, Sherry J. Saxonhouse, Gregory W. Woo, Thomas A. Burkart, William M. Miles, Jamie B. Conti, Richard S. Schofield, Samuel F. Sears, Juan M. Aranda, Jr</description><dc:title>Inside This Issue</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0735-1097(09)03546-3</dc:identifier><dc:source>Journal of the American College of Cardiology 54, 22 (2009)</dc:source><dc:date>2009-11-24</dc:date><prism:publicationName>Journal of the American College of Cardiology</prism:publicationName><prism:publicationDate>2009-11-24</prism:publicationDate><prism:volume>54</prism:volume><prism:number>22</prism:number><prism:issueIdentifier>S0735-1097(09)X0043-4</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A20</prism:startingPage><prism:endingPage>A20</prism:endingPage></item></rdf:RDF>