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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.heartrhythmjournal.com/?rss=yes"><title>Heart Rhythm</title><description>Heart Rhythm RSS feed: Current Issue. Heart Rhythm , the official Journal of the Heart Rhythm Society and the Cardiac Electrophysiology Society, is a unique journal 
for fundamental discovery and clinical applicability. Heart Rhythm  integrates the entire cardiac electrophysiology (EP) community 
from basic and clinical academic researchers, private practitioners, engineers, allied professionals, industry, and trainees, all of 
whom are vital and interdependent members of our EP community. Heart Rhythm  has an impact factor of 4.444, and remains the leading 
specialty journal in cardiology.  
 
The Heart Rhythm Society is the international leader in science, education, and advocacy for cardiac 
arrhythmia professionals and patients, and the primary information resource on heart rhythm disorders. Its mission is to improve the 
care of patients by promoting research, education, and optimal health care policies and standards. The Heart Rhythm Society is the preeminent 
professional group representing more than 5,100 specialists in cardiac pacing and electrophysiology from more than 70 countries.  The 
Society is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to sponsor continuing medical education for 
physicians.  For more information on the Heart Rhythm Society, please visit  www.HRSonline.org 
</description><link>http://www.heartrhythmjournal.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Heart Rhythm</prism:publicationName><prism:issn>1547-5271</prism:issn><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:publicationDate>March 2010</prism:publicationDate><prism:copyright> © 2010 Heart Rhythm Society. 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.heartrhythmjournal.com/article/PIIS1547527109012740/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013289/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014283/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109012685/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013034/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109012739/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013320/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109012995/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013332/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013058/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014167/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013319/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014775/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013368/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS154752710901385X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109012727/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527110000500/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013009/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527110000020/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013277/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013356/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013290/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109012570/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109013824/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109004627/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109007528/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS154752711000007X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527110000081/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014313/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014349/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014350/abstract?rss=yes"/><rdf:li rdf:resource="http://www.heartrhythmjournal.com/article/PIIS1547527109014362/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109012740/abstract?rss=yes"><title>P wave and the development of atrial fibrillation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109012740/abstract?rss=yes</link><description>Background: Terminal P-wave inversion in lead V1 representing left atrial overload has been considered a precursor of atrial fibrillation (AF).Objective: The purpose of this study was to determine whether this P-wave morphologic characteristic can predict the development of AF.Methods: Digital analysis of 12-lead ECGs was performed to enroll patients with P terminal force ≥0.06 s × 2 mm in lead V1 from among a database of 308,391 ECG recordings. The prognostic value of ECG characteristics for developing AF was determined.Results: A total of 78 patients (mean age 52 ± 19 years) with left atrial overload were chosen from among 102,065 patients in the database. During mean follow-up of 43 months, 15 (19%) patients developed AF (AF group) versus 63 (81%) patients who did not (non-AF group). No significant difference was noted between the AF and non-AF groups with regard to the area, duration, and amplitude of the P-wave terminal portion in lead V1. In contrast, the area, duration, and amplitude of the P-wave initial portion in the same lead were significantly greater in the AF group than in the non-AF group (114.6 ± 73.0 μV × ms vs 73.1 ± 59.3 μV × ms, 42.2 ± 12.4 ms vs 35.7 ± 10.1 ms, and 94.0 ± 39.9 μV vs 68.8 ± 49.4 μV, respectively; P &lt;.05 for each). Multivariate analysis confirmed that the area of the P-wave initial portion was independently associated with the development of AF (hazard ratio 4.02, 95% confidence interval 1.25–17.8; P = .018).Conclusion: P-wave initial portion in lead V1 was an independent risk stratifier of AF development in patients with marked left atrial overload.</description><dc:title>P wave and the development of atrial fibrillation</dc:title><dc:creator>Katsuya Ishida, Hideki Hayashi, Akashi Miyamoto, Yoshihisa Sugimoto, Makoto Ito, Yoshitaka Murakami, Minoru Horie</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.012</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-13</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-13</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Atrial Fibrillation</prism:section><prism:startingPage>289</prism:startingPage><prism:endingPage>294</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013289/abstract?rss=yes"><title>A critical decrease in dominant frequency and clinical outcome after catheter ablation of persistent atrial fibrillation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013289/abstract?rss=yes</link><description>Background: Termination of persistent atrial fibrillation (AF) by radiofrequency ablation (RFA) is associated with a high probability of freedom from AF but requires extensive ablation and long procedure times.Objective: The purpose of this study was to determine whether a critical decrease in the dominant frequency (DF) of AF is a sufficient endpoint for RFA of persistent AF.Methods: Antral pulmonary vein isolation (APVI) followed by RFA of complex fractionated atrial electrograms (CFAEs) in the atria and coronary sinus was performed in 100 consecutive patients with persistent AF. The DF of AF in lead V1 and in the coronary sinus was determined by fast Fourier transform (FFT) analysis at baseline and before termination of AF to identify a critical decrease in DF predictive of sinus rhythm after RFA.Results: A ≥11% decrease in DF had the highest accuracy in predicting freedom from atrial arrhythmias, with a sensitivity of 0.71 and a specificity of 0.82 (P &lt;.001). At a mean follow-up of 14 ± 3 months after one ablation procedure, sinus rhythm was maintained off antiarrhythmic drugs in 8/35 (23%) and 20/26 (77%) of patients with a &lt;11% and ≥11% decrease in DF, respectively (P &lt;.001). Sinus rhythm was maintained in 24/39 patients (62%) in whom RFA terminated AF. The duration of RFA and total procedure time were longer in patients with AF termination (95 ± 23 and 358 ± 87 minutes) than in patients with a &lt;11% decrease in the DF (77 ± 16 and 293 ± 70 minutes) or ≥11% decrease in DF (80 ± 17 and 289 ± 73 minutes), respectively (P &lt;.01). Among the variables of age, gender, left atrial diameter, duration of AF, left ventricular ejection fraction, duration of RFA, a ≥11% decrease in DF, and termination of AF, a ≥11% decrease in DF (odds ratio = 9.89, 95% confidence interval [CI] 2.84–34.47) and termination during RFA (OR = 4.38, 95% CI 1.50–12.80) were the only independent predictors of freedom from recurrent atrial arrhythmias.Conclusion: In a retrospective analysis of consecutive patients with persistent AF, a decrease in the DF of AF by 11% in response to APVI and ablation of CFAEs was associated with a probability of maintaining sinus rhythm that was similar to that when RFA terminates AF.</description><dc:title>A critical decrease in dominant frequency and clinical outcome after catheter ablation of persistent atrial fibrillation</dc:title><dc:creator>Kentaro Yoshida, Aman Chugh, Eric Good, Thomas Crawford, James Myles, Srikar Veerareddy, Sreedhar Billakanty, Wai S. Wong, Matthew Ebinger, Frank Pelosi, Krit Jongnarangsin, Frank Bogun, Fred Morady, Hakan Oral</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.024</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Atrial Fibrillation</prism:section><prism:startingPage>295</prism:startingPage><prism:endingPage>302</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014283/abstract?rss=yes"><title>Ablation of complex fractionated electrograms in persistent atrial fibrillation: Have we reached the endpoint?</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014283/abstract?rss=yes</link><description>Since Nademanee et al first reported the utility of ablation of complex fractionated atrial electrograms (CFAEs) for cure of atrial fibrillation (AF), the approach has been widely adopted, particularly in patients with persistent AF. However, despite its widespread clinical use, the definition, significance, and efficacy of ablation of CFAEs remain uncertain. Furthermore, in patients with extensive CFAEs, ablation endpoints are unknown.</description><dc:title>Ablation of complex fractionated electrograms in persistent atrial fibrillation: Have we reached the endpoint?</dc:title><dc:creator>Jonathan M. Kalman, Andrew W. Teh</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.018</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-04</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-04</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Editorial Commentary</prism:section><prism:startingPage>303</prism:startingPage><prism:endingPage>304</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109012685/abstract?rss=yes"><title>Focal mechanism of ventricular tachycardia in coronary artery disease</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109012685/abstract?rss=yes</link><description>Background: Re-entry is the most common mechanism of sustained monomorphic ventricular tachycardia (VT) in patients with coronary artery disease and prior myocardial infarction (MI).Objective: This study sought to report the electrophysiological properties of a series of patients with prior MI who underwent radiofrequency ablation (RFA) for VT originating instead from a focal source.Methods: The electrophysiological properties of 46 patients with prior MI (male 89%, age 64.8 ± 10.2 years) who underwent RFA for sustained VT were studied. A total of 101 VTs were induced (92 [91%] macro–re-entrant VT and 9 [9%] focal VT).Results: One patient had adenosine-sensitive idiopathic focal VT. The focal VT group had a significantly shorter pre-systolic interval (electrogram to QRS) during VT compared with the macro–re-entrant VT group (36 ± 17 ms vs. 117 ± 67 ms, P = .001). The successful ablation sites in the focal VT group also had a significantly lower ratio (in percentage) of electrogram-QRS interval to diastolic interval (VT cycle length − QRS duration) during VT (14 ± 8%) as compared with macro–re-entrant VTs (48 ± 30%, P &lt;.001). Focal VTs demonstrated an apparent point source of endocardial activation and could not be entrained, whereas 77% of macro–re-entrant VTs were entrained. Successful ablation sites for focal VT (success rate 100%) were predominantly in the basal half of the left ventricle (75%), whereas only 60% of macro–re-entrant VTs (success rate 90.7%) were basal (P = .01). However, the procedure time, VT cycle length, number of RFA applications required for success, and acute success results were not significantly different in these 2 groups.Conclusion: A focal mechanism is present in up to 9% of VTs in patients with CAD and prior MI that are induced during electrophysiology study for RF ablation. Mechanistic distinction from more typical macro–re-entrant VT in this population is important because ablation site characteristics are very different.</description><dc:title>Focal mechanism of ventricular tachycardia in coronary artery disease</dc:title><dc:creator>Mithilesh K. Das, Luis R. Scott, John M. Miller</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.006</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-09</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-09</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Ventricular Tachycardia</prism:section><prism:startingPage>305</prism:startingPage><prism:endingPage>311</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013034/abstract?rss=yes"><title>Electrocardiographic and electrophysiologic features of ventricular arrhythmias originating from the right/left coronary cusp commissure</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013034/abstract?rss=yes</link><description>Background: Ventricular arrhythmias are known to originate from the aortic sinus of Valsalva.Objective: The purpose of this study was to identify the characteristics associated with ventricular arrhythmias originating from the right coronary cusp–left coronary cusp (RCC–LCC) commissure.Methods: Thirty-seven consecutive patients with ventricular arrhythmias originating from the aortic cusp region were studied. Intracardiac echocardiography and electroanatomic mapping were used to define coronary cusp anatomy and catheter position. Ventricular arrhythmias from the RCC–LCC commissure were compared with ventricular arrhythmias originating from other sites in the aortic cusp region.Results: Nineteen (51%) ventricular arrhythmias had an anatomic origin at the RCC–LCC commissure. Eighteen ventricular arrhythmias originated from other aortic cusp sites (4 right cusp, 7 left cusp, 3 left ventricular endocardium, 4 left ventricular epicardium anterior to aortic valve). A QS morphology in lead V1 with notching on the downward deflection was present in 15 of 19 ventricular arrhythmias originating from the RCC–LCC commissure compared to 2 of 18 ventricular arrhythmias from other aortic cusp sites (P &lt;.01). At the site of earliest activation, 13 of 19 patients with RCC–LCC ventricular arrhythmias had late potentials in sinus rhythm compared to 1 of 18 ventricular arrhythmias from other aortic cusp sites (P &lt;.01). The site of successful ablation was confirmed to be above the aortic valve plane in 15 (79%) of 19 patients with RCC–LCC ventricular arrhythmias.Conclusion: RCC–LCC aortic cusp ventricular arrhythmias are common and have a QS morphology in lead V1 with notching on the downward deflection with precordial transition at lead V3. In the majority of cases, the site of successful ablation has late potentials in sinus rhythm.</description><dc:title>Electrocardiographic and electrophysiologic features of ventricular arrhythmias originating from the right/left coronary cusp commissure</dc:title><dc:creator>Rupa Bala, Fermin C. Garcia, Mathew D. Hutchinson, Edward P. Gerstenfeld, Sandhya Dhruvakumar, Sanjay Dixit, Joshua M. Cooper, David Lin, John Harding, Michael P. Riley, Erica Zado, David J. Callans, Francis E. Marchlinski</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.017</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-19</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-19</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Ventricular Tachycardia</prism:section><prism:startingPage>312</prism:startingPage><prism:endingPage>322</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109012739/abstract?rss=yes"><title>Loss of pace capture on the ablation line: A new marker for complete radiofrequency lesions to achieve pulmonary vein isolation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109012739/abstract?rss=yes</link><description>Background: Catheter ablation procedures for atrial fibrillation (AF) often involve circumferential antral isolation of pulmonary veins (PV). Inability to reliably identify conduction gaps on the ablation line necessitates placing additional lesions within the intended lesion set.Objective: This pilot study investigated the relationship between loss of pace capture directly along the ablation line and electrogram criteria for PV isolation (PVI).Methods: Using a 3-dimensional anatomic mapping system and irrigated-tip radiofrequency (RF) ablation catheter, lesions were placed in the PV antra to encircle ipsilateral vein pairs until pace capture at 10 mA/2 ms no longer occurred along the line. During ablation, a circular mapping catheter was placed in an ipsilateral PV, but the electrograms were not revealed until loss-of-pace capture. The procedural end point was PVI (entrance and exit block).Results: Thirty patients (57 ± 12 years; 15 male [50%]) undergoing PVI in 2 centers (3 primary operators) were included (left atrial diameter 40 ± 4 mm, left ventricular ejection fraction 60 ± 7%). All patients reached the end points of complete PVI and loss of pace capture. When PV electrograms were revealed after loss of pace capture along the line, PVI was present in 57 of 60 (95%) vein pairs. In the remaining 3 of 60 (5%) PV pairs, further RF applications achieved PVI. The procedure duration was 237 ± 46 minutes, with a fluoroscopy time of 23 ± 9 minutes. Analysis of the blinded PV electrograms revealed that even after PVI was achieved, additional sites of pace capture were present on the ablation line in 30 of 60 (50%) of the PV pairs; 10 ± 4 additional RF lesions were necessary to fully achieve loss of pace capture. After ablation, the electrogram amplitude was lower at unexcitable sites (0.25 ± 0.15 mV vs. 0.42 ± 0.32 mV, P &lt; .001), but there was substantial overlap with pace capture sites, suggesting that electrogram amplitude lacks specificity for identifying pace capture sites.Conclusion: Complete loss of pace capture directly along the circumferential ablation line correlates with entrance block in 95% of vein pairs and can be achieved without circular mapping catheter guidance. Thus, pace capture along the ablation line can be used to identify conduction gaps. Interestingly, more RF ablation energy was required to achieve loss of pace capture along the ablation line than for entrance block into PVs. Further study is warranted to determine whether this method results in more durable ablation lesions that reduce recurrence of AF.</description><dc:title>Loss of pace capture on the ablation line: A new marker for complete radiofrequency lesions to achieve pulmonary vein isolation</dc:title><dc:creator>Daniel Steven, Vivek Y. Reddy, Keiichi Inada, Kurt C. Roberts-Thomson, Jens Seiler, William G. Stevenson, Gregory F. Michaud</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.011</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-13</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-13</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Ablation</prism:section><prism:startingPage>323</prism:startingPage><prism:endingPage>330</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013320/abstract?rss=yes"><title>Loss of pace capture on the ablation line: The quest for a more reliable endpoint for pulmonary vein isolation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013320/abstract?rss=yes</link><description>During the last decade we have witnessed an impressive worldwide race to improve the efficacy and safety of catheter ablation of atrial fibrillation. In spite of many different approaches to tackle the challenges to find a curative treatment for atrial fibrillation, the electrophysiological community has reached some common grounds. One of them is the need to achieve complete pulmonary vein (PV) electrical disconnection in all patients as the only valid endpoint of PV isolation. While it is preferable that entrance and exit block of the PV should be demonstrated, the standard procedure to check PV isolation is entrance block assessment during sinus rhythm or by pacing the left atrium while checking the PVs with a circular mapping catheter for absent or dissociated PV potentials. However, even after documenting PV electrical disconnection, the major cause of recurrent AF is reconnection of the PV(s).</description><dc:title>Loss of pace capture on the ablation line: The quest for a more reliable endpoint for pulmonary vein isolation</dc:title><dc:creator>Eduardo Back Sternick</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.028</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Editorial Commentary</prism:section><prism:startingPage>331</prism:startingPage><prism:endingPage>332</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109012995/abstract?rss=yes"><title>One-year follow-up after pulmonary vein isolation using a single mesh catheter in patients with paroxysmal atrial fibrillation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109012995/abstract?rss=yes</link><description>Background: Catheter-based pulmonary vein (PV) isolation has emerged as established therapy for patients with paroxysmal atrial fibrillation (AF).Objective: The purpose of this study was to determine the results at 1-year follow-up after PV isolation was performed using a single novel multipolar catheter for mapping and ablation.Methods: Patients with paroxysmal AF were screened by cardiac computed tomography for anatomic suitability to undergo PV ablation with the Bard HD Mesh Ablator Catheter (MESH). PV isolation with the MESH was performed only in patients who matched the criteria of four clearly separated PVs with an ostial diameter of 15 to 25 mm.Results: PV isolation with the MESH was performed in 36 (55%) of 65 screened patients. In all 36 patients, all PVs could be mapped with the MESH. Electrical isolation could be achieved in 135 (96%) of 140 PVs that revealed PV potentials. One-year follow-up was completed for 35 patients; one patient was lost to follow-up. Ten (29%) patients reported to be symptom-free and had no AF during three 48-hour ECGs, whereas 25 (71%) patients suffered from AF recurrences. Reablation performed in 11 patients revealed reconnection of three PVs in 6 patients and four PVs in 5 patients.Conclusion: The single-catheter approach using the MESH for mapping and ablation was associated with a high AF recurrence rate within the first year despite a high acute success rate. Thus, the minimalist complexity of the procedure must be balanced with the poor clinical success leading to a high number of second procedures.</description><dc:title>One-year follow-up after pulmonary vein isolation using a single mesh catheter in patients with paroxysmal atrial fibrillation</dc:title><dc:creator>Clemens Steinwender, Simon Hönig, Franz Leisch, Robert Hofmann</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.013</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Ablation</prism:section><prism:startingPage>333</prism:startingPage><prism:endingPage>339</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013332/abstract?rss=yes"><title>Cryoablation versus radiofrequency ablation for treatment of atrioventricular nodal reentrant tachycardia: Cryoablation with 6-mm-tip catheters is still less effective than radiofrequency ablation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013332/abstract?rss=yes</link><description>Background: The treatment of choice for atrioventricular nodal reentrant tachycardia (AVNRT) is catheter ablation of the atrioventricular nodal slow pathway.Objective: The purpose of this study was to ascertain whether cryoablation (Cryo) with 6-mm-tip catheters is as effective as radiofrequency ablation (RF).Methods: Patients who had catheter ablation for AVNRT between 2005 and 2008 were identified. The main outcome measure was overall success without the use of an alternative energy source and no recurrence.Results: Two hundred eighty-eight procedures in 272 patients were identified; 184 were female (68%), and the mean age was 53 ± 14 (17–88) years. There were 123 Cryo and 149 RF procedures. Cryo had a lower overall success rate (83% vs. 93%; P = .02). Mean procedure times were similar in both groups (90 minutes; P = .5). Fluoroscopy time was longer with Cryo: 16 (7–48) versus 14 (5–50) minutes (P = .04). Only one case of atrioventricular block was observed in the RF group (0.7%). Cryo was more expensive than RF (£3141 vs. £2153).Conclusion: Even when delivering multiple lesions with 6-mm-tip catheters, Cryo is less effective than RF. RF is recommended as a first-line treatment, although the only major complication occurred in the RF group.</description><dc:title>Cryoablation versus radiofrequency ablation for treatment of atrioventricular nodal reentrant tachycardia: Cryoablation with 6-mm-tip catheters is still less effective than radiofrequency ablation</dc:title><dc:creator>Aaisha Opel, Sam Murray, Nikhil Kamath, Mehul Dhinoja, Dominic Abrams, Simon Sporton, Richard Schilling, Mark Earley</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.029</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Ablation</prism:section><prism:startingPage>340</prism:startingPage><prism:endingPage>343</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013058/abstract?rss=yes"><title>Biventricular stimulation improves right and left ventricular function after tetralogy of Fallot repair: Acute animal and clinical studies</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013058/abstract?rss=yes</link><description>Background: Optimal treatment of right ventricular (RV) dysfunction observed in patients after tetralogy of Fallot (TOF) repair is unclear. Studies of biventricular (BiV) stimulation in patients with congenital heart disease have been retrospective or have included patients with heterogeneous disorders.Objective: The purpose of this study was to determine the effects on cardiac function of stimulating at various cardiac sites in an animal model of RV dysfunction and dyssynchrony and in eight symptomatic adults with repaired TOF.Methods: Pulmonary stenosis and regurgitation as well as RV scars were induced in 15 piglets to mimic repaired TOF. The hemodynamic effects of various configurations of RV and BiV stimulation were compared with sinus rhythm (SR) 4 months after surgery. In eight adults with repaired TOF, RV and left ventricular (LV) dP/dtmax were measured invasively during SR, apical RV stimulation, and BiV stimulation.Results: At 4 months, RV dilation, dysfunction, and dyssynchrony were present in all piglets. RV stimulation caused a decrease in LV function but no change in RV function. In contrast, BiV stimulation significantly improved LV and RV function (P &lt; .05). Echocardiography and epicardial electrical mapping showed activation consistent with right bundle branch block during SR and marked resynchronization during BiV stimulation. In patients with repaired TOF, BiV stimulation increased significantly RV and LV dP/dtmax (P &lt; .05).Conclusion: In this swine model of RV dysfunction and in adults with repaired TOF, BiV stimulation significantly improved RV and LV function by alleviating electromechanical dyssynchrony.</description><dc:title>Biventricular stimulation improves right and left ventricular function after tetralogy of Fallot repair: Acute animal and clinical studies</dc:title><dc:creator>Jean-Benoit Thambo, Pierre Dos Santos, Maxime De Guillebon, Francois Roubertie, Louis Labrousse, Frederic Sacher, Xavier Iriart, Stephane Lafitte, Sylvain Ploux, Pierre Jais, Xavier Roques, Michel Haissaguerre, Philippe Ritter, Jacques Clementy, Sanjiv M. Narayan, Pierre Bordachar</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.019</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-23</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Devices</prism:section><prism:startingPage>344</prism:startingPage><prism:endingPage>350</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014167/abstract?rss=yes"><title>Right ventricular or biventricular pacing in repaired tetralogy of Fallot?</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014167/abstract?rss=yes</link><description>Because asynchronous electrical activation of ventricular myocardium has detrimental effects on its mechanical function, cardiac resynchronization therapy by means of biventricular (BiV) pacing has been used in heart failure patients. Due to the positive effects of BiV pacing in patients with heart failure and intrinsic or right ventricular (RV) pacing-induced left bundle branch block (LBBB), other applications have been sought and suggested. However, failure of studies such as RethinQ (Cardiac-Resynchronization Therapy in Heart Failure with Narrow QRS Complexes) indicate that application of pacing should always be guided by considering the effect of the specific ventricular pacing site(s) and mode on ventricular activation, mechanics, and hemodynamics. After all, in hearts with normal impulse conduction, (even) BiV pacing creates, rather than reduces, asynchrony and thus can worsen patients' condition.</description><dc:title>Right ventricular or biventricular pacing in repaired tetralogy of Fallot?</dc:title><dc:creator>Tammo Delhaas, Frits W. Prinzen</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.015</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Editorial Commentary</prism:section><prism:startingPage>351</prism:startingPage><prism:endingPage>352</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013319/abstract?rss=yes"><title>Differences in effects of electrical therapy type for ventricular arrhythmias on mortality in implantable cardioverter-defibrillator patients</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013319/abstract?rss=yes</link><description>Background: Implantable cardioverter-defibrillator (ICD) shocks have been associated with an increased risk of death. It is unknown whether this is due to the ventricular arrhythmia (VA) or shocks and whether antitachycardia pacing (ATP) termination can reduce this risk.Objective: The purpose of this study was to determine whether mortality in ICD patients is influenced by the type of therapy (shocks of ATP) delivered.Methods: Cox models evaluated effects of baseline characteristics, ventricular tachycardia (VT; &lt;188 bpm), fast VT (FVT; 188–250 bpm), ventricular fibrillation (VF; &gt;250 bpm), and therapy type (shocks or ATP) on mortality among 2135 patients in four trials of ATP to reduce shocks.Results: Over 10.8 ± 3.3 months, 24.3% patients received appropriate shocks (50.6%) or ATP only (49.4%), and 6.6% died. Mortality predictors were age (hazard ratio 1.07, 95% confidence interval 1.04–1.08, P &lt;.0001), New York Heart Association class III/IV (3.50 [2.27–5.41]; P &lt;.0001), coronary disease (3.08 [1.31–7.25]; P = .01), and cumulative VA (VT + FVT + VF) episodes shocked (1.20 [1.13, 1.29]; P &lt;.0001). Beta-blockers (0.65, 0.46–0.92; P &lt;.0001) and remote myocardial infarction (0.53, [0.38–0.76] P = .0004) predicted reduced risk. Since 92% of VT and all VF received a single therapy type (ATP and shocks, respectively), the effect of therapy on episode risk could not be established. For FVT (32% shocked, 68% ATP), episode and therapy effects could be uncoupled; ATP-terminated FVT did not increase episode mortality risk, whereas shocked FVT increased risk by 32%. Survival rates were highest among patients with no VA (93.8%) of ATP-only (94.7%) and lowest for shocked patients (88.4%). Monthly episode rates were 80% higher among shocked versus ATP-only patients.Conclusions: Shocked VA episodes are associated with increased mortality risk. Shocked patients have substantially higher VA episode burden and poorer survival compared with ATP-only-treated patients.</description><dc:title>Differences in effects of electrical therapy type for ventricular arrhythmias on mortality in implantable cardioverter-defibrillator patients</dc:title><dc:creator>Michael O. Sweeney, Lou Sherfesee, Paul J. DeGroot, Mark S. Wathen, Bruce L. Wilkoff</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.027</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Devices</prism:section><prism:startingPage>353</prism:startingPage><prism:endingPage>360</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014775/abstract?rss=yes"><title>The paradox of ICD shocks: Sudden cardiac death prevention—Heart failure death acceleration</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014775/abstract?rss=yes</link><description>Multiple major clinical trials over the last 2 decades have established the central role of implantable cardioverter defibrillators (ICDs) as a life-saving therapy in patients with ventricular arrhythmias (VA) as well as ischemic and nonischemic cardiomyopathy. Additional benefit is seen when an ICD is combined with cardiac resynchronization therapy (CRT) in heart failure patients. Appropriate shocks have been seen as a life-saving therapy with a sudden cardiac death (SCD) aborted without any other consequences.</description><dc:title>The paradox of ICD shocks: Sudden cardiac death prevention—Heart failure death acceleration</dc:title><dc:creator>Jason Bradfield, Noel G. Boyle</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.028</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-04</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-04</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Editorial Commentary</prism:section><prism:startingPage>361</prism:startingPage><prism:endingPage>362</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013368/abstract?rss=yes"><title>S38G single-nucleotide polymorphism at the KCNE1 locus is associated with heart failure</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013368/abstract?rss=yes</link><description>Background: Prolongation of the action potential duration, whose major determinants are the delayed-rectifier potassium currents, is a hallmark of failing ventricular myocardium. Genetic variants in the KCNE1 gene, encoding for the β-subunit (minK) of a slowly activated cardiac potassium channel (Iks), may impair myocardial repolarization. Experimental data demonstrated a higher KCNE1 expression in heart failure (HF).Objective: The purpose of this study was to investigate the association between a KCNE1 S38G single-nucleotide polymorphism (SNP) and HF.Methods: We genotyped 197 out of 323 previously investigated patients and 352 healthy controls comparable for age and sex. This study was replicated in 186 HF patients and in 200 healthy subjects comparable for age and sex and recruited from the Department of Cardiovascular Medicine of the National Research Council, Pisa, Italy.Results: A significant difference in genotype distribution and allele frequency between patients and controls was observed for the KCNE1 S38G SNP (P = .002 and P = .0008, respectively). The KCNE1 38G variant was associated with a significant predisposition to HF under a dominant (odds ratio [OR] = 2.22 [1.23–3.28]; P = .008) and additive (OR = 2.13 [1.09–4.15]; P = .03) model, after adjustment for age, sex, and traditional cardiovascular risk factors. No difference in genotype distribution and allele frequency for the KCNE1 S38G SNP according to functional New York Heart Association class was found (P = .4 and P = .3, respectively). In the HF replication study, the KCNE1 38G allele frequency was significantly higher in comparison with that observed in the control population (38G = 0.59 vs. 0.49; P = .004). The 38G allele was associated with HF predisposition under the recessive (OR [95% confidence interval (CI)] = 2.49 [1.45–4.29]; P = .001) and additive models (OR [95% CI] = 2.63 [1.29–5.35]; P = .008), after adjustment for traditional risk factors.Conclusion: KCNE1 S38G SNP is associated with HF predisposition in two study populations. Nevertheless, further studies performed in larger populations and aimed to better define the role of this locus are required.</description><dc:title>S38G single-nucleotide polymorphism at the KCNE1 locus is associated with heart failure</dc:title><dc:creator>Cinzia Fatini, Elena Sticchi, Rossella Marcucci, Valerio Verdiani, Carlo Nozzoli, Cristina Vassallo, Michele Emdin, Rosanna Abbate, Gian Franco Gensini</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.032</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Genetic</prism:section><prism:startingPage>363</prism:startingPage><prism:endingPage>367</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752710901385X/abstract?rss=yes"><title>Association of a common KCNE1 variant with heart failure</title><link>http://www.heartrhythmjournal.com/article/PIIS154752710901385X/abstract?rss=yes</link><description>Heart failure is a common multifactorial disease with substantial morbidity and mortality. The main clinical manifestations of heart failure include limited exercise tolerance, fluid retention with predisposition to edematous states and acute pulmonary edema, and other organ dysfunction such as hepatic and renal insufficiency. Heart failure is associated with a shortened life expectancy, with a median survival of 1.7 years in men and 3.2 years in women according to epidemiologic data from the Framingham Heart Study. A significant cause of mortality in heart failure is sudden cardiac death, in many cases as result of ventricular arrhythmias. Cardiac myocytes from failing hearts exhibit abnormal repolarization suggesting a predisposition to reentrant arrhythmia. Understanding risk factors for heart failure should promote the development of improved therapies and preventive measures to lessen this public health burden.</description><dc:title>Association of a common KCNE1 variant with heart failure</dc:title><dc:creator>Alfred L. George</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.014</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Editorial Commentary</prism:section><prism:startingPage>368</prism:startingPage><prism:endingPage>369</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109012727/abstract?rss=yes"><title>Percutaneous left atrial appendage closure with an epicardial suture ligation approach: A prospective randomized pre-clinical feasibility study</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109012727/abstract?rss=yes</link><description>Background: Percutaneous approaches to left atrial appendage (LAA) closure are being developed for stroke prophylaxis in atrial fibrillation (AF) patients as an alternative to warfarin. A pericardial suture ligation approach has the advantage of ultimately leaving no permanent implant within the blood pool, but the potential disadvantage of inadequate placement, thereby not excluding the entire LAA from the circulation.Objective: This study sought to investigate the ability of a novel percutaneous pericardial snare and suture ligation device to achieve complete LAA exclusion.Methods: Ten animals underwent LAA exclusion with a pericardial snare and suture ligation in this prospective randomized feasibility study. Animals were randomized to concomitant use of a transseptally placed endoluminal balloon within the LAA to aid in proximal positioning and stabilization of the pericardial snare and suture. The level of LAA appendage exclusion was determined at necropsy.Results: Nine animals completed the study, 5 with and 4 without the use of the endoluminal LAA balloon. In all animals, LAA closure was complete without a leak. The level of LAA closure was at the base without a proximal residual LAA remnant in 5 of 5 (100%) animals when the endoluminal balloon was used, but in only 1 of 4 (25%) of animals when it was not used. No acute procedural complications occurred.Conclusion: Percutaneous epicardial suture ligation of the LAA is feasible with this novel device. The concomitant use of an endoluminal balloon catheter placed in the LAA significantly increases the likelihood of excluding the entire LAA from the circulation.</description><dc:title>Percutaneous left atrial appendage closure with an epicardial suture ligation approach: A prospective randomized pre-clinical feasibility study</dc:title><dc:creator>Sheldon M. Singh, Srinivas R. Dukkipati, Andre d'Avila, Shephal K. Doshi, Vivek Y. Reddy</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.010</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Experimental</prism:section><prism:startingPage>370</prism:startingPage><prism:endingPage>376</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527110000500/abstract?rss=yes"><title>Percutaneous closure of the left atrial appendage: A finger in the dyke?</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527110000500/abstract?rss=yes</link><description>Atrial fibrillation (AF) is common but rarely is life-threatening, yet technological innovation aimed at modification of the arrhythmic substrate has advanced rapidly. In contrast, stroke associated with AF is a common and serious cause of morbidity and mortality, yet the mainstay of stroke prophylaxis in 2010 remains dose-adjusted warfarin, a venerable pesticide approved for human use in the 1950s.</description><dc:title>Percutaneous closure of the left atrial appendage: A finger in the dyke?</dc:title><dc:creator>Peter Anthony Brady</dc:creator><dc:identifier>10.1016/j.hrthm.2010.01.019</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-25</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Editorial Commentary</prism:section><prism:startingPage>377</prism:startingPage><prism:endingPage>378</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013009/abstract?rss=yes"><title>Mechanisms for initiation of reentry in acute regional ischemia phase 1B</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013009/abstract?rss=yes</link><description>Background: During phase 1B of acute regional ischemia, the subepicardial and subendocardial layers coupled to the inexcitable midmyocardium remain viable.Objective: The purpose of this study was to examine how the degree of hyperkalemia in the surviving layers, the lateral width of border zone between the normal tissue and the central ischemic zone, and the degree of cellular uncoupling between the surviving layers and the midmyocardium contribute to initiation of reentry.Methods: Simulations were conducted on the state-of-the-art model of rabbit ventricles with realistic representation of the spatial distribution of the ischemic insult.Results: Hyperkalemia in the surviving layers led to induction of reentry by increasing refractoriness and slowing conduction in the layers. Such reentries were formed solely in the subepicardium. A minimal level of hyperkalemia was required for induction of reentry. Progress increase in hyperkalemia led to a biphasic change in vulnerability to reentry. For each level of hyperkalemia, increased cellular uncoupling between subepicardium and midmyocardium increased inducibility of reentry by restoring subepicardial tissue excitability via blocking midmyocardial electrotonic effect. In addition, increased lateral width of the border zone prevented inducibility of reentry as conduction block occurred in the central ischemic zone when the wave propagated across the border zone from the normal zone.Conclusion: The degree of hyperkalemia in the surviving subepicardium, the lateral width of border zone, and cellular uncoupling between the subepicardium and midmyocardium determine dispersion of refractoriness, conduction velocity, excitability, and, therefore, inducibility of reentry during phase 1B.</description><dc:title>Mechanisms for initiation of reentry in acute regional ischemia phase 1B</dc:title><dc:creator>Xiao Jie, Natalia A. Trayanova</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.014</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-16</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-16</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Experimental</prism:section><prism:startingPage>379</prism:startingPage><prism:endingPage>386</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527110000020/abstract?rss=yes"><title>Mechanisms of lethal arrhythmias due to acute myocardial ischemia: Regional factors and challenges in sudden death prevention</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527110000020/abstract?rss=yes</link><description>Although the occurrence rate of sudden cardiac death (SCD) has decreased somewhat, in part because of wider use of implantable defibrillators, SCD due to ventricular tachyarrhythmias (VTs) continues to be a significant problem. Ischemic heart disease (IHD) is a major risk factor for SCD, which is in turn a substantial contributor to IHD mortality. Efforts at diminishing the SCD burden in IHD patients include improved risk stratification, as well as the continued assessment of underlying pathophysiology to establish novel mechanistically based therapeutic interventions.</description><dc:title>Mechanisms of lethal arrhythmias due to acute myocardial ischemia: Regional factors and challenges in sudden death prevention</dc:title><dc:creator>Stanley Nattel</dc:creator><dc:identifier>10.1016/j.hrthm.2010.01.001</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-07</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-07</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Basic/Clinical Relevance</prism:section><prism:startingPage>387</prism:startingPage><prism:endingPage>388</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013277/abstract?rss=yes"><title>Distinguishing epicardial fat from scar: Analysis of electrograms using high-density electroanatomic mapping in a novel porcine infarct model</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013277/abstract?rss=yes</link><description>Background: The presence of epicardial fat can confound the quantification of scar during transpericardial electroanatomic mapping. The electrogram (EGM) characteristics of epicardial fat have not been systematically compared with infarct scar using gross and histopathological analysis as a gold standard.Objective: The purpose of this study was to compare the EGM characteristics of epicardial fat with infarct scar.Methods: A closed-chest infarction was created in 40–50 kg pigs by occlusion of the circumflex artery for 150 minutes using an angioplasty balloon. This artery was chosen to minimize any potential overlap of epicardial fat with infarct and to spare any septal involvement. After 4–12 weeks of infarct healing, epicardial mapping was performed. EGMs in low-voltage regions (&lt;1.5 mV) were analyzed, and bipolar amplitude, duration, number of deflections, and the presence of late potentials were recorded. Statistical analysis was performed using unpaired t-test and χ2 analysis. Gross and histopathological examination was used to confirm areas of fat and infarct scar.Results: Seven porcine hearts were analyzed after high-density epicardial mapping (364 ± 92 points) was performed 48 ± 19 days after infarction. The mean bipolar EGM amplitude was similar in fat and scar (0.77 ± 0.34 vs. 0.75 ± 0.38 mV; P = not significant). The mean EGM duration was longer in scar than in fat (68.8 ± 18.9 vs. 50.1 ± 11.6 ms; P  4 mm in thickness registered low-voltage bipolar EGMs.Conclusion: Scar from healed myocardial infarction exhibits more fractionation and longer EGM duration when compared with fat. Late potentials are highly specific for locating infarct scars.</description><dc:title>Distinguishing epicardial fat from scar: Analysis of electrograms using high-density electroanatomic mapping in a novel porcine infarct model</dc:title><dc:creator>Roderick Tung, Shiro Nakahara, Rafael Ramirez, Chi Lai, Michael C. Fishbein, Kalyanam Shivkumar</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.023</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Experimental</prism:section><prism:startingPage>389</prism:startingPage><prism:endingPage>395</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013356/abstract?rss=yes"><title>Short-term hypertension is associated with the development of atrial fibrillation substrate: A study in an ovine hypertensive model</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013356/abstract?rss=yes</link><description>Background: Hypertension is frequently complicated by the development of atrial fibrillation (AF). However, the mechanisms of this link remain poorly understood. In addition, whether short-term hypertension can result in a substrate for AF is not known.Objective: The purpose of this study was to characterize the atrial substrate predisposing to AF due to short-duration hypertension.Methods: Sixteen sheep were studied: 10 had induced hypertension for 7 ± 4 weeks via the “one-kidney, one-clip” model, and six were controls. Cardiac magnetic resonance imaging was used to assess functional changes. Open-chest electrophysiological study was performed using a custom-made 128-electrode epicardial plaque applied to both right (RA) and left atria (LA), including the Bachmann's bundle, to determine effective refractory periods (ERPs) and conduction velocity at four pacing cycle lengths from six sites. Tissue specimens were harvested for structural analysis.Results: The hypertensive group demonstrated the following compared with controls: higher blood pressure (P &lt;.0001), enlarged LA (P &lt;.05), reduced LA ejection fraction (P &lt;.05), uniformly higher mean ERP (P &lt;.001), slower mean conduction velocity (P &lt;.001), higher conduction heterogeneity index (P &lt;.0001), greater AF inducibility (P = .03), and increased AF durations (P = .04). Picrosirius red staining of atrial tissues revealed increased interstitial fibrosis (P &lt;.0001). There was also evidence of increased inflammatory cell infiltrates (P &lt;.0001).Conclusion: Short-duration hypertension is associated with significant atrial remodeling characterized by atrial enlargement/dysfunction, interstitial fibrosis, inflammation, slowed/heterogeneous conduction, increased ERP, and greater propensity for AF.</description><dc:title>Short-term hypertension is associated with the development of atrial fibrillation substrate: A study in an ovine hypertensive model</dc:title><dc:creator>Dennis H. Lau, Lorraine Mackenzie, Darren J. Kelly, Peter J. Psaltis, Michael Worthington, Arumuga Rajendram, Douglas R. Kelly, Adam J. Nelson, Yuan Zhang, Pawel Kuklik, Anthony G. Brooks, Stephen G. Worthley, Randall J. Faull, Mohan Rao, James Edwards, David A. Saint, Prashanthan Sanders</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.031</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Experimental</prism:section><prism:startingPage>396</prism:startingPage><prism:endingPage>404</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013290/abstract?rss=yes"><title>Purkinje activation precedes myocardial activation following defibrillation after long-duration ventricular fibrillation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013290/abstract?rss=yes</link><description>Background: While reentry within the ventricular myocardium (VM) is responsible for the maintenance of short-duration ventricular fibrillation (SDVF; VF duration &lt;1 minute), Purkinje fibers (PFs) are important in the maintenance of long-duration ventricular fibrillation (LDVF; VF duration &gt;1 minute).Objective: The purpose of this study was to test the hypothesis that the mechanisms of defibrillation may also be different for SDVF and LDVF.Methods: A multielectrode basket catheter was deployed in the left ventricle of eight beagles. External defibrillation shocks were delivered with a ramp-up protocol after SDVF (20 seconds) and LDVF (150 seconds). Earliest VM and PF activations were identified after the highest energy shock that failed to terminate VF and the successful shock.Results: Defibrillation was successful after 36 ± 12 and 181 ± 14 seconds for SDVF and LDVF, respectively. The time after shock delivery until earliest activation was detected for failed shocks and was significantly longer after LDVF (138.7 ± 24.1 ms) than after SDVF (75.6 ± 8.7 ms). Earliest postshock activation after SDVF typically initiated in the VM (14 of 16 episodes), while it always initiated in the PF (16 of 16 episodes) after LDVF. Sites of earliest activity during sinus rhythm correlated with sites of earliest postshock activation for PF-led cycles but not for VM-led cycles.Conclusion: Earliest recorded postshock activation is in the Purkinje system after LDVF but not after SDVF. This difference raises the possibility that the optimal defibrillation strategy is different for SDVF and LDVF.</description><dc:title>Purkinje activation precedes myocardial activation following defibrillation after long-duration ventricular fibrillation</dc:title><dc:creator>Derek J. Dosdall, Jose Osorio, Robert P. Robichaux, Jian Huang, Li Li, Raymond E. Ideker</dc:creator><dc:identifier>10.1016/j.hrthm.2009.11.025</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-03</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Experimental</prism:section><prism:startingPage>405</prism:startingPage><prism:endingPage>412</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109012570/abstract?rss=yes"><title>Transconduit puncture for catheter ablation of atrial tachycardia in a patient with extracardiac Fontan palliation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109012570/abstract?rss=yes</link><description>Fontan palliation and its variants are the most widely used and accepted approach for regulating pulmonary blood flow and relieving cyanosis in patients with single-ventricle physiology. First-generation Fontan procedures involved connection of the right atrium (RA) to the pulmonary artery (PA). However, this frequently caused RA dilation, sluggish RA flow, and atrial fibrosis and was associated with a high incidence of atrial arrhythmias. Exclusion of most or all of the RA decreases the incidence of atrial arrhythmias; therefore, the Fontan procedure evolved with the establishment of a total cavopulmonary connection by way of either the lateral tunnel (an intra-atrial tunnel) or the extracardiac Fontan. Patients who have undergone first-generation RA–PA Fontan surgery with subsequent development of atrial arrhythmias may benefit from surgical conversion to total cavopulmonary connection with concomitant arrhythmia surgery. Despite a significant reduction in arrhythmia burden, a subgroup of patients still develop recurrent arrhythmias. The extracardiac Fontan consists of an inferior vena cava to PA conduit and direct connection of the superior vena cava to the PA. As the procedure is performed completely outside the heart, it is thought to be associated with fewer arrhythmic sequelae. However, the conduit is made of stiff Gore-Tex, which precludes access into the heart. This report outlines an approach to catheter ablation in a patient with extracardiac Fontan palliation in which the heart was accessed via the conduit.</description><dc:title>Transconduit puncture for catheter ablation of atrial tachycardia in a patient with extracardiac Fontan palliation</dc:title><dc:creator>Amish S. Dave, Jamil Aboulhosn, John S. Child, Kalyanam Shivkumar</dc:creator><dc:identifier>10.1016/j.hrthm.2009.10.037</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-11-09</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-11-09</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Case Report</prism:section><prism:startingPage>413</prism:startingPage><prism:endingPage>416</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109013824/abstract?rss=yes"><title>The year in arrhythmias—2009: Part I</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109013824/abstract?rss=yes</link><description>It is impossible to summarize all advances made in clinical and basic cardiac electrophysiology in 2009. In this article, we have attempted to select and condense the key literature published during the year. We are bound to err both by inclusion and by omission. We apologize to investigators and authors whose worthy contributions are not mentioned because of space and/or our own ignorance, and we welcome the input and criticisms of the Heart Rhythm readership, as these will assist in identifying the directions to be taken in “The Year in Arrhythmias 2010.” What follows is a subjective sample of highlighted articles exemplifying the recent advances in our field.</description><dc:title>The year in arrhythmias—2009: Part I</dc:title><dc:creator>Brian Olshansky, Mario Delmar, Gordon F. Tomaselli</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.011</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-25</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Contemporary Review--Associate Editor: Sami Viskin</prism:section><prism:startingPage>417</prism:startingPage><prism:endingPage>426</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109004627/abstract?rss=yes"><title>Paradoxical nodal response during parahisian pacing: What is the mechanism?</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109004627/abstract?rss=yes</link><description>A 24-year-old woman underwent electrophysiologic study for recurrent palpitations and syncope. Baseline ECG did not show any evidence of preexcitation. She had no structural heart disease. Head-up tilt test was negative for neurocardiogenic syncope. During electrophysiologic study, baseline AH interval was 82 ms, and HV interval was 39 ms. Programmed ventricular stimulation revealed dual retrograde AV nodal physiology with single echo but no inducible tachycardia. Atrial activation during ventricular pacing was central and decremental. Programmed atrial stimulation did not induce any tachycardia, and no evidence of anterograde dual AV nodal physiology was seen. Parahisian pacing was performed (). During His-bundle capture as evidenced by relatively narrow QRS complex, the stimulus to atrial (SA) interval was 271 ms. During His-bundle noncapture as evidenced by wider QRS complex, the SA interval was 181 ms. What is the mechanism of paradoxical prolongation of the SA interval during His-bundle capture compared with during His-bundle noncapture?</description><dc:title>Paradoxical nodal response during parahisian pacing: What is the mechanism?</dc:title><dc:creator>Anandaraja Subramanian, Menashe Waxman</dc:creator><dc:identifier>10.1016/j.hrthm.2009.04.027</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-04-29</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-04-29</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Featured Arrhythmia--Associate Editor: Fred Morady</prism:section><prism:startingPage>427</prism:startingPage><prism:endingPage>428</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109007528/abstract?rss=yes"><title>Atrial tachycardia arising from “right top pulmonary vein”</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109007528/abstract?rss=yes</link><description>We report a 51-year-old male presenting with palpitations, anxiety, and shortness of breath for the past 2 years. Atrial tachycardia (AT) as well as atrial fibrillation (AF) were first documented 1 year before the radiofrequency ablation attempt. The decision for left atrial (LA) ablation was made in light of remaining symptoms and documented episodes of AF under class IA antiarrhythmic drug treatment.</description><dc:title>Atrial tachycardia arising from “right top pulmonary vein”</dc:title><dc:creator>Martin Martinek, Said Hassanein, Helmut Purerfellner</dc:creator><dc:identifier>10.1016/j.hrthm.2009.07.013</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-07-16</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-07-16</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Image--Associate Editor: David S. Rosenbaum</prism:section><prism:startingPage>429</prism:startingPage><prism:endingPage>430</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752711000007X/abstract?rss=yes"><title>Basic and Translational</title><link>http://www.heartrhythmjournal.com/article/PIIS154752711000007X/abstract?rss=yes</link><description>Jarecki BW et al (JCI 2009 Epub, PMID: 20038812) demonstrated that a paroxysmal extreme pain disorder (PEPD) mutation in the human peripheral neuronal sodium channel Nav1.7, a paramyotonia congenita (PMC) mutation in the human skeletal muscle sodium channel Nav1.4, and a long-QT3/SIDS mutation in the human cardiac sodium channel Nav1.5 all substantially increased the amplitude of resurgent sodium currents. Computer simulations indicated that resurgent currents associated with the Nav1.7 mutation could induce high-frequency action potential firing in nociceptive neurons and that resurgent currents associated with the Nav1.5 mutation could broaden the action potential in cardiac myocytes. These effects are consistent with the pathophysiology associated with the respective channelopathies. Conclusion: Resurgent currents are associated with multiple channelopathies and are likely to be important contributors to neuronal and muscle disorders of excitability.</description><dc:title>Basic and Translational</dc:title><dc:creator>Peng-Sheng Chen</dc:creator><dc:identifier>10.1016/j.hrthm.2010.01.005</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-29</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-29</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>EP News--Associate Editors: Peng-Sheng Chen and N. A. Mark Estes III</prism:section><prism:startingPage>431</prism:startingPage><prism:endingPage>431</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527110000081/abstract?rss=yes"><title>Clinical</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527110000081/abstract?rss=yes</link><description>Yu et al (N Engl J Med 2009;361:2123–2134; PMID: 19915220) evaluated whether biventricular (BiV) pacing is superior to right ventricular apical (RVA) pacing in preventing deterioration of left ventricular (LV) systolic function and cardiac remodeling in patients with bradycardia and a normal ejection fraction (EF). In this prospective, double-blind, multicenter study, 177 patients with implantation of a BiV pacemaker were randomized to BiV pacing (89 patients) or RVA pacing (88 patients). The primary end points were the LVEF and LV end-systolic volume. At 12 months, the mean LVEF was significantly lower with RVA pacing than in the BiV pacing (54.8+/-9.1% vs. 62.2+/-7.0%, P&lt;0.001).The LV end-systolic volume was significantly higher in the RVA pacing group than in the BiV group (35.7+/-16.3 ml vs. 27.6+/-10.4 ml, P&lt;0.001). The authors conclude that in patients with normal LVEF, RVA pacing resulted in adverse LV remodeling and in a reduction in the LVEF. These effects were prevented by biventricular pacing.</description><dc:title>Clinical</dc:title><dc:creator>N.A. Mark Estes</dc:creator><dc:identifier>10.1016/j.hrthm.2010.01.006</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-29</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-29</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>EP News--Associate Editors: Peng-Sheng Chen and N. A. Mark Estes III</prism:section><prism:startingPage>432</prism:startingPage><prism:endingPage>432</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014313/abstract?rss=yes"><title>To the Editor—Long term gastroesophageal reflux after atrial fibrillation ablation</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014313/abstract?rss=yes</link><description>I read with interest the paper by Martinek et al entitled “Acute development of gastroesophageal reflux after radiofrequency catheter ablation of atrial fibrillation.” While the authors' concern is the contribution that the development of gastroesophageal reflux may make to atrioesophageal fistulas, I think it is important to realize that reflux disease as a complication of the procedure may present long-term morbidity to the patient.</description><dc:title>To the Editor—Long term gastroesophageal reflux after atrial fibrillation ablation</dc:title><dc:creator>Deborah Callanan</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.021</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2010-01-04</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2010-01-04</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e1</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014349/abstract?rss=yes"><title>To the Editor Response—Gastroesophageal reflux by RF injury</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014349/abstract?rss=yes</link><description>We are grateful for all of the interesting comments on our manuscript entitled “Acute development of gastroesophageal reflux after radiofrequency catheter ablation of atrial fibrillation” and would like to discuss a few statements that have been made.</description><dc:title>To the Editor Response—Gastroesophageal reflux by RF injury</dc:title><dc:creator>Martin Martinek, Rainer Schoefl, Helmut Puererfellner</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.024</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-31</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-31</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e1</prism:startingPage><prism:endingPage>e2</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014350/abstract?rss=yes"><title>To the Editor—Gastroesophageal reflux after RF ablation of AF</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014350/abstract?rss=yes</link><description>We read with great interest the manuscript of Martinek et al recently published in Heart Rhythm entitled “Acute development of gastroesophageal reflux after radiofrequency catheter ablation of atrial fibrillation.”</description><dc:title>To the Editor—Gastroesophageal reflux after RF ablation of AF</dc:title><dc:creator>Georg Nölker, Anil-Martin Sinha</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.025</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-31</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-31</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e2</prism:startingPage><prism:endingPage>e3</prism:endingPage></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527109014362/abstract?rss=yes"><title>To the Editor Response—Esophageal lesions following pulmonary vein isolation for AF</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527109014362/abstract?rss=yes</link><description>We thank you for all your interesting comments on our article, “Acute development of gastroesophageal reflux after radiofrequency catheter ablation of atrial fibrillation,” and would like to discuss a few of the aspects that were mentioned.</description><dc:title>To the Editor Response—Esophageal lesions following pulmonary vein isolation for AF</dc:title><dc:creator>Martin Martinek, Rainer Schoefl, Helmut Puererfellner</dc:creator><dc:identifier>10.1016/j.hrthm.2009.12.026</dc:identifier><dc:source>Heart Rhythm 7, 3 (2010)</dc:source><dc:date>2009-12-31</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2009-12-31</prism:publicationDate><prism:volume>7</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1547-5271(10)X0002-9</prism:issueIdentifier><prism:section>Letters to the Editor</prism:section><prism:startingPage>e3</prism:startingPage><prism:endingPage>e4</prism:endingPage></item></rdf:RDF>