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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//inpress?rss=yes"><title>Heart Rhythm - Articles in Press</title><description>Heart Rhythm RSS feed: Articles in Press.    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.  
 
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//inpress?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2012 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:publicationDate>2012-05-14</prism:publicationDate><prism:copyright> © 2012 Heart Rhythm Society. Published by Elsevier Inc. 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Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS) - Corrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112002937/abstract?rss=yes</link><description>The purpose of this consensus statement is to provide up-to-date clinical practice guidelines on the evaluation and management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW) electrocardiographic (ECG) pattern. The terminology WPW was first used to describe a “bundle-branch pattern” with a short PR interval in healthy young people prone to paroxysmal tachycardia and/or atrial fibrillation. Although isolated case reports preceded the 1930 landmark manuscript, history correctly credits identification of the syndrome to Drs. Wolff, Parkinson, and White. Over the years, the syndrome evolved through observations by anatomists and electrophysiologists to appreciate a reentrant circuit involving both the AV node–His axis as well as the accessory pathway. Isolated ventricular preexcitation refers to the abnormal ECG pattern in the absence of any clinical cardiovascular symptoms. Isolated ventricular preexcitation has historically been termed “asymptomatic WPW” or asymptomatic WPW syndrome. This manuscript provides guidelines only for individuals with an abnormal ECG pattern of ventricular preexcitation without symptoms. In response to recently published literature regarding patients with WPW, the Pediatric and Congenital Electrophysiology Society (PACES) in conjunction with the Heart Rhythm Society (HRS) created a writing committee to provide helpful clinical guidelines for asymptomatic patients with WPW. There are at present no specific guidelines addressing risk stratification in the asymptomatic young patient with WPW. Selected members from within PACES and HRS have reviewed and analyzed the published scientific literature, carefully assessing the absolute and relative risks of invasive procedures and therapies so as to provide a practical approach to optimize patient care.</description><dc:title>PACES/HRS Expert Consensus Statement on the Management of the Asymptomatic Young Patient with a Wolff-Parkinson-White (WPW, Ventricular Preexcitation) Electrocardiographic Pattern: Developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Endorsed by the governing bodies of PACES, HRS, the American College of Cardiology Foundation (ACCF), the American Heart Association (AHA), the American Academy of Pediatrics (AAP), and the Canadian Heart Rhythm Society (CHRS) - Corrected Proof</dc:title><dc:creator>Mitchell I. Cohen, John K. Triedman, Bryan C. Cannon, Andrew M. Davis, Fabrizio Drago, Jan Janousek, George J. Klein, Ian H. Law, Fred J. Morady, Thomas Paul, James C. Perry, Shubhayan Sanatani, Ronn E. Tanel</dc:creator><dc:identifier>10.1016/j.hrthm.2012.03.050</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-14</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-14</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004924/abstract?rss=yes"><title>Biological Pacemakers: the oscillatory road ahead - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004924/abstract?rss=yes</link><description></description><dc:title>Biological Pacemakers: the oscillatory road ahead - Accepted Manuscript</dc:title><dc:creator>Sandeep V. Pandit, José Jalife</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.010</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-14</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-14</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004936/abstract?rss=yes"><title>Cell-Specific Nanoplatform-Enabled Photodynamic Therapy for Cardiac Cells - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004936/abstract?rss=yes</link><description></description><dc:title>Cell-Specific Nanoplatform-Enabled Photodynamic Therapy for Cardiac Cells - Accepted Manuscript</dc:title><dc:creator>Uma Mahesh R. Avula, Gwangseong Kim, Yong-Eun Koo Lee, Fred Morady, Raoul Kopelman, Jérôme Kalifa</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.011</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-14</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-14</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004948/abstract?rss=yes"><title>Demonstration of Anatomical Reentrant Tachycardia Circuit in Verapamil-Sensitive Atrial Tachycardia Originating from the Vicinity of the Atrioventricular Node - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004948/abstract?rss=yes</link><description>Abstract: 
Background:: 
The anatomical location of reentry circuit in verapamil-sensitive atrial tachycardia originating from the vicinity of atrioventricular node (V-AT) is not well clarified.

Objective:: 
The purpose of this study was to define the reentry circuit of V-AT.

Methods:: 
In 17 patients with V-AT, rapid atrial pacing at a rate 5 beats/minute faster than the tachycardia rate was delivered from multiple sites of the right atrium (RA) during tachycardia to define the direction of the proximity of the slow conduction area of reentry circuit. After identification of manifest entrainment and orthodromic capture of the earliest atrial activation site (EAAS), radiofrequency energy was delivered starting at a site 2 cm away from the EAAS in the direction of pacing site. Radiofrequency energy application site was then gradually advanced toward EAAS until termination of tachycardia to define the entrance of the slow conduction area.

Results:: 
The EAAS was orthodromically captured by pacing delivered from one of the high antero-lateral RA (n=6), high postero-septal RA (n=9) and RA appendage (n=2). Radiofrequency energy delivery to the site, 10.1±2.8 mm away from EAAS, terminated V-AT immediately after the onset of delivery (2.9±1.0 sec). The successful ablation site located outside the Koch’s triangle, being more distant from His bundle (HB) site than EAAS (12.4±2.9 vs. 6.4±1.9 mm, p&lt;0.0001).

Conclusion:: 
The reentry circuit of V-AT located outside the Koch’s triangle. V-AT was eliminated by the radiofrequency energy delivered to the entrance of reentry circuit, which was more distant from HB site than EAAS, under the navigation of entrainment.
</description><dc:title>Demonstration of Anatomical Reentrant Tachycardia Circuit in Verapamil-Sensitive Atrial Tachycardia Originating from the Vicinity of the Atrioventricular Node - Accepted Manuscript</dc:title><dc:creator>Hiroshige Yamabe, Ken Okumura, Kenji Morihisa, Junjiroh Koyama, Hisanori Kanazawa, Tadashi Hoshiyama, Hisao Ogawa</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.012</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-14</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-14</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752711200495X/abstract?rss=yes"><title>QRS Prolongation Induced by Cardiac Resynchronization Therapy Correlates with Deterioration in Left Ventricular Function - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS154752711200495X/abstract?rss=yes</link><description>Abstract: 
Background:: 
The benefits of cardiac resynchronization in inducing reverse ventricular remodeling in patients with left ventricular (LV) systolic dysfunction have been well established. Still, up to 30% of patients fail to derive significant improvement from this therapy. A subset of “non- responders” experience deterioration in LV function following CRT. Characteristics of this patient population, however, have not been studied.

Objective:: 
This study sought to determine characteristics of patients who experience deterioration in LV function following CRT.

Methods:: 
Clinical, electrocardiographic, and echocardiographic data were collected in 856 consecutive patients presenting for a new CRT device. For inclusion, all patients had a left ventricular ejection fraction =40%, a QRS duration =120 ms, and available baseline and follow up echocardiograms and electrocardiograms. Deterioration in LV function was defined as an absolute decrease in ejection fraction of 5% or greater from baseline. Multivariate models were constructed to identify variables significantly associated with deterioration.

Results:: 
507 patients met inclusion criteria of which 60 met criteria for deterioration (11.8%). Patients with deterioration were more likely to be male (86.7% vs. 66.9%, p=0.002.), have a non-left bundle branch block morphology (41.7% vs. 23.7%, p= 0.001), and a history of atrial fibrillation (66.7% vs. 51.7%, p=0.03). Comparing the pre-CRT QRS duration to the first biventricular-paced QRS duration post-CRT implant, patients with LV deterioration had significant QRS widening compared to those without deterioration(ms)(+3.9±34.1 vs. -9.0±27.4, p=0.007, respectively). In multivariate analysis, QRS widening indexed to the baseline QRS duration was significantly associated with LV deterioration ((odds ratio 1.14(1.06-1.23), p=0.001)).

Conclusion:: 
QRS widening is associated with deterioration in LV function following CRT.
</description><dc:title>QRS Prolongation Induced by Cardiac Resynchronization Therapy Correlates with Deterioration in Left Ventricular Function - Accepted Manuscript</dc:title><dc:creator>John Rickard, Gregory Jackson, David D. Spragg, Edmond M. Cronin, Bryan Baranowski, W.H. Wilson Tang, Bruce L. Wilkoff, Niraj Varma</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.013</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-14</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-14</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004961/abstract?rss=yes"><title>High frequency stimulation of the atria increases early recurrence following pulmonary vein isolation in patients with persistent atrial fibrillation - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004961/abstract?rss=yes</link><description>Abstract: 
Background: 
High frequency stimulation of the atria (HFS) induces atrial fibrillation (AF) when applied during sinus rhythm and elicits a parasympathetic response when delivered at sites where ganglionated plexi (GPs) are located. However, little is known about its impact after an electrophysiological study.
Objective We aimed to evaluate the impact of HFS on the short-term and long-term outcomes after ablation of persistent AF.

Methods: 
Thirty consecutive patients with persistent or longstanding persistent AF were randomly assigned to either receive HFS of the left atrium (LA) (n = 15), or not (n = 15) during their electrophysiological studies. Patients receiving HFS were examined to determine whether or not a vagal response was elicited by the HFS at sites where GPs were located before and after conventional pulmonary vein (PV) isolation without any ablation targeting the GPs. Patients not receiving the HFS only underwent the ablation procedure. The rate of recurrence of AF within 3 months of the procedure (early recurrence [ER]), and the frequency of that occurring after that period (late recurrence [LR]), were compared between the patient groups.

Results: 
The incidence of ER occurred more frequently in patients with HFS than in those without (80% vs. 40%; p = 0.015), whereas the occurrence of LR was similar between the two groups (27% vs. 33%; p = 0.73). In the HFS group, the number of GPs decreased from 3.5 ± 1.1 to 1.6 ± 0.9 after the PV isolation (p &lt;0.0001), and the decrease was smaller in the patients experiencing ER than in those without.

Conclusion: 
HFS increases the incidence of ER in patients with persistent AF despite a partial GP modification resulting from the PV isolation.
</description><dc:title>High frequency stimulation of the atria increases early recurrence following pulmonary vein isolation in patients with persistent atrial fibrillation - Accepted Manuscript</dc:title><dc:creator>Akinori Sairaku, Yukihiko Yoshida, Hiroki Kamiya, Yasushi Tatematsu, Mamoru Nanasato, Haruo Hirayama, Yukiko Nakano, Yasuki Kihara</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.014</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-14</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-14</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004894/abstract?rss=yes"><title>Genetic Marker of Torsades de Pointes Risk Following Myocardial Infarction - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004894/abstract?rss=yes</link><description></description><dc:title>Genetic Marker of Torsades de Pointes Risk Following Myocardial Infarction - Accepted Manuscript</dc:title><dc:creator>Alfred L. George</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.007</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-10</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-10</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004857/abstract?rss=yes"><title>Every Life Counts - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004857/abstract?rss=yes</link><description></description><dc:title>Every Life Counts - Accepted Manuscript</dc:title><dc:creator>Bruce D. Lindsay, Bruce L. Wilkoff</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.004</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-09</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-09</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004870/abstract?rss=yes"><title>Letter response to “Deaths Caused by the Failure of Riata and Riata ST Implantable Cardioverter-Defibrillator Leads,” by Dr. Robert Hauser, et al. - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004870/abstract?rss=yes</link><description></description><dc:title>Letter response to “Deaths Caused by the Failure of Riata and Riata ST Implantable Cardioverter-Defibrillator Leads,” by Dr. Robert Hauser, et al. - Accepted Manuscript</dc:title><dc:creator>Mark Carlson</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.006</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-09</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-09</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004821/abstract?rss=yes"><title>ICD replacement using a functioning Fidelis lead; Vigilance is the word - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004821/abstract?rss=yes</link><description></description><dc:title>ICD replacement using a functioning Fidelis lead; Vigilance is the word - Accepted Manuscript</dc:title><dc:creator>Charles J. Love</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.001</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004833/abstract?rss=yes"><title>Desmopressin acutely decreases tachycardia and improves symptoms in the Postural Tachycardia Syndrome (POTS) - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004833/abstract?rss=yes</link><description>Abstract: 
Background: 
Postural Tachycardia Syndrome (POTS) induces disabling chronic orthostatic intolerance with an excessive increase in heart rate (HR) upon standing, and many POTS patients have low blood volume. Increasing blood volume is a promising approach to this problem.

Objective: 
We tested the hypothesis that desmopressin (DDAVP) will attenuate the tachycardia and improve symptom burden in patients with POTS.

Methods: 
In this protocol, patients with POTS (n=30) underwent acute drug trials with DDAVP 0.2 mg orally and placebo, on separate mornings, in a randomized crossover design. Blood pressure, HR and symptoms were assessed while seated and after standing for up to 10 minutes prior to and hourly for 4 hours following study drug.

Results: 
Standing HR was significantly lower following DDAVP compared to placebo (101.9 ± 14.5 vs. 109.2 ± 17.4 bpm (P&lt;0.001)). Standing blood pressure was not affected (P=0.28). The symptom burden improved with DDAVP (from a score of 18 ± 18 to 13 ± 15 arbitrary units [au] at 2 hours) compared with placebo (from 18 ± 17 to 19 ± 16 au; P=0.010).

Conclusion: 
Oral desmopressin significantly attenuated tachycardia and improved symptoms in POTS. The safety profile of this approach would need to be examined before it can be recommended for routine treatment of these patients.
</description><dc:title>Desmopressin acutely decreases tachycardia and improves symptoms in the Postural Tachycardia Syndrome (POTS) - Accepted Manuscript</dc:title><dc:creator>Samuel T. Coffin, Bonnie K. Black, Italo Biaggioni, Sachin Y. Paranjape, Carlos Orozco, Phillip W. Black, William D. Dupont, David Robertson, Satish R. Raj</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.002</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004845/abstract?rss=yes"><title>Arrhythmia Discrimination Using Hemoglobin Spectroscopy in Humans - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004845/abstract?rss=yes</link><description>Abstract: 
Background: 
Inappropriate therapies are frequently delivered by implantable cardioverter-defibrillators (ICD). We have investigated muscle perfusion as a means of augmenting arrhythmia discrimination using implanted near-infrared spectroscopy.

Objective: 
To evaluate hemodynamic stability by monitoring muscle perfusion from within the ICD pocket, in fresh tissue and inside the scar capsule on pre-existing ICD generators, during induced cardiac arrhythmias, in humans.

Methods: 
The sensor was implanted on or under the pectoral muscle, during ICD defibrillation threshold testing. A microvascular oxygenation trend indicator (O2 Index) was computed during 74 induced ventricular fibrillation (VF) and 34 normal sinus rhythm (NSR) episodes in 34 patients and also during 28 atrial and 90 ventricular overdrive pacing episodes as simulations of supraventricular and ventricular tachycardias, respectively.

Results: 
On average, the change in oxygenation, based on the O2 Index, was statistically significant (p&lt;0.003) from baseline within 3 seconds following cardiac arrest. An optimized O2 Index, used for detecting the hemodynamic trend, exhibited a decreasing trend during VF (p&lt;0.0001) and was different from that during NSR (p&lt;0.0001). The sensitivity for the detection of VF was 100% and specificity for the rejection of NSR was 82%, in the presence of scar tissue on the optical sensor. For a 35 mmHg drop in the mean arterial pressure as the threshold for hemodynamic instability, the specificity for the rejection of hemodynamically stable atrial and ventricular pacing episodes were 93% and 71%, respectively.

Conclusion: 
An implantable near-infrared spectroscopic sensor may be useful for hemodynamic monitoring during cardiac arrhythmias to prevent inappropriate therapy.
</description><dc:title>Arrhythmia Discrimination Using Hemoglobin Spectroscopy in Humans - Accepted Manuscript</dc:title><dc:creator>S.J. Compton, C.D. Swerdlow, R.C. Canby, G.G. Strobel, J.D. Zagrodzky, C. Cinbis, J.K. Carney, S.K. Bhunia</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.003</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004869/abstract?rss=yes"><title>In search of the shocking truth - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004869/abstract?rss=yes</link><description></description><dc:title>In search of the shocking truth - Accepted Manuscript</dc:title><dc:creator>Károly Kaszala, Kenneth A. Ellenbogen</dc:creator><dc:identifier>10.1016/j.hrthm.2012.05.005</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-07</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-07</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004808/abstract?rss=yes"><title>Response to Letter to the Editor: Nodo-ventricular pathways - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004808/abstract?rss=yes</link><description></description><dc:title>Response to Letter to the Editor: Nodo-ventricular pathways - Accepted Manuscript</dc:title><dc:creator>Reginald T. Ho, David L. Fischman</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.040</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-03</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752711200481X/abstract?rss=yes"><title>Pulmonary vein hematoma after atrial fibrillation cryoablation: A new complication - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS154752711200481X/abstract?rss=yes</link><description></description><dc:title>Pulmonary vein hematoma after atrial fibrillation cryoablation: A new complication - Accepted Manuscript</dc:title><dc:creator>Francis Bessière, Philippe Chevalier</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.041</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-03</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-03</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004778/abstract?rss=yes"><title>Learning from Clinical Experience - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004778/abstract?rss=yes</link><description></description><dc:title>Learning from Clinical Experience - Accepted Manuscript</dc:title><dc:creator>Jeffrey L. Williams</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.037</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752711200478X/abstract?rss=yes"><title>Spinal Cord Stimulation Protects Against Atrial Fibrillation Induced by Tachypacing - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS154752711200478X/abstract?rss=yes</link><description>Abstract: 
Background: 
Spinal cord stimulation (SCS) has been shown to modulate atrial electrophysiology and confer protection against ischemia and ventricular arrhythmias in animal models.

Objective: 
Determine whether SCS reduces the susceptibility to atrial fibrillation (AF) induced by tachypacing (TP).

Methods: 
In 21 canines, upper thoracic SCS systems and custom cardiac pacing systems (PM) were implanted. Right atrial (RA) and left atrial (LA) effective refractory periods (ERPs) were measured at baseline and after 15 minutes of SCS. Following recovery in a subset of canines, PM was turned on to induce AF by alternately delivering TP and searching for AF. Canines were randomized to no SCS therapy (CTL) or intermittent SCS therapy upon initiation of TP (EARLY) or after 8 weeks of TP (LATE). AF burden (percent AF relative to total sense time) and AF inducibility (percent of TP periods resulting in AF) were monitored weekly. After 15 weeks, echocardiography and histology were performed.

Results: 
ERPs increased by 21±14ms (p=0.001) in LA and 29±12ms (p=0.002) in RA after acute SCS. AF burden was reduced for 11 weeks in EARLY compared to CTL (p&lt;0.05). AF inducibility remained lower by week 15 in EARLY compared to CTL (32±10% vs 91±6%, p&lt;0.05). AF burden and inducibility were not significantly different between LATE and CTL animals. There were no structural differences among any groups.

Conclusions: 
SCS prolonged atrial ERPs and reduced AF burden and inducibility in a canine AF model induced by TP. These data suggest that SCS may represent a treatment option for AF.
</description><dc:title>Spinal Cord Stimulation Protects Against Atrial Fibrillation Induced by Tachypacing - Accepted Manuscript</dc:title><dc:creator>Scott A. Bernstein, Brian Wong, Carolina Vasquez, Stuart P. Rosenberg, Ryan Rooke, Laura M. Kuznekoff, Joshua M. Lader, Vanessa M. Mahoney, Tatyana Budylin, Marie Älvstrand, Tammy Rakowski-Anderson, Rupinder Bharmi, Riddhi Shah, Steven Fowler, Douglas Holmes, Taraneh G. Farazi, Larry A. Chinitz, Gregory E. Morley</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.038</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004791/abstract?rss=yes"><title>Resetting Atrioventricular Nodal Reentrant Tachycardia: The Impact of Nodal Extensions - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004791/abstract?rss=yes</link><description></description><dc:title>Resetting Atrioventricular Nodal Reentrant Tachycardia: The Impact of Nodal Extensions - Accepted Manuscript</dc:title><dc:creator>Demosthenes G. Katritsis</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.039</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-05-01</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-05-01</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004766/abstract?rss=yes"><title>Impact of QRS Duration of Frequent Premature Ventricular Complexes on the Development of Cardiomyopathy - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004766/abstract?rss=yes</link><description>Abstract: 
Background: 
Patients with frequent premature ventricular complexes (PVCs) are at risk of developing reversible PVC–induced cardiomyopathy (rPVC-CMP). Not all determinants of rPVC-CMP are known. The purpose of this study was to assess the impact of QRS duration of PVCs on the development of rPVC-CMP.

Methods: 
In a consecutive series of 294 patients with frequent idiopathic PVCs referred for PVC ablation, the width of the PVC-QRS complex was assessed. The QRS width was correlated with the presence of rPVC-CMP.

Results: 
The PVC-QRS width was significantly greater in patients with rPVC-CMP than in patients without rPVC-CMP (164±20 vs 149±17 ms, p&lt;0.0001). The site of origin of the PVC impacted on the PVC-QRS width, with epicardial PVCs having the broadest QRS complexes. Patients with PVCs originating from the right ventricular outflow tract or the fascicles had the narrowest QRS complexes. After adjusting for PVC burden, symptom duration, and PVC site of origin, PVC-QRS width and an epicardial PVC origin were independently associated with rPVC-CMP. Based on ROC analysis, a QRS duration &gt;150 ms best differentiated patients with and without rPVC-CMP (AUC: 0.66; sensitivity 80%, specificity 52%). The PVC burden for developing rPVC-CMP is significantly lower in patients with a PVC-QRS width ≥150 ms compared to patients with a narrower PVC-QRS complex (22±13% vs 28±12%; p&lt;0.0001).

Conclusion: 
Broader PVCs and an epicardial PVC origin are associated with the development of rPVC-CMP independent of the PVC burden.
</description><dc:title>Impact of QRS Duration of Frequent Premature Ventricular Complexes on the Development of Cardiomyopathy - Accepted Manuscript</dc:title><dc:creator>Miki Yokokawa, Hyungjin Myra Kim, Eric Good, Thomas Crawford, Aman Chugh, Frank Pelosi, Rakesh Latchamsetty, William Armstrong, Craig Alguire, Hakan Oral, Fred Morady, Frank Bogun</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.036</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-30</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-30</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003591/abstract?rss=yes"><title>EP News: Clinical - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003591/abstract?rss=yes</link><description>Lakkireddy et al (J Am Coll Cardiol 2012;59:1168–1174, PMID 22305113) evaluated the safety of dabigatran (D) during atrial fibrillation ablation in a multicenter, observational study of consecutive patients at 8 centers. All patients had the D dose held on the morning of the procedure. A total of 290 patients, including 145 taking D, and an equal number of matched patients taking uninterrupted warfarin (W), were included in the study. Three thromboembolic complications (2.1%) occurred in the D group compared with none in the W group (P &lt;.25). The D group had a significantly higher major bleeding rate (6% vs 1%; P &lt;.019), total bleeding rate (14% vs 6%; P &lt;.031), and composite of bleeding and thromboembolic complications (16% vs 6%; P &lt;.009) compared with the W group. D use was an independent predictor of bleeding or thromboembolic complications (odds ratio 2.76; P &lt;.01). The authors conclude that in patients undergoing atrial fibrillation ablation, D use significantly increases the risk of bleeding or thromboembolic complications compared with uninterrupted W therapy.</description><dc:title>EP News: Clinical - Uncorrected Proof</dc:title><dc:creator>N.A. Mark Estes</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.007</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-27</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-27</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003608/abstract?rss=yes"><title>EP News: Basic and Translational - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003608/abstract?rss=yes</link><description>The susceptibility to ventricular arrhythmia or sudden death is determined by the duration (eg, short or long QT syndromes and heart failure) or pattern (eg, Brugada syndrome) of ventricular repolarization. It is also known that there is circadian variation of the susceptibility to ventricular arrhythmias. However, the molecular mechanism by which the body's diurnal biological clock controls the circadian variations of repolarization remains unknown. Jeyaraj et al (Nature 2012;483:96, PMID 22367544) used the mice model to study the relationship between Krüppel-like family of transcription factors (Klfs) and myocardial repolarization. The term Krüppel (German for “cripple”) describes the crippled appearance of fruit fly larva caused by the mutation of the Krüppel gap gene. The Klfs are named for their homology to the fruit fly Krüppel protein. The Klfs have been extensively studied for their roles in cell proliferation, differentiation, and survival. Among them, Klf15 is linked to the pathobiology in heart failure. Jeyaraj et al show in mice heart that the cardiac ion-channel expression and QT-interval duration exhibit endogenous circadian rhythmicity under the control of Klf15, which is a biological clock–dependent oscillator. Klf15 transcriptionally controls the rhythmic expression of Kv channel interacting protein 2, a critical subunit required for generating the transient outward potassium (K) current. Because the transient outward K current of mice is primarily responsible for cardiomyocyte repolarization, deficiency or excess of Klf15 causes loss of rhythmic QT variation, abnormal repolarization, and enhanced susceptibility to ventricular arrhythmias. Klf15 is the first link between the biological clock and arrhythmogenesis. The authors conclude that circadian transcription of ion channels is a mechanism for cardiac arrhythmogenesis.</description><dc:title>EP News: Basic and Translational - Uncorrected Proof</dc:title><dc:creator>Peng-Sheng Chen</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.008</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-27</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-27</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004237/abstract?rss=yes"><title>Isolated Epicardial Ultra Rapid Activity - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004237/abstract?rss=yes</link><description></description><dc:title>Isolated Epicardial Ultra Rapid Activity - Accepted Manuscript</dc:title><dc:creator>Shinsuke Miyazaki, Kenji Koura, Yoshito Iesaka</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.035</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-27</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-27</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004195/abstract?rss=yes"><title>Pharmacotherapy in Medicare beneficiaries with atrial fibrillation - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004195/abstract?rss=yes</link><description>
Background: 
There are limited data regarding national patterns of pharmacotherapy for atrial fibrillation (AF) among older patients. Drug exposure data are now captured for Medicare beneficiaries enrolled in prescription drug plans.

Objective: 
To describe pharmacotherapy for AF among Medicare beneficiaries.

Methods: 
By using a 5% national sample of Medicare claims data, we compared demographic characteristics, comorbidity, and treatment patterns according to Medicare Part D status among patients with prevalent AF in 2006 and 2007.

Results: 
In 2006, 27,174 patients (29.3%) with prevalent AF were enrolled in Medicare Part D. In 2007, enrollment increased to 45,711 (49.1%). Most enrollees were taking rate-control agents (74.0% in 2007). β-Blocker use was higher in those with concomitant AF and heart failure and increased with higher CHADS2 scores (P &lt;.001). Antiarrhythmic use was 18.7% in 2006 and 19.1% in 2007, with amiodarone accounting for more than 50%. Class Ic drugs were used in 3.2% of the patients in 2007. Warfarin use was &lt;60% and declined with increasing stroke risk (P &lt;.001).

Conclusion: 
Pharmacotherapy for AF varied according to comorbidity and underlying risk. Amiodarone was the most commonly prescribed antiarrhythmic agent. Postmarketing surveillance using Medicare Part D claims data linked to clinical data may help inform comparative safety, effectiveness, and net clinical benefit of drug therapy for AF in older patients in real-world settings.
</description><dc:title>Pharmacotherapy in Medicare beneficiaries with atrial fibrillation - Uncorrected Proof</dc:title><dc:creator>Jonathan P. Piccini, Xiaojuan Mi, Tracy A. DeWald, Alan S. Go, Adrian F. Hernandez, Lesley H. Curtis</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.031</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-25</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004201/abstract?rss=yes"><title>A conflict of evidence: AVNRT or junctional tachycardia? - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004201/abstract?rss=yes</link><description>A 49-year-old woman who had previously undergone atrioventricular node (AVN) slow pathway cryoablation for typical AVN reentry tachycardia (AVNRT) presented with recurrent supraventricular tachycardia (SVT). During a transvenous electrophysiologic study, the SVT was reproducibly inducible with programmed atrial stimulation that resulted in an atrio-His (AH) interval “jump.” Other features of the SVT that were compatible with a recurrence of typical AVNRT included central atrial activation, AH interval &gt;&gt; HA interval, and a septal ventriculoatrial interval of 40 ms. Despite several radiofrequency energy applications in the region between the os of the coronary sinus and the tricuspid valve annulus that caused slow junctional rhythm, the SVT remained inducible. A spontaneous premature atrial contraction (PAC) during tachycardia advanced the immediate His potential without terminating the SVT (A). After this observation, atrial diastole in the SVT was scanned with paced PACs, and those delivered prior to His bundle depolarization had the same effect (B). A paced PAC later in atrial diastole that was timed to His bundle refractoriness, however, advanced the subsequent His potential by 34 ms (A), and a PAC delivered just after the His potential was still able to advance the subsequent His timing by 20 ms (B). What is the mechanism of the SVT?</description><dc:title>A conflict of evidence: AVNRT or junctional tachycardia? - Uncorrected Proof</dc:title><dc:creator>Christopher Lane, George Veenhuyzen, Russell Quinn</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.032</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-25</prism:publicationDate><prism:section>FEATURED ARRHYTHMIA</prism:section></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004213/abstract?rss=yes"><title>Lead electrical parameters may not predict integrity of the Sprint Fidelis ICD lead - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004213/abstract?rss=yes</link><description>
Background: 
The reported failure rate of the Medtronic Sprint Fidelis defibrillator lead continues to increase over time. Clinicians and patients count on the electrical analysis of leads through device interrogation to determine whether a lead is functioning “normally.” Most importantly, this analysis is often the basis for decision making around the ongoing use of this lead at the time of generator change. Can clinicians count on this analysis and feel confident that this “advisory” lead is “normal?”

Objective: 
To describe the incidence of unexpected lead abnormalities among Sprint Fidelis leads removed without prior evidence of electrical abnormalities.

Methods: 
We performed a retrospective cohort study of Medtronic Sprint Fidelis (6930, 6931, 6948, 6949) leads extracted at a single high-volume center. Medtronic analyzed all returned leads for abnormalities. The presence and type of lead abnormalities in addition to patient characteristics, indications for extraction, implant duration, and use of extraction sheath assistance are reported.

Results: 
Between September 2005 and January 2011, 209 Sprint Fidelis leads were extracted from 208 patients. The average duration of implant was 38.9 months (range 0.2–67.2). Of the analyzed leads, the majority of the extracted leads (63.1%) were active, normal functioning leads (83.8% prophylactically, 9.1% infection, and 7.1% other indication) while 36.9% had clinical evidence of a fracture. Extraction was achieved with simple traction in 39.5% of the leads; extraction sheath assistance was employed in 94 cases (59.9%), and surgical extraction at the time of transplant occurred in 1 case. Analysis of the 99 functionally “normal” leads removed determined that 20 leads had evidence of fractures (20.2%) not related to extraction. Of the fractured leads, 4 leads (20%) had more than 1 fracture and 1 lead had 3 separate fracture sites. There were 17 pacing conductor (10 proximal and 7 distal conductor) and 6 high-voltage conductor (1 superior vena cava and 5 right ventricle defibrillator conductor) fractures observed. Five additional leads (5.2%) had evidence of explant damage.

Conclusions: 
Functionally “normal” Fidelis leads demonstrate an alarmingly high rate of “subclinical” fractures. Recommendations regarding prophylactic Sprint Fidelis lead extraction, especially at the time of generator change, may warrant reconsideration. To aid in the design of better leads, all leads should be returned for analysis, regardless of the indication for extraction.
</description><dc:title>Lead electrical parameters may not predict integrity of the Sprint Fidelis ICD lead - Uncorrected Proof</dc:title><dc:creator>Melanie Maytin, Laurence M. Epstein</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.033</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-25</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004225/abstract?rss=yes"><title>The voltage-sensitive dye di-4-ANEPPS slows conduction velocity in isolated guinea pig hearts - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004225/abstract?rss=yes</link><description>
Background: 
Voltage-sensitive dyes are important tools for mapping electrical activity in the heart. However, little is known about the effects of voltage-sensitive dyes on cardiac electrophysiology.

Objective: 
To test the hypothesis that the voltage-sensitive dye di-4-ANEPPS modulates cardiac impulse propagation.

Methods: 
Electrical and optical mapping experiments were performed in isolated Langendorff perfused guinea pig hearts. The effect of di-4-ANEPPS on conduction velocity and anisotropy of propagation was quantified. HeLa cells expressing connexin 43 were used to evaluate the effect of di-4-ANEPPS on gap junctional conductance.

Results: 
In electrical mapping experiments, di-4-ANEPPS (7.5 μM) was found to decrease both longitudinal and transverse conduction velocities significantly compared with control. No change in the anisotropy of propagation was observed. Similar results were obtained in optical mapping experiments. In these experiments, the effect of di-4-ANEPPS was dose dependent. Nonetheless, di-4-ANEPPS had no effect on connexin 43–mediated gap junctional conductance in transfected HeLa cells.

Conclusion: 
Our results demonstrate that the voltage-sensitive dye di-4-ANEPPS directly and dose-dependently modulates cardiac impulse propagation. The effect is not likely mediated by connexin 43 inhibition. Our results highlight an important caveat that should be taken into account when interpreting data obtained by using di-4-ANEPPS in cardiac preparations.
</description><dc:title>The voltage-sensitive dye di-4-ANEPPS slows conduction velocity in isolated guinea pig hearts - Uncorrected Proof</dc:title><dc:creator>Anders Peter Larsen, Katie J. Sciuto, Alonso P. Moreno, Steven Poelzing</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.034</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-25</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-25</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003657/abstract?rss=yes"><title>Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003657/abstract?rss=yes</link><description>We read the article by Baranowski et al with great interest. We thank the authors for publishing their experience in dealing with a difficult and challenging clinical scenario of CIED leads jailed by an endovascular stent. While we agree with the fact that there is no conclusively established safe approach to removing jailed leads, respectfully, we sense that the conclusion of the abstract might be somewhat misleading in that the approach presented in the article insinuated an established safety. Indeed, from a technical standpoint, leads were successfully removed. However, on the basis of a rather strong tone of the conclusion of the abstract, we believe that the high success rate of jailed lead removal might be used as a justification to jail leads with stents. Because of an immense academic status and an undisputed expertise of the authors in the area of cardiac rhythm devices, some clarification of this issue would be much appreciated.</description><dc:title>Uncorrected Proof</dc:title><dc:creator>Loay Salman, Arif Asif</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.012</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate><prism:section>LETTERS TO THE EDITOR</prism:section></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752711200402X/abstract?rss=yes"><title>Cause for concern - Corrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS154752711200402X/abstract?rss=yes</link><description>I do not write many editorials because I feel my role as editor-in-chief is to be as impartial as possible. In my mind, being editor does not automatically instill in me wisdom exceeding that possessed by any other, nor thoughts more interesting or profound, that readers want to hear what I have to say on a regular basis. However, the recent events that transpired following publication in HeartRhythm of R. Hauser's article (“Deaths Caused by the Failure of Riata and Riata ST Implantable Cardioverter-Defibrillator Leads”) have compelled me to speak out.</description><dc:title>Cause for concern - Corrected Proof</dc:title><dc:creator>Douglas P. Zipes</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.014</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate><prism:section>EDITORIAL</prism:section></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004079/abstract?rss=yes"><title>Atrioventricular node functional remodeling induced by atrial fibrillation - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004079/abstract?rss=yes</link><description>
Background: 
The atrioventricular node (AVN) plays a vital role in determining the ventricular rate during atrial fibrillation (AF). AF results in profound electrophysiological and structural remodeling in the atria as well as the sinus node. However, it is unknown whether AVN undergoes remodeling during AF.

Objective: 
To determine whether AVN undergoes functional remodeling during AF.

Methods: 
AVN conduction properties were studied in vitro in 9 rabbits with AF and 10 normal controls. A previously validated index of AVN dual-pathway electrophysiology, His-electrogram alternans, was used to monitor fast-pathway or slow-pathway (SP) AVN conduction in these experiments. AVN conduction properties were further studied in vivo in 7 dogs with chronic AF and 8 controls.

Results: 
Compared with the control rabbits, the rabbits with AF had a longer AVN conduction time (83 ± 16 ms vs 68 ± 7 ms; P &lt;.01), longer AVN effective refractory period (141 ± 27 ms vs 100 ± 9 ms; P &lt;.01), an earlier transition from fast-pathway to SP conduction (at a longer prematurity, 249 ± 60 ms vs 171 ± 24 ms; P &lt;.01), and a slower ventricular rate during simulated AF (RR interval 249 ± 42 ms vs 202 ± 12 ms; P &lt;.01). Notably, a larger proportion of conducted beats utilized the SP in AF preparations (92% ± 12% vs 63% ± 32%; P &lt;.05). Long-term AF in dogs resulted in a longer atrioventricular conduction time and AVN effective refractory period and a slower ventricular rate during AF compared with the controls.

Conclusions: 
Pronounced AVN functional electrophysiological remodeling occurs after long-term AF, which could lead to a spontaneous slowing of the ventricular rate. Furthermore, the SP dominance during AF underscores the effectiveness of its modification by ablation for ventricular rate control during AF.
</description><dc:title>Atrioventricular node functional remodeling induced by atrial fibrillation - Uncorrected Proof</dc:title><dc:creator>Youhua Zhang, Todor N. Mazgalev</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.019</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004080/abstract?rss=yes"><title>Biological pacemaker created by percutaneous gene delivery via venous catheters in a porcine model of complete heart block - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004080/abstract?rss=yes</link><description>
Background: 
Pacemaker-dependent patients with device infection require temporary pacing while the infection is treated. External transthoracic pacing is painful and variably effective, while temporary pacing leads are susceptible to superinfection.

Objective: 
To create a biological pacemaker delivered via venous catheters in a porcine model of complete heart block, providing a temporary alternative/adjunct to external pacing devices without additional indwelling hardware.

Methods: 
Complete atrioventricular (AV) nodal block was induced in pigs by radiofrequency ablation after the implantation of a single-chamber electronic pacemaker to maintain a ventricular backup rate of 50 beats/min. An adenoviral vector cocktail (KAAA + H2), expressing dominant-negative inward rectifier potassium channel (Kir2.1AAA) and hyperpolarization-activated cation channel (HCN2) genes, was injected into the AV junctional region via a NOGA Myostar catheter advanced through the femoral vein.

Results: 
Animals injected with KAAA + H2 maintained a physiologically relevant ventricular rate of 93.5 ± 7 beats/min (n = 4) compared with control animals (average rate, 59.4 ± 4 beats/min; n = 6 at day 7 postinjection; P &lt;.05). Backup electronic pacemaker utilization decreased by almost 4-fold in the KAAA + H2 group compared with the control (P &lt;.05), an effect maintained for the entire 14-day window. In contrast to the efficacy of gene delivery into the AV junctional region, open-chest, direct injection of KAAA + H2 (or its individual vectors) into the ventricular myocardium failed to elicit significant pacemaker activity.

Conclusions: 
The right-sided delivery of KAAA + H2 to the AV junctional region provided physiologically relevant biological pacing over a 14-day period. Our approach may provide temporary, bridge-to-device pacing for the effective clearance of infection prior to the reimplantation of a definitive electronic pacemaker.
</description><dc:title>Biological pacemaker created by percutaneous gene delivery via venous catheters in a porcine model of complete heart block - Uncorrected Proof</dc:title><dc:creator>Eugenio Cingolani, Kristine Yee, Michael Shehata, Sumeet S. Chugh, Eduardo Marbán, Hee Cheol Cho</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.020</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004109/abstract?rss=yes"><title>Contemporary and Future Trends in Cardiac Resynchronization Therapy Pacing to Enhance Response - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004109/abstract?rss=yes</link><description>Abstract: 
The rationale for cardiac resynchronization therapy (CRT), expectations in terms of patient benefit, patient selection for CRT, the selection of a CRT pacemaker (CRT-P) versus CRT plus implantable cardioverter defibrillator (CRT-D) platform, and studies evaluating device programming to enhance benefit from CRT are reviewed. The notion of an "optimal" left ventricular (LV) pacing site, the rationale for identifying and avoiding LV pacing in regions of scar, the use of anatomic, hemodynamic, and electrical parameters to identify an optimal LV pacing site, and the potential utility of multi-site LV pacing to enhance benefit from CRT are discussed. Finally, the advantages and disadvantages of the various methods for LV lead delivery are reviewed.
</description><dc:title>Contemporary and Future Trends in Cardiac Resynchronization Therapy Pacing to Enhance Response - Accepted Manuscript</dc:title><dc:creator>Derek V. Exner, Angelo Auricchio, Jagmeet P. Singh</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.022</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004110/abstract?rss=yes"><title>Advances in Electrical Therapy for Heart Failure: Papers from the International ADVANCE CRT Summit - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004110/abstract?rss=yes</link><description></description><dc:title>Advances in Electrical Therapy for Heart Failure: Papers from the International ADVANCE CRT Summit - Accepted Manuscript</dc:title><dc:creator>Jagmeet P. Singh</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.023</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004122/abstract?rss=yes"><title>The challenge of nonresponders to cardiac resynchronization therapy: Lessons learned from oncology - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004122/abstract?rss=yes</link><description>Cardiovascular diseases (CVD) are the leading cause of death in high- and middle-income societies and the number two cause of death in low-income societies. However, it is the end-stage of CVD—heart failure (HF)—that imposes one of the highest disease burdens of any medical condition. An estimated 5.8 million patients were diagnosed with HF in the United States in 2006, more than 600,000 new cases of HF are diagnosed annually in the United States, and, as of 2006, 34% of all deaths in the United States (approximately 280,000) were attributed either directly or indirectly to HF. Importantly, HF remains the most common cause of hospitalization and rehospitalization among elderly patients, for whom the mortality rate at 60 to 90 days postdischarge is as high as 15%.</description><dc:title>The challenge of nonresponders to cardiac resynchronization therapy: Lessons learned from oncology - Uncorrected Proof</dc:title><dc:creator>Frank Ruschitzka</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.024</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004134/abstract?rss=yes"><title>Thinking beyond resynchronization therapy in the failing heart - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004134/abstract?rss=yes</link><description>Heart failure (HF) is a chronic, progressive disease that leads to high morbidity and mortality. In 2010, approximately 5.8 million people in the United States were diagnosed with HF. Each year, approximately 670,000 people are diagnosed with HF, and more than 290,000 deaths are associated with the disease. Despite advances in medical therapy, the incidence of HF continues to rise, mainly due to the growth of the aging population and the increased risk of HF with advancing age.</description><dc:title>Thinking beyond resynchronization therapy in the failing heart - Uncorrected Proof</dc:title><dc:creator>Kimberly A. Parks, Maria Rosa Costanzo</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.025</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004146/abstract?rss=yes"><title>Cardiac Resynchronization Therapy (CRT): Clinical Trials, Guidelines, and Target Populations - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004146/abstract?rss=yes</link><description>Abstract: 
Over the last 10 years several large, well-designed clinical trials have firmly established the role of cardiac resynchronization therapy (CRT) as a recommended treatment strategy for moderate-to-severe heart failure (HF). A review of the relevant results from the MUSTIC, MIRACLE, CONAK-CD, and MIRACLE ICD trials reveals that in patients with NYHA class III–IV HF, CRT produces consistent improvements in quality of life, functional status, and exercise capacity while also providing strong evidence for reverse remodeling and diminished functional mitral regurgitation, resulting in reductions in both HF hospitalizations and all-cause morbidity and mortality. In patients with earlier NYHA class I–II HF, the benefit of CRT has been more controversial. The principal ongoing challenges addressed in this article include the substantial 30% of patients who receive a CRT device but fail to respond, the wide variations in how to define “response” vs “non-response,” and how to identify patients who will benefit from CRT, especially narrow QRS (&lt;120 msec), those with right bundle branch block, and those with mild-to-moderate (NYHA class I–II HF). An important result of this uncertainty is that there is not yet a good sense of what the optimal rate of CRT implantation should be, making consideration of the data reviewed in this article crucial for identifying important gaps of knowledge and mechanisms of action that need to be studied in the near future.
</description><dc:title>Cardiac Resynchronization Therapy (CRT): Clinical Trials, Guidelines, and Target Populations - Accepted Manuscript</dc:title><dc:creator>Cecilia Linde, Kenneth Ellenbogen, Finlay A. McAlister</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.026</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004158/abstract?rss=yes"><title>Understanding the Cardiac Substrate and the Underlying Physiology: Implications for Individualized Treatment Algorithm - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004158/abstract?rss=yes</link><description></description><dc:title>Understanding the Cardiac Substrate and the Underlying Physiology: Implications for Individualized Treatment Algorithm - Accepted Manuscript</dc:title><dc:creator>John Gorcsan, Frits W. Prinzen</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.027</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS154752711200416X/abstract?rss=yes"><title>Multispecialty Approach: The Need for Heart Failure Disease Management for Refining Cardiac Resynchronization Therapy - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS154752711200416X/abstract?rss=yes</link><description>Abstract: 
Cardiac resynchronization therapy (CRT) has been proven in clinical trials to be a very effective therapy in appropriate patients. However, while the literature has primarily focused on appropriate implanting techniques and inclusion criteria for CRT devices by electrophysiologists, most patients who receive CRT are managed by their primary care providers with the help of general cardiologists and/or heart failure (HF) specialists. As CRT has been more broadly applied over the past decade, the fragmentation and specialization of care in the current healthcare system has created challenges in optimizing this otherwise invasive but potentially beneficial intervention in the complex HF patient. Furthermore, cost considerations as well as appropriate follow-up care continue to challenge the optimal application of these devices, particularly when evidence to support multidisciplinary approaches is lacking. The challenge begins with identification of appropriate candidates for CRT, which is an evolving concept due to data emerging from new studies with a wide range of inclusion and exclusion criteria coupled with increasing oversight from providers or even logistical hurdles from patients. Post-implant management practices and procedures are still evolving. The important and so-far unresolved concept of the "non-responder" to CRT remains largely subjective and is variably defined in the literature, and the lack of understanding of the underlying mechanisms of "non-response" continues to challenge long-term management of CRT, even given the recent developments in advanced sensor technologies. Therefore, further investigations into HF disease management with a multispecialty approach, pre- and post-CRT, are warranted.
</description><dc:title>Multispecialty Approach: The Need for Heart Failure Disease Management for Refining Cardiac Resynchronization Therapy - Accepted Manuscript</dc:title><dc:creator>W.H. Wilson Tang, John Boehmer, Daniel Gras</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.028</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004171/abstract?rss=yes"><title>The quest for rotors in atrial fibrillation: Different nets catch different fishes - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004171/abstract?rss=yes</link><description>Despite remarkable progress in the catheter ablation of atrial fibrillation (AF), primarily based on the elimination of pulmonary vein arrhythmogenicity, the identification of drivers beyond the thoracic veins specifically in patients with persistent AF remains problematic. The hypothesis that AF could be maintained by drivers in the form of reentrant circuits was first proposed about 100 years ago. However, during the second half of the 20th century, the prevailing hypothesis was that AF maintenance depended on multiple wavelets that randomly propagate across the atria and perpetually annihilate and regenerate. With the development of high-resolution optical mapping techniques, the original thought of a single or a small number of reentrant drivers of AF has reemerged. Both simulation and experimental studies in animal models have demonstrated that despite the spatiotemporal complexity of wave propagation during AF, measurable deterministic properties of high-frequency sources, rotors, and the hierarchical distribution of dominant frequency play a critical role in the perpetuation of AF. However, these important mechanistic studies involved toxic voltage-sensitive dyes and high-density mapping ex vivo with detailed offline analysis of electrograms, primarily in the frequency domain. Therefore, the clinical utility of these seminal findings has been limited.</description><dc:title>The quest for rotors in atrial fibrillation: Different nets catch different fishes - Uncorrected Proof</dc:title><dc:creator>Omer Berenfeld, Hakan Oral</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.029</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate><prism:section>EDITORIAL COMMENTARY</prism:section></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004183/abstract?rss=yes"><title>Managing Atrial Fibrillation in the CRT Patient: Controversy or Consensus? - Accepted Manuscript</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004183/abstract?rss=yes</link><description></description><dc:title>Managing Atrial Fibrillation in the CRT Patient: Controversy or Consensus? - Accepted Manuscript</dc:title><dc:creator>Gaurav A. Upadhyay, Jonathan S. Steinberg</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.030</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-23</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-23</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004092/abstract?rss=yes"><title>The mode of death in implantable cardioverter-defibrillator and cardiac resynchronization therapy with defibrillator patients: Results from routine clinical practice - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004092/abstract?rss=yes</link><description>
Background: 
Although data on the mode of death of implantable cardioverter-defibrillator (ICD) and cardiac resynchronization therapy with defibrillator (CRT-D) patients have been examined in randomized clinical trials, in routine clinical practice data are scarce. To provide reasonable expectations and prognosis for patients and physicians, this study assessed the mode of death in routine clinical practice.

Objective: 
To assess the mode of death in ICD/CRT-D recipients in routine clinical practice.

Methods: 
All patients who underwent an ICD or CRT-D implantation at the Leiden University Medical Center, the Netherlands, between 1996 and 2010 were included. Patients were divided into primary prevention ICD, secondary prevention ICD, and CRT-D patients. For patients who died during follow-up, the mode of death was retrieved from hospital and general practitioner records and categorized according to a predetermined classification: heart failure death, other cardiac death, sudden death, noncardiac death, and unknown death.

Results: 
A total of 2859 patients were included in the analysis. During a median follow-up of 3.4 years (interquartile range 1.7–5.7 years), 107 (14%) primary prevention ICD, 253 (28%) secondary prevention ICD, and 302 (25%) CRT-D recipients died. The 8-year cumulative incidence of all-cause mortality was 39.9% (95% confidence interval 37.0%–42.9%). Heart failure death and noncardiac death were the most common modes of death for all groups. Sudden death accounted for approximately 7%–8% of all deaths.

Conclusion: 
For all patients, heart failure and noncardiac death are the most common modes of death. The proportion of patients who died suddenly was low and comparable for primary and secondary ICD and CRT-D patients.
</description><dc:title>The mode of death in implantable cardioverter-defibrillator and cardiac resynchronization therapy with defibrillator patients: Results from routine clinical practice - Uncorrected Proof</dc:title><dc:creator>Joep Thijssen, Johannes B. van Rees, Jeroen Venlet, C. Jan Willem Borleffs, Ulas Höke, Hein Putter, Enno T. van der Velde, Lieselot van Erven, Martin J. Schalij</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.021</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-20</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-20</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004067/abstract?rss=yes"><title>Baseline functional capacity and the benefit of cardiac resynchronization therapy in patients with mildly symptomatic heart failure enrolled in MADIT-CRT - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004067/abstract?rss=yes</link><description>
Background: 
Mildly symptomatic heart failure (HF) patients were shown to derive substantial clinical benefit from cardiac resynchronization therapy with defibrillator (CRT-D) in Multicenter Automatic Defibrillator Implantation Trial in Cardiac Resynchronization Therapy. However, the relationship between functional capacity (FC) and CRT-D benefit in the trial was not assessed.

Objective: 
To evaluate the association between FC and response to CRT-D in Multicenter Automatic Defibrillator Implantation Trial in Cardiac Resynchronization Therapy.

Methods: 
We evaluated the association between preimplantation FC and the benefit of CRT-D in reducing the risk of HF or death in Multicenter Automatic Defibrillator Implantation Trial in Cardiac Resynchronization Therapy. Functional status was assessed by a 6-minute walk test (6MWT), dichotomized at the median value as poor (&lt;350 m) or good (≥350 m).

Results: 
Implantable cardioverter-defibrillator–only patients with a poor FC had an adjusted 73% increased risk for HF or death (P &lt;.001) and a 2.4-fold (P = .001) increased risk for all-cause mortality. CRT-D therapy was associated with 63% (P &lt;.001) and 44% (P &lt;.001) reductions in the risk of HF or death among left bundle branch block patients with a poor FC and a good FC, respectively (P for interaction = .10). Among left bundle branch block patients with a poor FC, CRT-D was also associated with a significant reduction in the risk of all-cause mortality (hazard ratio 0.52; P = .015) whereas the survival benefit of CRT-D was not observed among those who had a higher FC at enrollment (hazard ratio 1.01; P = .98; P for interaction = .10).

Conclusions: 
Poor FC is a strong independent predictor for mortality and HF events in patients with mildly symptomatic HF. Left bundle branch block patients with poor baseline FC derive a pronounced benefit from CRT-D, manifest by a significant reduction in mortality.
</description><dc:title>Baseline functional capacity and the benefit of cardiac resynchronization therapy in patients with mildly symptomatic heart failure enrolled in MADIT-CRT - Uncorrected Proof</dc:title><dc:creator>Andrew Brenyo, Ilan Goldenberg, Arthur J. Moss, Mohan Rao, Scott McNitt, David T. Huang, Wojciech Zareba, Alon Barsheshet</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.018</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-19</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-19</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004031/abstract?rss=yes"><title>Simulator training reduces radiation exposure and improves trainees' performance in placing electrophysiologic catheters during patient-based procedures - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004031/abstract?rss=yes</link><description>
Background: 
Currently, training in interventional electrophysiology is based on conventional methodologies, and a paucity of data on the usefulness of simulation in this field is available.

Objective: 
The purpose of this study was to evaluate the impact of simulator training on trainees' performance in electrophysiologic catheter placement during the early phase of their learning curve.

Methods: 
Inexperienced electrophysiology fellows were considered. A hybrid high-fidelity simulator (Procedicus VIST, version 7.0, Mentice AB Gothenburg, Sweden for Biosense Webster) was used. The following parameters were evaluated in 3 consecutive patient-based procedures before and after two training sessions of at least 1.5 hours on the simulator: (1) ability to place catheters in conventional recording/pacing sites (coronary sinus, His-bundle area, high right atrium, and right ventricular apex); (2) amount of help provided by the supervisor (scale from 1–3; 3 for maximal help); (3) fluoroscopy time; and (4) positioning time.

Results: 
Seven fellows performed 168 catheter placements during 42 patient-based procedures with no complications. Comparing parameters before and after simulator training, there was a significant reduction in the mean amount of help and in fluoroscopy and positioning times per placement: from 1.71 ± 1.24 to 0.42 ± 0.68 (P &lt;.001), from 121 ± 88 seconds to 76 ± 54 seconds (P &lt;.001), and from 175 ± 138 seconds to 102 ± 74 seconds (P &lt;.001), respectively. Overall fluoroscopy time per patient decreased from 567 ± 220 seconds to 305 ± 111 seconds (P &lt;.0001). Improvement appeared to be related to simulator training alone and not to the previously performed patient-based procedures.

Conclusion: 
During the early phase of the trainees' learning curve, simulator training significantly improves the independent trainees' performance with reduction in radiation exposure.
</description><dc:title>Simulator training reduces radiation exposure and improves trainees' performance in placing electrophysiologic catheters during patient-based procedures - Uncorrected Proof</dc:title><dc:creator>Roberto De Ponti, Raffaella Marazzi, Lorenzo Doni, Claudio Tamborini, Sergio Ghiringhelli, Jorge A. Salerno-Uriarte</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.015</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004043/abstract?rss=yes"><title>The course of the sinus node artery and its impact on achieving linear block at the left atrial roof in patients with persistent atrial fibrillation - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004043/abstract?rss=yes</link><description>
Background: 
Linear block at the left atrial (LA) roof may be challenging in some patients undergoing an ablation procedure for atrial fibrillation.

Objective: 
To identify factors that may influence the likelihood of achieving roof block.

Methods: 
Seventy-four patients (61 ± 10 years; 59 men [80%); LA diameter, 46 ± 6 mm; ejection fraction 0.55 ± 0.10) underwent linear ablation at the LA roof for persistent atrial fibrillation. The morphology of the roof and its anatomical relationship to adjacent structures were analyzed on a preprocedure computed tomography scan.

Results: 
Complete block along the LA roof was achieved in 61 of the 74 patients (82%). There was no significant difference in the myocardial thickness, length, or other morphological aspects of the LA roof between patients with and without complete block. The sinus node artery (SNA) originated from the right coronary artery in 52 patients (70%) and the left circumflex artery in 22 patients (30%). The prevalence of a left SNA (from the circumflex) among patients with and without linear block at the roof was 21% and 69%, respectively (P = .001). On multivariate analysis, a left SNA was the only independent predictor of incomplete conduction block at the LA roof (odds ratio 6.8; 95% confidence interval 1.7–28; P = .007).

Conclusions: 
A left SNA identifies patients in whom conduction block at the roof is more difficult to achieve. A left SNA may act as an epicardial heat sink, preventing adequate heating of the LA roof during linear ablation.
</description><dc:title>The course of the sinus node artery and its impact on achieving linear block at the left atrial roof in patients with persistent atrial fibrillation - Uncorrected Proof</dc:title><dc:creator>Miki Yokokawa, Baskaran Sundaram, Hakan Oral, Fred Morady, Aman Chugh</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.016</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112004055/abstract?rss=yes"><title>Spontaneous baroreflex sensitivity: Prospective validation trial of a novel technique in survivors of acute myocardial infarction - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112004055/abstract?rss=yes</link><description>
Background: 
Low baroreflex sensitivity (BRS) indicates poor prognosis after acute myocardial infarction. Noninvasive BRS assessment is complicated by nonstationarities and noise in electrocardiogram and pressure signals. Phase-rectified signal averaging is a novel signal processing technology overcoming these problems.

Objective: 
To prospectively validate a BRS measure (baroreflex sensitivity assessed by means of phase-rectified signal averaging [BRSPRSA]) based on this technology.

Methods: 
Nine hundred forty-one consecutive acute myocardial infarction survivors aged 80 years or younger in sinus rhythm were prospectively enrolled at 2 German university hospitals. All patients underwent 30-minute recordings of electrocardiogram and arterial blood pressures (Portapres; TNO-TPD Biomedical Instrumentation, Amsterdam, Netherlands) within the first 2 weeks after myocardial infarction. BRSPRSA was prospectively dichotomized at 1.58 ms/mm Hg. Primary end point was all-cause mortality at 5 years. Multivariable analyses included Global Registry of Acute Coronary Events score (dichotomized at ≥120), sex, BRSPRSA, left ventricular ejection fraction (dichotomized at ≤35%), and diabetes mellitus. BRSPRSA was compared with 3 standard noninvasive BRS measures, that is, the sequence method, the transfer function method, and the correlation method.

Results: 
During follow-up, 72 patients (7.7%) died. BRSPRSA stratified the study population into a high-risk group of 405 patients (≤1.58 ms/mm Hg) with an estimated 5-year mortality of 14.2% and a low-risk group of 536 patients (&gt;1.58 ms/mm Hg) with a 5-year mortality of 2.8% (P &lt;.0001). On multivariable analysis, BRSPRSA ≤ 1.58 ms/mm Hg was associated with a hazard ratio of 3.1 (confidence interval 1.7–5.6; P = .001). Predictive power of BRSPRSA ≤ 1.58 ms/mm Hg was particularly strong in patients with a Global Registry of Acute Coronary Events score of ≥120 or with a left ventricular ejection fraction of ≤35%.

Conclusion: 
BRSPRSA is a powerful and independent predictor of mortality in postinfarction patients especially when assessed in patients with a Global Registry of Acute Coronary Events score of ≥120 or a left ventricular ejection fraction of ≤35%.
</description><dc:title>Spontaneous baroreflex sensitivity: Prospective validation trial of a novel technique in survivors of acute myocardial infarction - Uncorrected Proof</dc:title><dc:creator>Petra Barthel, Axel Bauer, Alexander Müller, Katharina M. Huster, Jørgen K. Kanters, Vijayapraveena Paruchuri, Xiaoyun Yang, Kurt Ulm, Marek Malik, Georg Schmidt</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.017</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-18</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-18</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003621/abstract?rss=yes"><title>Alcohol ablation of the vein of Marshall: Is it the answer for mitral isthmus ablation? - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003621/abstract?rss=yes</link><description>Catheter ablation of atrial fibrillation in patients with structural heart disease may include isolation of the pulmonary veins and modification of the atrial substrate by a combination of ablation of complex fractionated atrial electrograms and left atrial linear ablation. Left atrial roof and mitral isthmus lines are the most commonly used, and these are important adjuncts to pulmonary vein isolation in achieving successful catheter ablation of atrial fibrillation, especially in persistent atrial fibrillation. However, paradoxically, improved success rate of ablation of atrial fibrillation comes at the cost of increasing the incidence of macro-reentrant left atrial tachycardia during follow-up. Perimitral flutter is the commonest left atrial reentrant tachycardia occurring after atrial fibrillation ablation. Interestingly though, linear ablation of mitral isthmus, which would be useful in treating perimitral flutter, can lead to increased risk of the same arrhythmia. This phenomenon is explained by inadvertent gaps left in the linear mitral isthmus ablation line, facilitating reentrant circuits for the development of atrial tachycardia. A durable bidirectional block across mitral isthmus is of utmost importance in achieving freedom from atrial flutter in these patients.</description><dc:title>Alcohol ablation of the vein of Marshall: Is it the answer for mitral isthmus ablation? - Uncorrected Proof</dc:title><dc:creator>Prabhat Kumar, J. Paul Mounsey</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.009</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate><prism:section>EDITORIAL COMMENTARY</prism:section></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003633/abstract?rss=yes"><title>Riata externalized conductors: Cosmetic defect or manifestation of a more serious design flaw? - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003633/abstract?rss=yes</link><description>Approximately 227,000 Riata and Riata ST implantable cardioverter-defibrillator leads (St Jude Medical [SJM], Inc, Sylmar, CA) had been sold worldwide when the manufacturer abruptly removed them from the market in December 2010. In a letter to physicians, SJM stated that its newer Riata ST and Durata leads with Optim insulation were more resistant to abrasion than the Riata and Riata ST leads that were not covered by Optim. Also, for the first time, SJM explained that externalized conductors were the result of inside-out abrasions caused by the movement of the cables within the leads' lumens. Although case reports describing externalized cables have been published since 2008, it was the Northern Ireland study presented at the European Society of Cardiology in August 2011 that suggested that this unique structural failure could be found in a high proportion of patients who had Riata and Riata ST leads.</description><dc:title>Riata externalized conductors: Cosmetic defect or manifestation of a more serious design flaw? - Uncorrected Proof</dc:title><dc:creator>Robert G. Hauser</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.010</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate><prism:section>EDITORIAL COMMENTARY</prism:section></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003645/abstract?rss=yes"><title>Percutaneous extraction of stented device leads - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003645/abstract?rss=yes</link><description>We would like to thank doctors Salman and Asif for their comments regarding our recently published experience with percutaneous extraction of stented device leads. We would like to emphasize several points: 1) We feel strongly that the practice of jailing leads to a vein wall with a stent creates a highly undesirable situation 2) This practice should be strongly discouraged 3) We strongly support the Heart Rhythm Society's expert consensus document's recommendation that all transvenous leads be extracted prior to any stenting procedure due to the risk of lead entrapment.</description><dc:title>Percutaneous extraction of stented device leads - Uncorrected Proof</dc:title><dc:creator>Brian Baranowski, Bruce Wilkoff</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.011</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003669/abstract?rss=yes"><title>Syncope in Brugada syndrome patients: Prevalence, characteristics, and outcome - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003669/abstract?rss=yes</link><description>
Background: 
The report from the 2nd Consensus Committee on BrS suggests that all patients with syncope without a “clear extracardiac cause” should have an implantable cardioverter-defibrillator (ICD). However, a clear extracardiac cause for syncope may be difficult to prove.

Objective: 
The purpose of this study was to characterize syncope in patients with Brugada syndrome (BrS).

Methods: 
All patients diagnosed with BrS at our institution between 1999 and 2010 were enrolled in a prospective registry. Patients with suspected arrhythmic syncope (group 1) were compared to patients with nonarrhythmic syncope (group 2) and to patients with syncope of doubtful origin (group 3).

Results: 
Of 203 patients with BrS, 57 (28%; 44 male, age 46 ± 12 years) experienced at least 1 syncope. Group 1 consisted of 23 patients, all of whom received an ICD. In group 2 (17 patients), 3 received an ICD because of a positive electrophysiologic study. In group 3 (17 patients), 6 received an implantable loop recorder and 6 received an ICD. After mean follow-up of 65 ± 42 months, 14 patients in group 1 remained asymptomatic, 4 had recurrent syncope, and/or 6 had appropriate ICD therapy. In group 2, 9 patients remained asymptomatic and 7 had recurrent neurocardiogenic syncope. In group 3, 7 remained asymptomatic and 9 had recurrent syncope. One patient from each group died from a noncardiac cause.

Conclusion: 
In the present study, syncope occurred in 28% of patients with BrS. The ventricular arrhythmia rate was 5.5% per year in group 1. In 30%, the etiology of the syncope was questionable. No sudden cardiac death occurred in groups 2 and 3.
</description><dc:title>Syncope in Brugada syndrome patients: Prevalence, characteristics, and outcome - Uncorrected Proof</dc:title><dc:creator>Frédéric Sacher, Florence Arsac, Stephen B. Wilton, Nicolas Derval, Arnaud Denis, Maxime de Guillebon, Khaled Ramoul, Pierre Bordachar, Philippe Ritter, Mélèze Hocini, Jacques Clémenty, Pierre Jaïs, Michel Haïssaguerre</dc:creator><dc:identifier>10.1016/j.hrthm.2012.04.013</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-12</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-12</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003475/abstract?rss=yes"><title>Fragmented and delayed electrograms within fibrofatty scar predict arrhythmic events in arrhythmogenic right ventricular cardiomyopathy: Results from a prospective risk stratification study - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003475/abstract?rss=yes</link><description>
Background: 
Islets of myocytes within fibrofatty scars represent the substrate for reentrant ventricular arrhythmias in arrhythmogenic right ventricular cardiomyopathy (ARVC). Electroanatomic mapping can reliably identify such areas.

Objective: 
To prospectively test the association between late and fragmented electrograms within scar and arrhythmic events in patients with ARVC.

Methods: 
High-density right ventricle electroanatomic mapping was performed in 32 patients with ARVC without history of cardiac arrest or sustained ventricular arrhythmias. Standard definitions of electroanatomic scars and fragmented, isolated, and very late potentials were used. All patients received an implantable cardioverter-defibrillator for the primary prevention of sudden death.

Results: 
After a mean follow-up of 25 ± 7 months, 12 (38%) patients received appropriate implantable cardioverter-defibrillator shock for sustained ventricular arrhythmias. With the exception of a higher rate of previous syncope (P = .053), patients with arrhythmic events at follow-up did not differ from those who remained free from arrhythmic events in terms of other clinical variables, including cardiac magnetic resonance findings. Electroanatomic scars were present in all patients. The distribution and extent of electroanatomic scars were similar in the 2 groups (38 ± 25 cm2 vs 33 ± 20 cm2; P = .51). However, patients with implantable cardioverter-defibrillator shock had a higher prevalence of fragmented electrograms (92% vs 20%; P &lt;.001), of isolated late potentials (75% vs 20%; P = .004), and of very late potentials (67% vs 25%; P = .030). Fragmented electrograms were the only variable independently associated with arrhythmic events at follow-up (hazard ratio 21; P = .015).

Conclusion: 
The presence of fragmented and delayed electrograms within the scar predicts arrhythmic events in ARVC.
</description><dc:title>Fragmented and delayed electrograms within fibrofatty scar predict arrhythmic events in arrhythmogenic right ventricular cardiomyopathy: Results from a prospective risk stratification study - Uncorrected Proof</dc:title><dc:creator>Pasquale Santangeli, Antonio Dello Russo, Maurizio Pieroni, Michela Casella, Luigi Di Biase, J. David Burkhardt, Javier Sanchez, Dhanunjaya Lakkireddy, Corrado Carbucicchio, Martina Zucchetti, Gemma Pelargonio, Sakis Themistoclakis, Antonia Camporeale, Antonio Rossillo, Salwa Beheiry, Richard Hongo, Fulvio Bellocci, Claudio Tondo, Andrea Natale</dc:creator><dc:identifier>10.1016/j.hrthm.2012.03.057</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate></item><item rdf:about="http://www.heartrhythmjournal.com/article/PIIS1547527112003487/abstract?rss=yes"><title>Correlation between substrate location and ablation strategy in patients with ventricular tachycardia late after myocardial infarction - Uncorrected Proof</title><link>http://www.heartrhythmjournal.com/article/PIIS1547527112003487/abstract?rss=yes</link><description>
Background: 
The requirement for epicardial radiofrequency ablation (RFA) is still undefined in ventricular tachycardia (VT) late after myocardial infarction (MI).

Objective: 
The purpose of this study was to evaluate the correlation between the need for epicardial RFA and the clinical and electrophysiologic characteristics of VT late after MI.

Methods: 
Endocardial mapping and RFA were performed for VT late after MI, followed by epicardial mapping and RFA if no endocardial substrate was present or endocardial RFA failed.

Results: 
Seventy patients with VT late after MI (30 anterior MI [A-MI] and 40 posteroinferior MI [PI-MI]) were included in the study. Forty-one VTs in patients with A-MI and 64 VTs in patients with PI-MI were targeted for RFA. Epicardial mapping and ablation were attempted in 6 patients and performed successfully in only 4 patients. All 6 (100%) patients requiring epicardial access had PI-MIs. Patients with epicardial RFA had endocardial low-voltage areas of smaller size compared to patients without epicardial RFA (21 ± 13 cm2 vs 68 ± 40 cm2; P &lt;.01). During 25 ± 19 months of follow-up, recurrence after the initial procedure was noted in 12 of 30 patients (40%) with A-MI and in 18 of 40 patients (45%) with PI-MI. There was no significant difference between groups.

Conclusion: 
In the majority of patients, clinical and slower VTs late after MI can be abolished using endocardial RFA. Rarely indicated, epicardial RFA is more commonly required in patients with small-sized PI-MI. During follow-up, VT recurrence after successful RFA is common.
</description><dc:title>Correlation between substrate location and ablation strategy in patients with ventricular tachycardia late after myocardial infarction - Uncorrected Proof</dc:title><dc:creator>Yasuhiro Yoshiga, Shibu Mathew, Erik Wissner, Roland Tilz, Alexander Fuernkranz, Andreas Metzner, Andreas Rillig, Melanie Konstantinidou, Miyako Igarashi, Karl-Heinz Kuck, Feifan Ouyang</dc:creator><dc:identifier>10.1016/j.hrthm.2012.03.058</dc:identifier><dc:source>Heart Rhythm (2012)</dc:source><dc:date>2012-04-05</dc:date><prism:publicationName>Heart Rhythm</prism:publicationName><prism:publicationDate>2012-04-05</prism:publicationDate></item></rdf:RDF>
