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Rheumatic heart disease results in significant remodeling of the atria that provides the milieu for maintaining atrial fibrillation. Some electrical remodeling is reversible and hence early intervention may prove useful. Active screening for atrial fibrillation in high-risk subset and instituting anticoagulation may reduce the devastating complications that follow. Age older than 50 years, NYHA functional class II symptoms, left atrial dimension >4.0 cm on echocardiogram in parasternal long-axis view, and gradients across the mitral valve >10 mm Hg are clinical indicators that identify the high-risk subset. Ablation strategy in this population may differ compared with the nonvalvular group.

Background and objectives: Right ventricular (RV) pacing can lead to progressive ventricular dysfunction over a certain period. This pacemaker-induced cardiomyopathy (PiCMP) may be more common than previously reported. Speckle tracking imaging is a recent development in echocardiography that can identify left ventricular (LV) dysfunction even before the LV ejection fraction (LVEF) value decreases. Three-dimensional (3D) echocardiography has made more accurate assessment of LVEF possible. The objectives of this study are to study the incidence of RV PiCMP using 3D echocardiography and LV strain analysis over a follow-up of 6 months, and to identify its predictors. Methods: This is an observational study of consecutive patients without structural heart disease and with a baseline EF of more than 45% who received a permanent pacemaker. They were observed over a 6-month period. PiCMP was defined as a decrease in LVEF by 10 percentage points or a decrease in LV strain by 15% from baseline in the absence of other known causes of cardiomyopathy. PiCMP incidence and its associations were analyzed over a 6-month period. Results: The incidence of PiCMP was not only significant over a period of 6 months but also at 24 hours. Significant drops in 3D EF were noted in one (2.8%) patient at 24 hours and in another four (11.1%) patients at 6 months. A significant decrease in LV global longitudinal strain was noted in 23 (63.9%) patients by 6 months. In seven of these patients, there was significant decrease in global longitudinal strain 24 hours after implantation. In analyzing longitudinal strain, the parameter significantly influencing a decrease was a pacing percentage of ≥20% (p = 0.023). Conclusions: PiCMP is not uncommon in patients undergoing pacemaker implantation and is associated with RV pacing. PiCMP was associated with a ventricular pacing percentage of ≥20%. 3D echocardiography with LV strain analysis plays a vital role in identifying LV dysfunction at an earlier stage compared to EF. PiCMP, if picked up and intervened upon early, can help impede its progression. Keywords: Ejection fraction, Incidence, Pacing induced cardiomyopathy, Predictors, Three-dimensional echocardiography

Background It has been suggested that ethnicity can make a significant difference to the likelihood of thromboembolic stroke related to atrial fibrillation. Ethnic differences have been shown to alter inflammatory and haemostatic factors; however, this may all be confounded by differences in cardiovascular risk factors between different ethnicity. The impact of different ethnicities on the thrombogenic profile is not known. The aim of this study was to investigate differences in markers of inflammation, endothelial function and tissue remodelling between Caucasian and Indian populations with supraventricular tachycardia (SVT). Methods Patients with structurally normal hearts undergoing catheter ablation for SVT were studied. This study included 23 Australian (Caucasian) patients from the Royal Adelaide Hospital, Adelaide, Australia and 24 Indian (Indian) patients from the Christian Medical College, Vellore, India. Blood samples were collected from the femoral vein, and right and left atria. Blood samples were analysed for the markers of endothelial function (ADMA, ET-1), inflammation (CD40L, VCAM-1, ICAM-1), and tissue remodelling (MMP-9, TIMP-1) using ELISA. Results The study populations were well matched for cardiovascular risk factors and the absence of structural heart disease. No difference in the echocardiographic measurements between the two ethnicities was found. In this context, there was no difference in markers of inflammation, endothelial function or tissue remodelling between the two SVT populations. Conclusion Caucasian and Indian populations demonstrate similar inflammatory, endothelial function or tissue remodelling profiles. This study suggests a lack of an impact of different ethnicity in these populations in terms of thrombogenic risk.

Refractory and fatal hemodynamic depression remarkably occurred eight hours after left carotid artery stenting in a 62-year-old male who had no hemodynamic instability till then; possible contributory factors were pre-existing moderate left ventricular systolic dysfunction and new-onset complete heart block caused by vasopressor-induced sympathetic stimulation in the presence of covert distal conduction system disease.

Patients with lone atrial fibrillation (AF) have an abnormal atrial substrate.The purpose of this study was to determine the role of direction-dependent conduction in patients with lone AF.Twenty-four patients with paroxysmal lone AF and 24 reference patients with left-sided accessory pathways were studied. Multipolar catheters placed at the lateral right atrium, crista terminalis, coronary sinus (CS), and left atrial roof were used to determine direction-dependent conduction characteristics. Biatrial electroanatomic maps were created during sinus rhythm and with distal CS pacing to characterize direction-dependent differences in conduction velocities, electrogram complexity, and voltage.Differing wavefront directions caused changes in conduction velocity (P.001), biatrial activation times (P.001), electrogram fragmentation (P.001), site-specific conduction delays (P.001), and voltage (P.001) in both lone AF and reference patients. These direction-dependent abnormalities were amplified in lone AF patients compared to reference patients, who exhibited greater slowing in conduction velocities (P = .02), prolongation of biatrial activation time (P = .04), increase in number (P.001) and length (P.001) of lines of conduction block, increase in proportion of fractionated electrograms (P.001), and decrease in voltage (P = .03) during distal CS pacing compared to sinus rhythm.This study demonstrates the marked direction-dependent conduction abnormalities present in patients with lone AF. These results provide further insights into the critical interplay between the underlying abnormal substrate and differing wavefront directions. The study suggests that direction-dependent conduction abnormalities may explain in part the greater arrhythmogenicity of ectopic triggers from the left atrium rather than the right atrium.

Sinus Node Mapping. Introduction: The area of the functional sinus node complex exceeds that of the anatomical sinus node; however, reasons for this discrepancy are unknown. We aimed to characterize the functional sinus node complex in health and disease with high-density simultaneous mapping. Methods and Results: Sinus node activity was characterized in 15 reference patients after ablation for supraventricular tachycardia. A further 16 patients were studied following ablation of chronic atrial flutter to determine effects of atrial remodeling. High-density simultaneous mapping of the sinus node complex was performed using a multi-electrode array. In reference patients, distance from superior vena cava-right atrial (SVC-RA) junction to earliest activation (EA) was 4 ± 4 mm and sinus break-out (SBO) 9 ± 6 mm. Preferential pathways of conduction were observed between EA and SBO. For patients with flutter, these distances were greater (EA: 15 ± 12 mm, P = 0.003; SBO: 23 ± 11 mm, P < 0.001). Conduction time along preferential pathways was 15 ± 5 ms for reference patients and 23 ± 8 ms for patients with flutter (P = 0.005). Following pacing, distance from SVC–RA junction to EA and SBO lengthened to 13 ± 8 mm (P = 0.006) and 16 ± 10 mm (P = 0.02), respectively, in reference patients, and 19 ± 12 mm (P = 0.045), 28 ± 9 mm (P = 0.02) in patients with flutter. This resulted in caudal shifts in EA and SBO of 10 ± 9 mm and 7 ± 8 mm in reference patients but diminished shifts in patients with flutter; 4 ± 7 mm and 4 ± 6 mm. Conclusion: The functional sinus node complex demonstrates dynamic changes in activation. There are preferential pathways of conduction from sinus node to atrial myocardium. The remodeled atria demonstrate longer conduction times along preferential pathways and a restricted functional sinus node complex. (J Cardiovasc Electrophysiol, Vol. 21, pp. 532-539, May 2010)

The left atrium is a complex chamber, which plays an integral role in the maintenance of physiologic hemodynamic and electrical stability of the heart and is involved in many disease states, most commonly atrial fibrillation. Preserving regions of the left atrium that contribute the greatest to atrial mechanical function during curative strategies for atrial fibrillation are important. We present here a new application of the CARTO electroanatomical mapping system in the assessment of the left atria mechanical function. Electroanatomical data were collected in course of the electrophysiological procedure in 11 control patients and 12 patients with paroxysmal atrial fibrillation. The three-dimensional geometry of the left atria was reconstructed in 10 ms intervals and segmented into distinct regions. For each segment, a regional ejection fraction was calculated. We found that anterior, septal and lateral segments have significantly greater regional ejection fraction than atria roof, inferior and posterior segments. Therefore, we hypothesize that in order to minimize the impact on atrial mechanical function, an important determinant of thromboembolic risk, damage should be minimized to these atrial regions.

Objectives: The aim of this report was to study the effect of chronic stretch reversal on the electrophysiological characteristics of the atria in humans.Background: Atrial stretch is an important ...

Information regarding left atrial (LA) substrate in conditions predisposing to atrial fibrillation (AF) is limited.This study sought to characterize the left atrial remodeling that results from chronic atrial stretch caused by atrial septal defect (ASD).Eleven patients with hemodynamically significant ASDs and 12 control subjects were studied. The following were evaluated using multipolar catheters: effective refractory period (ERP) at 7 sites, P-wave duration (PWD), conduction time, and inducibility of AF. LA electroanatomic maps were created to determine atrial activation, and regional conduction and voltage abnormalities.Patients with ASDs showed significant LA enlargement (P0.001), unchanged or prolonged atrial ERPs, increase in LA conduction times (P = 0.03), prolonged PWD (P0.001), regional conduction slowing (P0.001), greater number of double potentials or fractionated electrograms (P0.0001), reduced atrial voltage (P0.001), and more frequent electrical scar (P = 0.005) compared with control subjects. In addition, patients with ASDs showed a greater propensity for sustained AF with single extrastimuli (4 of 11 vs. 0 of 12, P = 0.04).ASDs are associated with chronic left atrial stretch, which results in remodeling characterized by LA enlargement, loss of myocardium, and electrical scar that results in widespread conduction abnormalities but with no change or an increase in ERP. These abnormalities were associated with a greater propensity for sustained AF.

Objectives The purpose of this study was to determine whether patients with paroxysmal “lone” atrial fibrillation (AF) have an abnormal atrial substrate. Background While “AF begets AF,” prompt termination to prevent electrical remodeling does not prevent disease progression. Methods Twenty-five patients with paroxysmal lone AF, without arrhythmia in the week prior, and 25 reference patients with left-sided accessory pathways were studied. Multipolar catheters placed at the lateral right atrium (RA), crista terminalis, coronary sinus, septal RA, and sequentially within the left atrium (LA) determined the effective refractory period (ERP) at 10 sites, conduction time along linear catheters, and conduction characteristics at the crista terminalis. Bi-atrial electroanatomic maps were created to determine regional differences in conduction velocity and voltage. Results Patients with AF demonstrated the following compared with reference patients: larger atrial volumes (RA: 94 ± 18 ml vs. 69 ± 9 ml, p = 0.003; LA: 99 ± 19 ml vs. 77 ± 17 ml, p = 0.006); longer ERP (at 600 ms: 255 ± 25 ms vs. 222 ± 16 ms, p Conclusions Patients with paroxysmal lone AF, remote from arrhythmia, demonstrate bi-atrial abnormalities characterized by structural change, conduction abnormalities, and sinus node dysfunction. These factors are likely contributors to the “second factor” that predisposes to the development and progression of AF.

Aims To characterize the atrial remodelling in mitral stenosis (MS). Methods and results Twenty-four patients with severe MS undergoing commissurotomy and 24 controls were studied. Electrophysiological evaluation was performed in 12 patients in each group by positioning multi-electrode catheters in both atria to determine the following: effective refractory period (ERP) at 10 sites at 600 and 450 ms; conduction time; conduction delay at the crista terminalis (CT); and vulnerability for atrial fibrillation (AF). P-wave duration (PWD) was determined on the surface ECG. In the remaining 12 patients in each group, electroanatomic maps of both atria were created to determine conduction velocity and identify regions of low voltage and electrical silence. Patients with MS had larger left atria (LA) ( P < 0.0001); prolonged PWD ( P = 0.0007); prolonged ERP in both LA ( P < 0.0001) and right atria (RA) ( P < 0.0001); reduced conduction velocity in the LA ( P = 0.009) and RA ( P < 0.0001); greater number ( P < 0.0001) and duration ( P < 0.0001) of bipoles along the CT with delayed conduction; lower atrial voltage in the LA ( P < 0.0001) and RA ( P < 0.0001); and more frequent electrical scar ( P = 0.001) compared with controls. Five of twelve with MS and none of the controls developed AF with extra-stimulus ( P = 0.02). Conclusion Atrial remodelling in MS is characterized by LA enlargement, loss of myocardium, and scarring associated with widespread and site-specific conduction abnormalities and no change or an increase in ERP. These abnormalities were associated with a heightened inducibility of AF.

Sites of complex fractionated atrial electrograms (CFAEs) and highest dominant frequency (DF) have been proposed as critical regions maintaining atrial fibrillation (AF). This study aimed to determine the minimum electrogram recording duration that accurately characterizes CFAE or DF sites for ablation without unduly lengthening the procedure.Fourteen patients with AF undergoing catheter ablation had high-density (498 +/- 174 points) biatrial mapping performed during AF before ablation. At each point, 8-second electrograms were recorded. CFAE characterization using the NavX software provided a representation of electrogram complexity (CFE-mean). CFE-mean for each point from 7-, 6-, 5-, 4-, 3-, 2-, and 1-second subsamples were compared with the index 8-second CFE-mean. Offline spectral analysis defined DF as the frequency with greatest power, and DF of subsamples were compared with index DF. Index 8-second electrogram CFE-mean was 114 +/- 20 ms for right atria and 102 +/- 17 ms for left atria (P = 0.01); DF was 5.7 +/- 0.8 Hz for right atria and 6.0 +/- 0.8 Hz for left atria (P = 0.02). Means from shorter electrograms were nonsignificantly decreased for CFE-mean and overestimated for DF (P0.001). Mean absolute differences between subsampled and index values ranged from 3.3 to 20.1 ms for CFE-mean and 0.11 to 1.18 Hz for DF. Subsampled electrograms deviating10% from index values ranged from 2.5 to 56% for CFE-mean and 3.5 to 41% for DF. Intraclass correlation coefficients ranged from 0.992 to 0.788 for CFE-mean and 0.897 to 0.233 for DF. Unacceptable differences from index values were found with CFE-mean and DF from electrograms5 seconds.Electrograms ofor=5-second duration are required to accurately characterize CFAE and DF sites for ablation.

Evidence from noninvasive studies suggests magnesium has a differential effect on atrioventricular nodal (AVN) pathways. To further explore the electrophysiologic effects of intravenous magnesium sulfate (MgSO(4)) on supraventricular tachycardia, with particular reference to AVN conduction pathways, we studied 23 patients with supraventricular tachycardia at the time of electrophysiologic study. Tachycardia cycle length; AH, HV, and VA intervals; anterograde and retrograde Wenckebach thresholds; slow and fast pathway effective refractory periods (ERPs); accessory pathway ERP; right atrial and ventricular ERPs; blood pressure; and serum magnesium were evaluated before and after administration of MgSO(4) during sustained tachycardia. AVN reentry was induced in 14 patients and atrioventricular reentry was induced in 9; 1 of the latter had dual AVN physiology with tachycardia using the slow pathway. Serum magnesium level increased from 0.88 +/- 0.11 to 1.79 +/- 0.14 mmol/L (p

Aims There is increasing evidence of the role direction-dependent conduction plays in the arrhythmogenic interaction between ectopic triggers and abnormal atrial substrates. We thus sought to characterize direction-dependent conduction in chronically stretched atria. Methods and results Twenty-four patients with chronic atrial stretch due to mitral stenosis and 24 reference patients with left-sided accessory pathways were studied. Multipolar catheters placed at the lateral right atrium, crista terminalis, and coronary sinus (CS) characterized direction-dependent conduction along linear catheters and across the crista terminalis. Bi-atrial electroanatomic maps were created in both sinus rhythm and an alternative wavefront direction by pacing from the distal CS. This allowed an assessment of conduction velocities, electrogram, and voltage characteristics during wavefronts propagating in different directions. While differing wavefront directions caused changes in both chronic atrial stretch and reference patients ( P < 0.001 for all), these direction-dependent changes were greater in chronic atrial stretch compared with reference patients, who exhibited greater slowing in conduction velocities ( P = 0.09), prolongation of bi-atrial activation time ( P = 0.04), increase in number ( P < 0.001) and length ( P < 0.001) of lines of conduction block, increase in fractionated electrograms ( P < 0.001), and decrease in voltage ( P = 0.08) during left-to-right compared with right-to-left atrial activation. These direction-dependent changes were associated with a greater propensity for chronically stretched atria to develop atrial fibrillation ( P = 0.02). Conclusions Atrial remodelling in chronic atrial stretch exacerbates physiological direction-dependent conduction characteristics. Our data suggest that the greater direction-dependent conduction seen in patients with chronic atrial stretch may promote arrhythmogenesis due to ectopic triggers from the left atrium.

Atrial electrical remodeling has been shown after termination of atrial flutter (AFL); however, whether abnormalities persist beyond an arrhythmic episode is not known. We aimed to characterize the atrial substrate, remote from arrhythmia, in patients with typical AFL. We compared 20 patients, studied remote from episodes of typical AFL and without a history of atrial fibrillation, to 20 reference patients. Multipolar catheters placed at the lateral right atrium (RA), coronary sinus, crista terminalis, and septal RA measured the effective refractory period at 5 sites; conduction characteristics at the crista terminalis; and the conduction time along the lateral RA and coronary sinus. Electroanatomic right atrial maps were created to determine regional differences in voltage and conduction. Patients with AFL demonstrated the following compared to the reference patients: a larger right atrial volume (121 +/- 30 vs 83 +/- 24 ml, p = 0.005); a prolonged P-wave duration (122 +/- 18 vs 102 +/- 11 ms, p = 0.007); a longer right atrial activation time (107 +/- 23 vs 85 +/- 14 ms, p = 0.02); a prolonged conduction time along the lateral RA (67 +/- 4 vs 47 +/- 3 ms, p

Catheter ablation has rapidly gained acceptance as a mainstay of therapy for many symptomatic patients with atrial fibrillation since the original publication by the Bordeaux group [1]. Early on it became apparent that in most patients with par-oxysmal AF, the arrhythmia was initiated by focal firing in the pulmonary veins. Ablation focused on elimination of such triggers and was largely lim-ited to patients who would stay in sinus rhythm long enough to allow successful mapping within the pulmonary veins. As this was time consuming and was associated with high risk of developing pulmonary vein stenosis, ablation lesions were moved further and further away from the sources of focal firing with co-development of Circumfer-ential Pulmonary Vein Ablation (CPVA) [2] aim-ing to encompass pulmonary vein ostia with cir-cular lesions without verification of conduction block and Segmental Pulmonary Vein Isolation [3] evolving into Pulmonary Vein Antrum Isola-tion [4] with the targeted area similar to that in CPVA but with requisite documentation of entry and / or exit block of conduction. While successful in the majority of patients with paroxysmal AF, these approaches were lacking in patients with persistent and permanent AF. A concurrent ap-proach addressing the fibrillatory substrate was developed and proved to be a successful stand-alone alternative to lesions encircling the pulmo-nary veins at one center [5]. This approach had the advantage of better tailoring the lesion set to the individual patient and potentially limiting energy delivery and associated risks. Addressing fibrillatory conduction as an adjunct to ablating triggers had since become incorporated into the lesion set targeting persistent and permanent atri-al fibrillation in a stepwise approach popularized by the Bordeaux group [6]. At the same time better tools have enabled clinicians to probe deeper into the complex interaction of the mechanisms initi-ating and maintaining atrial fibrillation. So in ex-perimental models of atrial fibrillation “drivers” or areas of microreentry were seen surrounded by areas of fibrillatory conduction [7-9]. Research has pointed to the possibility of the “drivers” or “triggers” to be in close proximity to areas of atrial myocardium innervated by autonomic gan-glionated plexi with areas of fibrillatory conduc-tion 1-2 cm remote from these [10]. Relationship between areas of high dominant frequency and atrial tachyarrhythmias that follow AF ablation has been demonstrated [11] suggesting that such arrhythmias may actually drive AF prior to de-fragmentation.In their paper published last month [12], Drs Stiles and Brooks describe high-density bi-atrial map-ping during atrial fibrillation prior to ablation to identify areas of presumed drivers and fibrillato-ry conduction. The investigators collected around 500 points in each of the 20 patients during atrial fibrillation using a PentaRay (Biosense Webster, Diamond Bar, CA, USA) catheter and NavX soft-ware (St. Jude Medical, St. Paul, MN, USA). Each point was screened manually to eliminate points with unacceptable signal-to-noise ratio. Eight

Darryl P. Leong, Martin K. Stiles, Bobby John, Dennis H. Lau, Glenn D. Young and Prashanthan Sanders

We present a 51-year-old morbidly obese man who underwent insertion of a single-chamber implantable cardioverter defibrillator for monomorphic ventricular tachycardia occurring after myocardial infarction. After a period of satisfactory device function, a sudden change in R-wave with atrial over-sensing heralded inappropriate defibrillation and induction of ventricular fibrillation, with subsequent death of the patient.

Atrial fibrillation (AF) is the most common sustained arrhythmia to occur in humans. Several predisposing substrates such as increasing age, heart failure, hypertension and valvular heart disease have been identified. The use of illicit drugs as the substrate for AF is not frequently recognized.

Background: Arrhythmic events are one of the leading causes of death in patients after myocardial infarction. Tpeak-Tend interval (TpTe) on the surface ECG has been associated with increased of arrhythmia. We sought to investigate the effect of reperfusion therapy on this parameter and also as a predictor for mortality among patients with ST elevation myocardial infarction (STEMI). Method: Consecutive patients admitted to chest pain unit at a tertiary hospital with new-onset STEMI treated with thrombolysis, rescue percutaneous coronary intervention (PCI) and primary PCI were included. Digital ECGs at 50 mm/sec speed and 20 mm/mV gain were obtained before and after reperfusion therapy. TpTe interval was measured in leads with limited ST-segment deviation. Risk factors, clinical presentation and left ventricular function (LV EF) by echocardiography were noted. Results: From June 2013 to January 2014, 222 patients (14.9% Females; mean age 54.9 12.1 years) were enrolled. All forms of reperfusion resulted in significant reduction of TpTe [13.4ms (p < 0.0001), 13.7ms (p < 0.0001) and 18.8ms (p < 0.001) respectively]. TpTewas not significantly associated with the 12 (5.4%)deaths at 1month following STEMI. Change in TpTe was inversely related to duration of presenting complaint (p < 0.001 andLVEF (p < 0.001). It didnot correlatewith diabetes, hypertension, dyslipidaemia or tobacco use. Conclusion: In patients with STEMI there was significant reduction in repolarisation duration as assessed by TpTe following reperfusion. None of reperfusion modalities conferred greater change. This index could not predict subsequent 30 day mortality.

that irregular ventricular activation alters ion channel expression and cellular electrophysiology. Methods:mRNA expression of ion channels and accessory subunits was examined in neonatal rat ventricular myocytes (NVCMs) paced either regularly or irregularly for 24 hours to simulate ventricular activation in sinus rhythm (SR) and AF respectively. Relevant transmembrane currents were measured after 96 hours of regular vs irregular pacing using whole cell patch clamp approach. LV myocardium from end-stage heart failure (ESHF) patients in SR and chronic AF undergoing cardiac transplantation also underwent mRNA expression studies as guided by results from the NVCMmodel. Results: Irregular pacing induced a 48% increase in NVCMmRNA expression of KCNA4. However, there was no difference in Ito current density across pacing strategies. Irregular pacing induced trivial changes in NVCM mRNAexpression for theNa channel SCN5A (11% reduction), and the Ca channels CACNA1C (19% increase), and CACNA1H (8% decrease). No differences were observed for ion channels CACNA1G, KCNQ1, KCNH2, KCND3, KCNJ2, and KCNJ11; accessory subunits KCNE1, KCNE2, KCNIP2, and ABCC9; and gap junction subunits GJA1 and GJA5. There were no differences in mRNA expression of SCN5A, CACNA1C, CACNA1H, or KCNA4 in LV myocardium from ESHF patients in AF vs SR. Conclusion: In an acute model, irregular ventricular a i a a

Background: Incessant focal atrial tachycardia (AT)may be complicated by LV dysfunction. The aim was to characterise the incidence, ECG and EP features of incessant focal AT and identify predictors of tachycardia mediated cardiomyopathy (TCM). Methods: 82 of 345 (24%) pts with focal AT presenting for radiofrequency ablation between 1997 and 2008 were incessant. Incessant AT was defined as continuous tachycardia or recurrent paroxysms of tachycardia separated by ≤2 sinus beats. Results: The mean age was 42± 20 years, 57% were male and mean symptom duration was 5± 7 years. TCM was present in 30/82 (37%), defined as LVEF