Atrial Burst Pacing Research Articles

A Novel Mechanism of Failure to Detect Atrial Arrhythmias by Pacemakers and Implantable Cardioverter Defibrillators

A 64-year-old man with complete heart block, status post-Medtronic dual chamber pacemaker insertion, failed ablation for atrial tachycardia at an outside institution. Despite persistent palpitations and known unsuccessful ablation, pacemaker interrogation revealed no evidence of atrial arrhythmias. At electrophysiology study, burst pacing from the high right atrium and distal coronary sinus at 370 ms revealed bidirectional 2:1 interatrial conduction block. Left atrial burst pacing at 260 ms induced an atrial tachycardia (cycle length 340 ms) with 2:1 left to right atrial block and right atrial activation at 680 ms. The tachycardia was localized to the lateral left atrial roof. A series of ablation lesions from left to right superior pulmonary vein terminated the tachycardia. Left to right interatrial conduction block is a mechanism for underdetection of atrial arrhythmias with implantable devices not previously described. As the extent of atrial ablation increases, the incidence of this mechanism of underdetection may increase. Though devices are often considered ideal for atrial arrhythmia detection and are used in multiple trials, detection failures can occur despite appropriate device function. This case underscores the need for electrocardiographic monitoring in addition to device-based electrogram monitoring.

Atrial fibrillation and circulating endothelial progenitor cells

This editorial refers to ‘Relationship of circulating endothelial progenitor cells to the recurrence of atrial fibrillation after successful conversion and maintenance of sinus rhythm’ by C.-W. Siu et al. , on page 517. In atrial fibrillation (AF), mortality is increased largely due to associated stroke.1 Besides their inability to contract synchronously, fibrillating atria develop contractile dysfunction due to remodelling, including abnormalities in cellular calcium handling (for review see Dobrev2) Contractile dysfunction impairs blood flow in the atria and may, in part, be responsible for the prevalence of atrial thrombus formation leading to enhanced propensity for stroke. Evidence is accumulating that AF is associated with endothelial dysfunction3,4 that contributes to increased risk of thrombo-embolism via the mediation of a prothrombotic or hypercoagulable state. Platelet activation is enhanced5 and after induction of AF by atrial burst pacing local hypercoagulabity develops within a few minutes.6 AF-induced tachyarrhythmia causes beat-to-beat variation in peripheral blood flow, and … *Corresponding author. Tel: +49 351 458 6300; fax: +49 351 458 6315, Email: ravens{at}rcs.urz.tu-dresden.de

Electrical Remodeling in Fibrillating Canine Atrium Action Potential Alternans During Rapid Atrial Pacing and Late Phase 3 Early Afterdepolarization After Cessation of Rapid Atrial Pacing

Sustained atrial fibrillation (AF) was induced by atrial burst pacing, and monophasic action potentials (MAPs) were recorded. MAP alternans was observed at a cycle length (CL) of 167.5 ± 28.2 msec before burst pacing and 201.3 ± 40.2 msec after burst pacing. AF > 5 minutes duration was induced in 1 dog in the control condition but in all 8 dogs after burst pacing. The difference in RA MAPD(80) of the first spontaneous beat and steady-state sinus rhythm was significantly larger after atrial burst pacing than before atrial burst pacing (31.5 ± 15.9 msec versus 8.2 ± 9.0 msec) In 4 dogs, late phase 3 early after depolarization was observed after rapid atrial pacing. Rapid atrial pacing-induced electrical remodeling includes APD alternans during rapid atrial pacing and also causes an increase in the MAPD of the initial several beats and the development of late phase 3 early afterdepolarizations after a sudden increase in CL.

Persistent thebesian veins presenting with myocardial ischemia

An 82-year-old man presenting with acute coronary syndrome (exercise-induced chest pain, ST-T wave changes and troponin I 0.21 μg/L) underwent coronary angiography. The left anterior descending artery (LAD) and right coronary artery (RCA) had minor nonobstructive plaque (Figures 1A and ​and1B).1B). Left coronary injection demonstrated a capillary blush draining into the left ventricular (LV) cavity due to multiple microfistulae (Figure 1C and Video) all along the wall of the left ventricle, extensive enough to produce an LV angiogram (Figure 1D). In the absence of any myocardial tumour, ventricular hypertrophy or evidence of noncompaction (on echocardiography), this appearance suggested arterioluminal-type thebesian veins communicating between the coronary arteries and LV cavity. Figure 1 Although arterioluminal thebesian veins have a larger diameter, a network extensive enough to produce LV opacification is rare. These veins bypass myocardial capillaries and may give rise to myocardial ischemia due to coronary steal (1), because the normal circulation offers a greater resistance to flow than the fistula. Extensive communication, as in the present patient, may lead to myocardial ischemia, severe enough to cause enzyme leak. This is due to a considerable decrease in intracoronary diastolic perfusion pressure that diminishes in proportion to the size of the fistula, especially during exercise. Anginal symptoms with ST segment changes due to myocardial hypoxia confirmed by elevated coronary sinus lactate levels has been demonstrated after atrial burst pacing in patients with multiple coronary artery-LV fistulae and normal epicardial coronary arteries (2).

Age‐Related Increase in Atrial Fibrillation Induced by Transvenous Catheter‐Based Atrial Burst Pacing: An In Vivo Rat Model of Inducible Atrial Fibrillation

Large animal models of atrial fibrillation (AF) are well established, but limited experimental reports exist on small animal models. We sought to develop an in vivo rat model of AF using a transvenous catheter and to evaluate the model's underlying characteristics. Echocardiogram, surface electrocardiogram (ECG), and atrial effective refractory period (AERP) were recorded at baseline in young (3 months) and middle-aged (9 months) Wistar rats. AF inducibility and duration were measured through transvenous electrode catheter in young (n = 11) and middle-aged rats (n = 11) and middle-aged rats treated with either pilsicainide (1 mg/kg iv, n = 7) or amiodarone (10 mg/kg iv, n = 9). Degrees of interstitial fibrosis and cellular hypertrophy in the atria were assessed histologically. The P-wave duration and AERP were significantly longer and echocardiographic left atrial dimension significantly larger in middle-aged versus young rats. AF was inducible in >90% of all procedures in both untreated rat groups, whereas AF inducibility was reduced by the antiarrhythmic drugs. The AF duration was significantly longer in middle-aged than in young rats and was significantly shortened by treatment with either pilsicainide or amiodarone. Histologic analysis revealed significant increases in atrial interstitial fibrosis and cellular diameter in middle-aged versus young rats. Transvenous catheter-based AF is significantly longer in middle-aged than in young rats and is markedly reduced by treatment with antiarrhythmic drugs. This rat model of AF is simple, reproducible, and reliable for examining pharmacologic effects on AF and studying the process of atrial remodeling.

Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties.

AimIn contrast to extensive reports on the roles of Nav1.5 α-subunits, there have been few studies associating the β-subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b−/− mice.MethodsThe following properties were compared in the hearts of wild-type (WT) and Scn3b−/− mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the β3 protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts.ResultsScn3b mRNA was expressed in the atria of WT but not Scn3b−/− hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the β3 protein was expressed in WT and absent in Scn3b−/− cardiac myocytes. Lead I electrocardiograms from Scn3b−/− mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b−/− hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b−/− but hardly any WT hearts. Scn3b−/− hearts also demonstrated significantly longer sinus node recovery times than WT hearts.ConclusionThese findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion.

Inducibility of atrial fibrillation depends not on inflammation but on atrial structural remodeling in rat experimental autoimmune myocarditis

There is increasing evidence to support a link between inflammation and atrial fibrillation (AF). However, the role of inflammation on new-onset AF is still to be elucidated. Rats underwent induction of experimental autoimmune myocarditis (EAM). Atrial structural change was evaluated by echocardiography and histological analysis. Electrophysiological data and the in vivo atrial response to burst atrial pacing were evaluated in the acute (2 weeks after EAM induction) and chronic phases (8 weeks after induction). In addition, atrial pacing after 2, 4, and 6 h after lipopolysaccharide (LPS) infusion, when the expression of gap junctions was modified, were challenged with young healthy rats. AF was induced in 11 of 15 chronic phase EAM rats but not in either acute phase EAM rats or LPS infusion rats (P<.01). Echocardiography showed dilatation of both atrium and ventricle and a decrease in the ejection fraction in the chronic phase. Histology revealed severe inflammatory lesions only in the acute phase. Interstitial atrial fibrosis as well as the area of atrial myocyte increased in the chronic phase but not in the acute phase. AF could be induced in the chronic phase of myocarditis rats, but not in the acute phase of myocarditis rats or in rats with LPS infusion. Acute inflammation per se did not increase the occurrence of AF induction. Atrial structural remodeling caused by inflammation and hemodynamic effects is necessary to induce AF.

Decremental Accessory Pathway Conduction After Ablation and Antidromic Atrioventricular Reciprocating Tachycardia 8 Years After Successful Radiofrequency Ablation

This is a rare case of antidromic reciprocating tachycardia developing 8 years after successful catheter ablation. A 15-year-old girl had recurrence of palpitations 8 years after the ablation of manifest right posteroseptal accessory pathway. Atrial burst pacing revealed Wenckebach atrioventricular conduction with preexcitation. Wide QRS tachycardia with identical morphology to sinus rhythm associated with retrograde His potential recorded immediately after the V-wave was induced by isoproterenol infusion. Atrial premature stimulus applied at the identical timing of His potential advanced the subsequent ventricular beat and His potential. Catheter ablation may produce decremental accessory pathway conduction and rarely cause antidromic atrioventricular reciprocating tachycardia. This may be explained by a presence of "de novo" accessory pathway with decremental conduction properties that became manifest after the first ablation.

A unique iatrogenic organized left atrial tachycardia with a gap conduction in previously ablated lesions

This case concerns a 57-year-old woman with an organized left atrial tachycardia (AT) after pulmonary vein (PV) isolation. The left inferior PV (LIPV) exhibited a figure of eight tachycardia around the LIPV ostium with one loop at the anterior aspect and another at the posterior aspect, which corresponded to regular surface P waves. Although a gap ablation of fractionated electrograms changed the LIPV sequence, the atrial potentials were organized with a shortened cycle length accompanied by the same surface P-wave morphology. The elimination of the anterior loop and modification of the posterior loop after the gap ablation might have yielded that specific sequence change of the AT.

Atrial tachycardia initiating atrial fibrillation successfully ablated in the non-coronary cusp of the aorta

A 60-year-old woman was referred for catheter ablation of atrial fibrillation (AF). Atrial flutter and atrial tachycardia (AT) also had been clinically documented. During the electrophysiological study, the clinical AT was induced by burst atrial pacing during isoproterenol infusion and exhibited negative P waves in the inferior leads, positive P waves in leads I, aVL, and aVR, and biphasic P waves in lead V1. The AT repeatedly and spontaneously accelerated to initiate AF by causing fibrillatory conduction in the atria. Successful catheter ablation of the AT was achieved in the non-coronary cusp of the aorta (NCC) where the local atrio-ventricular electrogram amplitude ratio was >1 during both the AT and sinus rhythm. The tailored approach targeting the NCC AT alone without left atrial ablation completely eliminated the AF. In catheter ablation of AF in a patient with a co-existing clinical AT, it may be recommended to examine the clinical AT first. If the clinical AT initiates the AF and local atrial activations in the His bundle region precede the P wave onset during AT, mapping in the NCC should be considered prior to left atrial catheterization.

Inducibility of Atrial Fibrillation with a Synchronized External Low Energy Shock Post‐Pulmonary Vein Isolation Predicts Recurrent Atrial Fibrillation

Inducibility of atrial fibrillation (AF) with burst pacing after pulmonary vein (PV) isolation is associated with recurrent AF. This study evaluated whether an external 30 Joule (J) shock synchronized to the R wave, during the vulnerable period of atrial repolarization, is able to risk-stratify patients further for AF recurrence after PV isolation. One hundred and sixteen consecutive patients underwent PV isolation for AF. Atrial burst pacing was performed after PV isolation. In patients without AF induced by burst pacing, a biphasic external 30 J shock synchronized to the R wave was delivered as a further test for inducible AF. Patients were followed for a mean of 16 months, and recurrent AF was defined as more than 10 sec of AF on ambulatory monitoring. AF was induced in 19 (16%) of patients with burst pacing. Eighty-one patients who were noninducible with burst pacing had a 30 J shock administered, which induced AF in 16 (20%). In follow-up, 21% of patients who were noninducible with burst pacing or low-energy shock vs 54% who were inducible with either test developed recurrent AF at one year (HR 3.18, P = 0.0004 on multivariate analysis). Among patients who were noninducible with burst pacing, 18% who were noninducible with a low-energy shock vs 60% who were inducible with shock developed recurrent AF at one year (HR = 4.63, P = 0.0006 on multivariate analysis). Inducibility of AF by a 30 J shock delivered during atrial repolarization after PV isolation may predict AF recurrence. Evaluation of inducibility of AF with burst pacing and a biphasic external synchronized shock after PV isolation may help guide postprocedure management.

Identification and Radiofrequency Catheter Ablation of a Nonsustained Atrial Tachycardia at the Septal Mitral Annulus with the Use of a Noncontact Mapping System: A Case Report

Here we report a case of a 16-year old female with symptomatic nonsustained atrial tachycardia (NSAT) originating from the septal mitral annulus. NSAT was induced by atrial burst pacing after an intravenous isoproterenol (ISP) injection. The array mode of the noncontact mapping system (NCM) allowed us to quickly identify the tachycardia focus at the septal mitral annulus, where the contact bipolar voltage map revealed no low voltage area (<0.5 mV). The NSAT was eliminated by a radiofrequency energy application to the identified tachycardia focus during sinus rhythm, and the patient has been free from any symptoms during 10 months of follow-up.

Distinct contractile and molecular differences between two goat models of atrial dysfunction: AV block-induced atrial dilatation and atrial fibrillation

Atrial dilatation is an independent risk factor for thromboembolism in patients with and without atrial fibrillation (AF). In many patients, atrial dilatation goes along with depressed contractile function of the dilated atria. While some mechanisms causing atrial contractile dysfunction in fibrillating atria have been addressed previously, the cellular and molecular mechanisms of atrial contractile remodeling in dilated atria are unknown. This study characterized in vivo atrial contractile function in a goat model of atrial dilatation and compared it to a goat model of AF. Differences in the underlying mechanisms were elucidated by studying contractile function, electrophysiology and sarcoplasmic reticulum (SR) Ca 2+ load in atrial muscle bundles and by analyzing expression and phosphorylation levels of key Ca 2+-handling proteins, myofilaments and the expression and activity of their upstream regulators. In 7 chronically instrumented, awake goats atrial contractile dysfunction was monitored during 3 weeks of progressive atrial dilatation after AV-node ablation (AV block goats (AVB)). In open chest experiments atrial work index (AWI) and refractoriness were measured (10 goats with AVB, 5 goats with ten days of AF induced by repetitive atrial burst pacing (AF), 10 controls). Isometric force of contraction (FC), transmembrane action potentials (APs) and rapid cooling contractures (RCC, a measure of SR Ca 2+ load) were studied in right atrial muscle bundles. Total and phosphorylated Ca 2+-handling and myofilament protein levels were quantified by Western blot. In AVB goats, atrial size increased by 18% (from 26.6 ± 4.4 to 31.6 ± 5.5 mm, n = 7 p < 0.01) while atrial fractional shortening (AFS) decreased (from 18.4 ± 1.7 to 12.8 ± 4.0% at 400 ms, n = 7, p < 0.01). In open chest experiments, AWI was reduced in AVB and in AF goats compared to controls (at 400 ms: 8.4 ±0.9, n = 7, and 3.2 ± 1.8, n = 5, vs 18.9 ± 5.3 mm×mmHg, n = 7, respectively, p < 0.05 vs control). FC of isolated right atrial muscle bundles was reduced in AVB ( n = 8) and in AF ( n = 5) goats compared to controls ( n = 9) (at 2 Hz: 2.3 ± 0.5 and 0.7 ± 0.2 vs 5.5 ± 1.0 mN/mm 2, respectively, p < 0.05). APs were shorter in AF, but unchanged in AVB goats. RCCs were reduced in AVB and AF versus control (AVB, 3.4 ± 0.5 and AF, 4.1 ± 1.4 vs 12.2 ± 3.2 mN/mm 2, p < 0.05). Protein levels of protein kinase A (PKA) phosphorylated phospholamban (PLB) were reduced in AVB ( n = 8) and AF ( n = 8) vs control ( n = 7) by 37.9 ± 12.4% and 29.7 ± 10.1%, respectively ( p < 0.01), whereas calmodulin-dependent protein kinase II (CaMKII) phosphorylated ryanodine channels (RyR2) were increased by 166 ± 55% in AVB ( n = 8) and by 146 ± 56% in AF ( n = 8) goats ( p < 0.01). PKA-phosphorylated myosin-binding protein-C and troponin-I were reduced exclusively in AVB goat atria (by 75 ± 10% and 55 ± 15%, respectively, n = 8, p < 0.05). Atrial dilatation developing during slow ventricular rhythm after complete AV block as well as AF-induced remodeling are associated with atrial contractile dysfunction. Both AVB and AF goat atria show decreased SR Ca 2+ load, likely caused by PLB dephosphorylation and RYR2 hyperphosphorylation. While shorter APs further compromise contractility in AF goat atria, reduced myofilament phosphorylation may impair contractility in AVB goat atria. Thus, atrial hypocontractility appears to have distinct molecular contributors in different types of atrial remodeling.

Abstract 3501: Calmodulin Kinase II Activation of Mutant Ryanodine Channels Promotes Ectopic Activity and Atrial Fibrillation

Some individuals with mutations in the cardiac ryanodine receptor gene (RyR2) develop stress-induced atrial fibrillation (AF), but the underlying mechanisms are unknown. This study explored the molecular basis of AF susceptibility in mice heterozygous for the human arrhythmia-linked RyR2 mutation R176Q (RQ mice). AF inducibility was assessed with atrial burst pacing in WT (n=34), RQ mice (n=43) and RQ mice crossed with transgenic mice expressing the CaMKII-inhibitory peptide AC3I (RQxAC3I, n=6) or the inactive analog AC3C (RQxAC3C, n=9). Dual voltage (RH237) and calcium (Rhod-2 AM) optical mapping was applied to monitor simultaneous Ca2+ and membrane-voltage changes. Ca2+ fluorescence (Fluo-4 AM) was used to study SR Ca2+ release. Expression/phosphorylation of CaMKII and RyR2 were determined by immunostaining in mice and human atrial biopsies from sinus rhythm (SR) (n=7) and chronic AF (n=7) patients. Atrial burst pacing-induced AF was more common in RQ (55%) than in WT mice (11%*; *P&lt;0.05) and was associated with ~50% higher CaMKII-dependent RyR2 phopshorylation (Ser2814 site). Expression and phosphorylation (Thr287) of CaMKIId were increased in AF patients by 63%* and 40%*, respectively, and CaMKII-phopshorylation of RyR2 at Ser2814 was 80%* higher in AF than in SR patients. Genetic inhibition of CaMKII reduced AF incidence in RQxAC3I (16%*), but not in RQxAC3C mice (62%). Optical mapping revealed more atrial burst pacing-induced ectopic beats (and re-entry) in RQ than WT atria (296 vs.19* ectopic beats, 120 ms cycle length) that were depressed by CaMKII inhibiton with KN-93 (1 μM). [Ca2+]i release by 10 mM local caffeine puffs (an index of SR Ca2+ content) were similar in RQ and WT mice (4.59±0.42 vs 4.04±0.41 [a.u.], respectively), whereas SR Ca2+ leak defined as tetracaine (5 μM)-sensitive decrease in diastolic [Ca2+]i was higher in RQ than in WT mice (% of SR Ca2+ content: 10.2±0.9 vs 7.7±0.8*). CaMKII inhibition with KN-93 suppressed SR Ca2+ leak. High rate-associated CaMKII activation promotes AF inducibility in mice with a stress-induced arrhythmia-linked R176Q mutation in RyR2. Inhibition of CaMKII may be a viable drug target for effective AF therapy. This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma &amp; Texas).

Acute Onset Human Atrial Fibrillation Is Associated With Local Cardiac Platelet Activation and Endothelial Dysfunction

The purpose of this study was to determine whether acute onset atrial fibrillation (AF), independent of other risk factors, predisposes to an early prothrombotic state. Several risk factors predispose to the hypercoagulable state in human AF, but whether acute onset AF alone is prothrombotic remains unclear. Patients with paroxysmal AF (n = 22) underwent radiofrequency catheter ablation. All patients presented in sinus rhythm. Baseline blood samples were obtained simultaneously from the femoral vein (systemic sample) and the coronary sinus (local cardiac sample). The AF was induced by burst atrial pacing in 14 patients (AF group). A control group (n = 8) underwent atrial pacing at 120 beats/min. Blood samples were recollected after 15 min. Platelet P-selectin expression (CD62) was measured using flow cytometry. Markers of thrombin generation (thrombin antithrombin complex, prothrombin fragment 1.2), inflammation (C-reactive protein, interleukin-6), and nitric oxide were measured using enzyme-linked immunosorbent assays. Neither local nor systemic platelet activation changed in the control group. In the AF group, local cardiac platelet activation (percent P-selectin [+] platelets) increased significantly (2.2 +/- 0.6% to 2.8 +/- 1.0%, p = 0.007); however, systemic platelet activation did not change. The AF group had increased local thrombin generation (thrombin antithrombin complex: 8.5 +/- 7.6 ng/ml to 33.2 +/- 17.4 ng/ml, p = 0.003; prothrombin fragment 1.2: 95.6 +/- 45.6 micromol/l to 243.8 +/- 120.1 micromol/l, p = 0.003), decreased nitric oxide production (25.2 +/- 10.8 micromol/l to 22.3 +/- 10.0 micromol/l, p < 0.02), and no change in inflammatory markers. Human AF causes local cardiac platelet activation within minutes of onset. The results demonstrate how AF alone, independent of other risk factors, may contribute to the hypercoagulable state.

Identification and Radiofrequency Catheter Ablation of a Nonsustained Atrial Tachycardia at the Septal Mitral Annulus with the Use of a Noncontact Mapping System: A Case Report

Here we report a case of a 16-year old female with symptomatic nonsustained atrial tachycardia (NSAT) originating from the septal mitral annulus. NSAT was induced by atrial burst pacing after an intravenous isoproterenol (ISP) injection. The array mode of the noncontact mapping system (NCM) allowed us to quickly identify the tachycardia focus at the septal mitral annulus, where the contact bipolar voltage map revealed no low voltage area (<0.5 mV). The NSAT was eliminated by a radiofrequency energy application to the identified tachycardia focus during sinus rhythm, and the patient has been free from any symptoms during 10 months of follow-up.

Omega-3 Polyunsaturated Fatty Acids Prevent Atrial Fibrillation Associated With Heart Failure but Not Atrial Tachycardia Remodeling

There is epidemiological evidence that omega-3 polyunsaturated fatty acids (PUFAs) reduce the risk of atrial fibrillation (AF), but clinical data are conflicting. The present study assessed the effects of PUFA on AF in experimental models. We studied the effects of oral PUFA supplements in 2 experimental AF paradigms: electrical remodeling induced by atrial tachypacing (400 bpm for 1 week) and congestive heart failure-associated structural remodeling induced by ventricular tachypacing (240 bpm for 2 weeks). PUFA pretreatment did not directly change atrial effective refractory period (128+/-6 [mean+/-SEM] versus 127+/-2 ms; all effective refractory periods at 300-ms cycle lengths) or burst pacing-induced AF duration (5+/-4 versus 34+/-18 seconds). Atrial tachypacing dogs had shorter refractory periods (73+/-6 ms) and greater AF duration (1185+/-300 seconds) than shams (119+/-5 ms and 20+/-11 seconds; P<0.01 for each). PUFAs did not significantly alter atrial tachypacing effects on refractory periods (77+/-8 ms) or AF duration (1128+/-412 seconds). PUFAs suppressed ventricular tachypacing-induced increases in AF duration (952+/-221 versus 318+/-249 seconds; P<0.05) and attenuated congestive heart failure-related atrial fibrosis (from 19.2+/-1.1% to 5.8+/-1.0%; P<0.001) and conduction abnormalities. PUFAs also attenuated ventricular tachypacing-induced hemodynamic dysfunction (eg, left ventricular end-diastolic and left atrial pressure from 12.2+/-0.5 and 11.4+/-0.6 mm Hg, respectively, to 6.4+/-0.5 and 7.0+/-0.8 mm Hg; P<0.01) and phosphorylation of mitogen-activated protein kinases (extracellular-signal related and P38 kinase). PUFAs suppress congestive heart failure-induced atrial structural remodeling and AF promotion but do not affect atrial tachycardia-induced electrical remodeling. The beneficial effects of PUFAs on structural remodeling, possibly related to prevention of mitogen-activated protein kinase activation, may contribute to their clinical anti-AF potential.

Atrial fibrillation reduces the atrial impedance amplitude during cardiac cycle: a novel detection algorithm to improve recognition of atrial fibrillation in pacemaker patients

In carriers of dual chamber pacemakers and implantable cardioverter-defibrillators (ICD), detection of atrial fibrillation (AF) is crucial for adequate mode switch function and to avoid inappropriate shock delivery. Detection algorithms rely on the atrial rate and on the relationship of atrial to ventricular intracardiac electrograms, but the relative portion of misclassified AF episodes remains high. Although myocardial impedance is a reliable indicator of contraction, little is known about atrial impedance as a marker of atrial arrhythmias. Methods During an electrophysiological study, we investigated the effect of induced AF on impedance at the right atrial free wall (RAFW) and right atrial appendage (RAA) in 20 patients. Using biphasic square-wave pulses (128 Hz, 200 microA/15 micros), impedance changes were recorded during sinus rhythm (SR-1), atrial pacing at 120 beats/min, AF induced by rapid atrial burst pacing, and after spontaneous AF termination (SR-2). Results At the RAA, peak-to-peak impedance amplitude during cardiac cycle (DeltaZ) dropped from 51.7 +/- 35.3 Omega (SR-1) or 49.6 +/- 30.6 Omega (pacing) to 24.6 +/- 22.0 Omega (AF, P< or =0.0005), and subsequently increased to 37.7 +/- 24.7 Omega (SR-2, P < or = 0.0004 v. AF). At the RAFW, DeltaZ changed from 16.2 +/- 15.5 Omega (SR-1) or 13.5 +/- 9.9 Omega (pacing) to 5.9 +/- 4.1 Omega (AF, P < or = 0.003), and to 11.4 +/- 10.7 Omega (SR-2, P < or = 0.015). Given a discrimination threshold of 65%, the sensitivity and the specificity of DeltaZ to detect AF were 79 +/- 18 and 89 +/- 14%, respectively (95% confidence interval). AF causes DeltaZ drop in pacemaker and ICD recipients. This impedance based algorithm can be used as an alternative method of AF detection.

A Wide QRS Complex Tachycardia with Different Initiation Patterns: What is the Mechanism?

A 47-year-old man with palpitations underwent electrophysiologic testing (EPS). Burst atrial pacing while infusing isoproterenol induced non-reproducible wide QRS tachycardias with an unusual pattern of an H-A-V activation with the same tachycardia cycle length and two different initiation patterns. The tachycardia had the earliest atrial activation at the His bundle region. No dual atrioventricular (AV) nodal physiology was demonstrated by programmed atrial stimulation. Though a definite diagnosis of AV nodal reentrant tachycardia was not obtained, slow pathway ablation was performed in order to avoid inadvertent AV block as a complication. Thereafter, no tachycardias were induced by repeat burst atrial pacing.

Focal Atrial Tachycardia Originating from the Left Atrial Appendage: Electrocardiographic and Electrophysiologic Characterization and Long‐Term Outcomes of Radiofrequency Ablation

This study sought to investigate electrophysiologic characteristics and radiofrequency ablation (RFA) in patients with focal atrial tachycardia (AT) arising from the left atrial appendage (LAA). This study included seven patients undergoing RFA with focal AT. Activation mapping was performed during tachycardia to identify an earlier activation in the left atria and the LAA. The atrial appendage angiography was performed to identify the origin in the LAA before and after RFA. AT occurred spontaneously or was induced by isoproterenol infusion rather than programmed extrastimulation and burst atrial pacing in any patient. The tachycardia demonstrated a characteristic P-wave morphology and endocardial activation pattern. The P wave was highly positive in inferior leads in all patients. Lead V1 showed upright or biphasic (+/-) component in all patients. Lead V2-V6 showed an isoelectric component in five patients or an upright component with low amplitude (<0.1 mV) in two patients. Earliest endocardial activity occurred at the distal coronary sinus (CS) ahead of P wave in all seven patients. Mean tachycardia cycle length was 381 +/- 34 msec and the earliest endocardial activation at the successful RFA site occurred 42.3 +/- 9.6 msec before the onset of P wave. RFA was acutely successful in all seven patients. Long-term success was achieved in seven of the seven over a mean follow-up of 24 +/- 5 months. The LAA is an uncommon site of origin for focal AT (3%). There were consistent P-wave morphology and endocardial activation associated with this type of AT. The LAA focal ablation is safe and effective. Long-term success was achieved with focal ablation in all patients.