bluuebunny/crossref_metadata_2025_split huggingface dataset:
Method for Simultaneous Epicardial and Endocardial Mapping of In Vivo Canine Heart: Application to Atrial Conduction Properties and Arrhythmia Mechanisms
Authors: DERAKHCHAN KATAYOUN , LI DANSHI , COURTEMANCHE MARC , SMITH BENJAMIN , BROUILLETTE JUDITH , PAGÉ PIERRE L. , NATTEL STANLEY 
Published: August 2003

Endocardial/Epicardial Mapping of AF.
Introduction: It has been suggested that the three‐dimensional structure of the atria may be crucial in arrhythmogenesis; however, previous in vivo atrial activation mapping studies have been limited to either endocardial or epicardial approaches. Methods and Results: To investigate the role of endocardial and epicardial structures and their interaction in atrial conduction and arrhythmias, we used five epicardial plaques and two intra‐atrial balloon arrays to record a total of 368 unipolar electrograms from the entire epicardial and endocardial surface of both atria. During regular 1:1 pacing from the right atrial appendage, right atrial endocardial activation spread considerably faster than epicardial (total activation time 45 ± 12 msec vs 60 ± 19 msec, respectively [mean ± SD]; P < 0.05), pointing to preferential conduction over structures like the crista terminalis and pectinate muscles. No such differences were noted in the left atrium. Transseptal spread occurred via discrete anterior and posterior pathways, causing separate breakthroughs in anterior and posterior atrial regions, respectively. Dissociation between septal pathways played a role in reentry during vagal atrial fibrillation. In 2 of 4 dogs with atrial fibrillation associated with congestive heart failure, single macroreentrant circuits involving endocardial and epicardial components were revealed during the arrhythmia. Conclusion: We conclude that activation mapping using simultaneous recording from both epicardial and endocardial surfaces provides potentially important insights into the mechanisms of atrial conduction and arrhythmogenesis.
Critically Timed Auxiliary Shock to Weak Field Area Lowers Defibrillation Threshold
Authors: WALKER ROBERT G. , KENKNIGHT BRUCE H. , IDEKER RAYMOND E. 
Published: August 2003

Auxiliary Shock Improves Defibrillation.
Introduction: This study tested the hypothesis that the defibrillation threshold (DFT) can be lowered by delivering a weak auxiliary shock in conjunction with a stronger primary shock to the cardiac region where the primary shock electric field is weakest. Methods and Results: Eight swine were studied in each of two study parts. In both parts, DFTs were determined for dual shocks delivered through two electrode pairs. The biphasic primary shock was delivered through electrodes in the right ventricle and superior vena cava. The auxiliary shock was delivered through a separate electrode in the superior vena cava and a left ventricular electrode placed where the primary shock field was presumed to be weakest. In part I, a monophasic auxiliary shock of 50, 100, or 150 V was delivered either simultaneously with or 1, 20, or 40 msec before primary shock. When auxiliary shock was delivered simultaneously with or 1 msec before primary shock, DFT energy was reduced by approximately 50% compared with primary shock alone. In part II, a 150‐V monophasic or biphasic auxiliary shock of either polarity was delivered 1 msec before or after primary shock. Regardless of waveform or polarity, all auxiliary shock delivered before primary shock lowered DFT energy by approximately 30% compared with primary shock alone. Depending on waveform and polarity, auxiliary shock delivered after primary shock either did not significantly change the DFT or elevated the DFT compared with primary shock alone. Conclusion: Application of a small auxiliary shock, just before or simultaneously with a primary shock, to the cardiac region where the primary shock field is weakest significantly lowers DFT.
Role of Calcium in Acute Hyperthermic Myocardial Injury
Authors: EVERETT THOMAS H. , NATH SUNIL , LYNCH CARL , BEACH JAMES M. , WHAYNE JAMES G. , HAINES DAVID E. 
Published: August 2003

Hyperthermic Myocardial Injury.
Introduction: We hypothesized that intracellular calcium overload may play an important role in heat‐induced myocardial injury. This postulate was investigated using a model of isolated guinea pig papillary muscle in which resting tension was measured as an indirect indicator of cytosolic free‐calcium concentration and the fluorescence changes of Fluo‐3 AM dye was measured as a direct indicator of cytosolic free‐calcium concentration. Methods and Results: Excised guinea pig right ventricular papillary muscles were attached to a force transducer in a high‐flow tissue bath and superfused with Tyrode's solution at 37°± 0.5°C. The temperature was rapidly changed to between 38.0° and 56.0°C for 60 seconds and then returned to 37.0°C. Hyperthermia caused a reversible increase in resting tension at temperatures between 45° and 50°C and irreversible contracture at ≥50°C. Rapid cooling contracture experiments and experiments measuring fluorescence of myocytes loaded with 5 μ M Fluo‐3 AM dye demonstrated that the hyperthermia‐induced rise in resting tension was likely due to an increase in intracellular calcium content. Inhibition of the sarcoplasmic reticulum calcium pump with 20 μ M thapsigargin resulted in irreversible contracture of the papillary muscles at temperatures between 45° and 50°C and significant increases in Fluo‐3 fluorescence at 48°C. Blockade of sarcolemmal calcium channels with 0.5 mM cadmium or 40 μ M verapamil did not attenuate the heat‐induced increase in resting tension and Fluo‐3 fluorescence. Conclusion: Hyperthermia causes an increase in resting tension of cardiac muscle that most likely is mediated by a calcium channel‐independent increase in calcium permeability of the sarcolemmal membrane and/or release of stored intracellular calcium.
Altering Ventricular Activation Remodels Gap Junction Distribution in Canine Heart
Authors: PATEL PRAVINA M. , PLOTNIKOV ALEXEI , KANAGARATNAM PRAPA , SHVILKIN ALEXEI , SHEEHAN CATHERINE T. , XIONG WEN , DANILO PETER , ROSEN MICHAEL R. , PETERS NICHOLAS S. 
Published: August 2003

Gap Junctional Remodeling in Paced Ventricle.
Introduction: Prolonged arrhythmic or paced ventricular activation causes persistent changes in myocardial conduction and repolarization that may result from altered electrotonic current flow, for which gap junctional coupling is the principal determinant. Remodeling of gap junctions and their constituent connexins modifies conduction and has been causally implicated in reentrant arrhythmogenesis. We hypothesized conversely that altering the pattern of ventricular activation causes gap junctional remodeling. Methods and Results: Seven dogs were paced from the left ventricular (LV) epicardium (VVO, ~120 beats/min) for 21 days before excision of transmural LV samples that were divided into endomyocardial, mid‐myocardial, and epimyocardial layers. Another five paced dogs had recording electrodes attached to multiple LV sites. All 12 dogs developed characteristic pacing‐induced persistent T wave changes of cardiac memory. After 21 days of pacing, the ventricularly paced QRS duration prolonged by a mean of 4 msec over baseline (P < 0.05), a change that was associated with significant slowing of intraventricular conduction to local sites. These changes in QRS duration and repolarization were associated with a reduction in epimyocardial connexin43 expression on quantitative Western blotting of LV myocardium from close to, but not distant from, the pacing site (61.7 ± 18.4 vs 100.9 ± 34.0; P < 0.02) and a marked disruption in immunolabeled connexin43 distribution in epimyocardium only. Conclusion: Spatially distinct transmural and regional gap junctional remodeling is a consequence of abnormal ventricular activation and is associated with consistent changes in activation that may alter patterns of repolarization and facilitate reentrant arrhythmogenesis.
Reentry Site During Fibrillation Induction in Relation to Defibrillation Efficacy for Different Shock Waveforms
Authors: IDEKER RAYMOND E. , ALFERNESS CLIF , MELNICK SHARON , SREENAN KATE M. , JOHNSON ERIC , SMITH WILLIAM M. 
Published: August 2003

Reentry Site and Defibrillation Waveform Efficacy.
Introduction: Unsuccessful defibrillation shocks may reinitiate fibrillation by causing postshock reentry. Methods and Results: To better understand why some waveforms are more efficacious for defibrillation, reentry was induced in six dogs with 1‐, 2‐, 4‐, 8‐, and 16‐msec monophasic and 1/1‐ (both phases 1 msec) 2/2‐, 4/4‐, and 8/8‐msec biphasic shocks. Reentry was initiated by 141 ± 15 V shocks delivered from a defibrillator with a 150‐ μ F capacitance during the vulnerable period of paced rhythm (183 ± 12 msec after the last pacing stimulus). The shock potential gradient field was orthogonal to the dispersion of refractoriness. Activation was mapped with 121 electrodes covering 4 × 4 cm of the right ventricular epicardium, and potential gradient and degree of recovery of excitability were estimated at the sites of reentry. Defibrillation thresholds (DFTs) were estimated by an up‐down protocol for the same nine waveforms in eight dogs internally and in nine other dogs externally. DFT voltages for the different waveforms were positively correlated with the magnitude of shock potential gradient and negatively correlated with the recovery interval at the site at which reentry was induced by the waveform during paced rhythm for both internal (DFT = 1719 + 64.5 ∇ V − 11.1RI; R2= 0.93) and external defibrillation (DFT = 3445 + 150 ∇ V − 22RI; R2= 0.93). Conclusion: The defibrillation waveforms with the lowest DFTs were those that induced reentry at sites of low shock potential gradient, indicating efficacious stimulation of myocardium. Additionally, the site of reentry induced by waveforms with the lowest DFTs was in myocardium that was more highly recovered just before the shock, perhaps because this high degree of recovery seldom occurs during defibrillation due to the rapid activation rate during fibrillation.
Focal Atrial Fibrillation: Experimental Evidence for a Pathophysiologic Role of the Autonomic Nervous System
Authors: SCHAUERTE PATRICK , SCHERLAG BENJAMIN J. , PATTERSON EUGENE , SCHERLAG MICHAEL A. , MATSUDARIA KAGARI , NAKAGAWA HIROSHI , LAZZARA RALPH , JACKMAN WARREN M. 
Published: August 2003

Focal AF and Autonomic Nerves.
Introduction: Focal paroxysmal atrial fibrillation (AF) was shown recently to originate in the pulmonary veins (PVs) and superior vena cava (SVC). In the present study, we describe an animal model in which local high‐frequency electrical stimulation produces focal atrial activation and AF/AT (atrial tachycardia) with electrogram characteristics consistent with clinical reports. Methods and Results: In 21 mongrel dogs, local high‐frequency electrical stimulation was performed by delivering trains of electrical stimuli (200 Hz, impulse duration 0.1 msec) to the PVs/SVC during atrial refractoriness. Atrial premature depolarizations (APDs), AT, and AF occurred with increasing highfrequency electrical stimulation voltage. APD/AT/AF originated adjacent to the site of high‐frequency electrical stimulation and were inducible in 12 of 12 dogs in the SVC and in 8 of 9 dogs in the left superior PV (left inferior PV: 7/8, right superior PV: 6/8; right inferior PV: 4/8). In the PVs, APDs occurred at 13 ± 8 V and AT/AF at 15 ± 9 V (P < 0.01; n = 25). In the SVC, APDs were elicited at 19 ± 6 V and AT/AF at 26 ± 6 V (P < 0.01; n = 12). High‐frequency electrical stimulation led to local refractory period shortening in the PVs. The response to high‐frequency electrical stimulation was blunted or prevented after beta‐receptor blockade and abolished by atropine. In vitro, high‐frequency electrical stimulation induced a heterogeneous response, with shortening of the action potential in some cells (from 89 ± 35 msec to 60 ± 22 msec; P < 0.001; n = 7) but lengthening of the action potential and development of early afterdepolarizations that triggered APD/AT in other cells. Action potential shortening was abolished by atropine. Conclusion: High‐frequency electrical stimulation evokes rapid ectopic beats from the PV/SVC, which show variable degrees of conduction block to the atria and induce AF, resembling findings in patients with focal idiopathic paroxysmal AF. The occurrence of the arrhythmia in this animal model was likely due to alterations in local autonomic tone by high‐frequency electrical stimulation. Further research is needed to prove absolutely that the observed effects of high‐frequency electrical stimulation were caused by autonomic nerve stimulation.
Dissociation Between Coronary Sinus and Left Atrial Conduction in Patients with Atrial Fibrillation and Flutter
Authors: NDREPEPA GJIN , ZRENNER BERNHARD , SCHNEIDER MICHAEL A.E. , SCHREIECK JÜRGEN , KARCH MARTIN R. , SCHÖMIG ALBERT , SCHMITT CLAUS 
Published: August 2003

Dissociation Between CS and LA Conduction.
Introduction: Coronary sinus (CS) recordings are routinely used during electrophysiologic studies for various supraventricular and ventricular arrhythmias with the understanding that they represent left atrial (LA) activity. However, the behavior of CS electrical activity during atrial arrhythmias has not drawn any special attention beyond standard considerations. Methods and Results: The study population consisted of 9 patients (3 women; mean age 59 ± 11 years) with atrial fibrillation (AF) and atrial flutter (AFL) who developed dissociation of conduction between the CS and posterior LA during spontaneous AF and AFL. In all patients, the LA and the CS were mapped using a 64‐electrode basket catheter and a multipolar electrode catheter, respectively. The right atrium (RA) was mapped simultaneously using a 24‐polar electrode catheter (7 patients) or a 64‐electrode basket catheter (2 patients). Eight patients showed stable double potentials in CS recordings during AF (9 episodes) and AFL (3 episodes). During ongoing arrhythmias, the first row of potentials maintained a constant relationship with the RA activity, whereas the second row of potentials was discordant with the posterior wall of the LA in 7 patients and concordant in 2 patients. In 1 patient with counterclockwise AFL, CS activation was isolated from the posterior wall of the RA until it reached the distal portion of the CS, after which it entered the lateral region of the LA. In 1 patient, a macroreentrant LA tachycardia involving CS muscle was observed. Rapid atrial pacing from the proximal CS and extrastimuli produced longitudinal dissociation of CS activation in all patients. Conclusion: Conduction between the CS and posterior LA can be dissociated during spontaneous atrial arrhythmias and provocative proximal CS pacing.
Possible Bradycardic Mode of Death and Successful Pacemaker Treatment in a Large Family with Features of Long QT Syndrome Type 3 and Brugada Syndrome
Authors: VAN DEN BERG MAARTEN P. , WILDE ARTHUR A.M. , VIERSMA JAN WILLEM , BROUWER JAN , HAAKSMA JAAP , VAN DER HOUT ANNEMIEKE H. , STOLTE‐DIJKSTRA IRENE , BEZZINA CONNIE R. , VAN LANGEN IRENE M. , BEAUFORT‐KROL GERTIE C.M. , CORNEL JAN HEIN , CRIJNS HARRY J.G.M. 
Published: August 2003

Pacemaker Treatment in LQT3 and Brugada Syndrome.
Introduction: We recently identified a novel mutation of SCN5A (1795insD) in a large family with features of both long QT syndrome type 3 and the Brugada syndrome. The purpose of this study was to detail the clinical features and efficacy of pacemaker therapy in preventing sudden death in this family. Methods and Results: The study group consisted of 116 adult family members: 60 carriers (29 males) and 56 noncarriers (28 males) of the mutant gene. Investigations included 24‐hour Holter monitoring, ergometry, and electrophysiologic studies. Mean, lowest, and highest heart rate were lower in the carriers, but heart rate variability was comparable. In carriers, disproportional QT prolongation was present during bradycardia. No complex ventricular ectopy was recorded, and there were fewer isolated premature beats (both ventricular and atrial) in carriers. All patients were asymptomatic, except for two individuals who experienced syncope; in one of these patients, asystolic episodes (up to 9 sec) were repeatedly recorded. Prolonged HV intervals were present in 5 of 6 patients. Thirty carriers received a prophylactic backup pacemaker. During median follow‐up of 4.5 years (range 0.0 to 22.6), their survival rate was 100%. There were five sudden deaths among the remaining 30 carriers without a pacemaker (P = 0.019). Conclusion: This family with a high incidence of nocturnal sudden death is characterized by bradycardia‐dependent QT prolongation, intrinsic sinus node dysfunction, and generalized conduction abnormalities. There is a striking absence of complex ventricular ectopy, and pacemaker implantation was effective in preventing sudden death. These findings raise the possibility of a bradycardic rather than tachycardic mode of death.
Simultaneous Analysis of Heart Rate Variability and Myocardial Contractility During Head‐Up Tilt in Patients with Vasovagal Syncope
Authors: MANGIN LAURENCE , KOBEISSI ADONIS , LELOUCHE DAVID , D' HÉROUVILLE YVES , MANSIER PASCALE , SWYNGHEDAUW BERNARD , MACQUIN‐MAVIER ISABELLE 
Published: August 2003

Cardiac Autonomic and Inotropic Changes in Vasovagal Syncope.
Introduction: The aim of this study was to evaluate simultaneously cardiac autonomic activity, through heart rate variability (HRV) analysis, and cardiac inotropic changes during head‐up tilt (HUT) in patients with recurrent vasovagal syncope. Methods and Results: Twelve subjects implanted with a permanent dual‐chamber pacemaker for recurrent vasovagal syncope characterized by marked bradycardia were studied. The tip of the right ventricular electrode was equipped with a sensor that measured peak endocardial acceleration (PEA) as an index of myocardial contractility. RR interval and PEA signals were acquired simultaneously and processed in the time and frequency (low frequencies [LF] and high frequencies [HF] of RR signal) domain during early HUT (T1), late HUT, or before syncope (T2). In the six subjects with positive HUT: (1) Abnormal heart rate oscillations were evidenced at T1 and discriminated this group from the negative group (LF/HF decreased by 46% from supine to T1, but increased by 55% in the negative group; P < 0.01 positive vs negative HUT). (2) Gradual diminution of the HF component was associated with an increase in PEA index during HUT with a correlation between PEA/RR interval (R =− 0.8, P < 0.001), PEA/HF components (R =− 0.6, P < 0.05). (3) Sympathetic stimulation responsible for changes in both HRV and PEA parameters occurred immediately before the faint (LF/LF+HF: 0.6 ± 0.2 to 0.8 ± 0.09; P < 0.05 T2 vs T1; PEA: 0.62 ± 0.10G to 0.83 ± 0.22G; P < 0.01 T2 vs T1). Conclusion: Our findings showed that a homogeneous subgroup of patients with recurrent vasovagal syncope and positive HUT exhibited abnormal cardiac autonomic and inotropic responses to an orthostatic stimulus. Continuous changes over time of HRV and PEA parameters highlight the dynamic behavior of the mechanisms leading to syncope.
Prognostic Significance of Risk Stratifiers of Mortality, Including T Wave Alternans, After Acute Myocardial Infarction: Results of a Prospective Follow‐Up Study
Authors: TAPANAINEN JARI M. , STILL AINO‐MAIJA , AIRAKSINEN K.E. JUHANI , HUIKURI HEIKKI V. 
Published: August 2003

Noninvasive Risk Assessment Including TWA After AMI.
Introduction: Occurrence of sustained microvolt‐level T wave alternans (TWA) at a specified heart rate has been suggested to predict life‐threatening arrhythmic events, but its prognostic value has not been well established in patients who survived an acute myocardial infarction (AMI). The purpose of this prospective study was to assess the predictive significance of various noninvasive risk indicators of mortality, including TWA, in consecutive post‐AMI patients with optimized medical therapy. Methods and Results: In addition to a symptom‐limited predischarge exercise test with measurement of TWA, mortality risk was assessed using heart rate variability, 24‐hour ECG recordings, baroreflex sensitivity, signal‐averaged ECG, QTc interval, QT dispersion, and echocardiographic wall‐motion index in 379 consecutive patients. Twenty‐six patients (6.9%) died during a mean follow‐up of 14 ± 8 months. Sustained TWA was found in 56 patients (14.7%), none of whom died. Several risk variables, e.g., incomplete TWA test (inability to perform the exercise test or reach the required target heart rate of 105 beats/min), increased QRS duration on signal‐averaged ECG, increased QT dispersion, long QTc interval, nondiagnostic baroreflex sensitivity result, and low wall‐motion index, predicted all‐cause mortality in univariate analyses. In multivariate analysis, the incomplete TWA test was the most significant predictor of cardiac death (relative risk 11.1, 95% confidence interval 2.4 to 50.8; P < 0.01). Conclusion: Sustained TWA during the predischarge exercise test after AMI does not indicate increased risk for mortality. An incomplete TWA test and several common risk variables provided prognostic information in this post‐AMI population.
Focal Atrial Tachycardia Arising from the Tricuspid Annulus: Electrophysiologic and Electrocardiographic Characteristics
Authors: MORTON JOSEPH B. , SANDERS PRASHANTHAN , DAS ARVIND , VOHRA JITENDRA K. , SPARKS PAUL B. , KALMAN JONATHAN M. 
Published: August 2003

Tricuspid Annular Tachycardia.
Introduction: Focal right atrial tachycardia (RAT) arising from the crista terminalis, para‐Hisian, and coronary sinus os regions are well described. Less information exists regarding RAT arising from the nonseptal region of the tricuspid annulus (TA). Methods and Results: From a consecutive series of 64 patients who had undergone successful radiofrequency ablation (RFA) of 67 RATs, the characteristics of 9 (13%) patients (6 men; mean age 50 ± 20 years) with a TA focus were reviewed. The annular focus was localized to the inferoanterior TA in 7 and the superior TA in 2. Mean tachycardia cycle length was 371 ± 66 msec. Mean activation time at the site of successful RFA in 9 of 9 patients was −43 ± 11 msec. At 9.3 ± 5.6 months of follow‐up, 1 of 9 patients had recurrent tachycardia successfully treated with repeat RFA. In 7 of 9 patients with RAT from the inferoanterior TA, the surface ECG P wave morphology was upright in aVL, inverted in III and V1, and either inverted or biphasic with an initial negative deflection from V2 to V6. Conclusion: The TA is an important site of origin of RAT. In the present study, the inferoanterior region of the TA was a preferential site of origin with resulting characteristic P wave morphology. Knowledge of this anatomic distribution and P wave morphology allows targeted mapping and may facilitate successful RFA.