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Ventricular Activation (ventricular + activation)

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Medical Sciences100%

Terms modified by Ventricular Activation

  • ventricular activation pattern
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    Selected Abstracts

    Preserving Normal Ventricular Activation Versus Atrioventricular Delay Optimization During Pacing: The Role of Intrinsic Atrioventricular Conduction and Pacing Rate

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2000
    IVAN ILIEV ILIEV
    The purpose of the study was to compare the effects of DDD pacing with optimal AV delay and AAI pacing on the systolic and diastolic performance at rest in patients with prolonged intrinsic AV conduction (first-degree AV block). We studied 17 patients (8 men, aged 69 ± 9 years) with dual chamber pacemakers implanted for sick sinus syndrome in 15 patients and paroxysmal high degree AV block in 2 patients. Aortic flow and mitral flow were evaluated using Doppler echocardiography. Study protocol included the determination of the optimal A V delay in the DDD mode and comparison between AAI and DDD with optimal A V delay for pacing rate 70/min and 90/min. Stimulus-R interval during AAI (AHI) was 282 ± 68 ms for rate 70/min and 330 ± 98 ms for rate 90/min (P < 0.01). The optimal A V delay was 159 ± 22 ms, A V delay optimization resulted in an increase of an aortic flow time velocity integral (AFTVI) of 16%± 9%. At rate 70/min the patients with ARI , 270 ms had higher AFTVI in AAI than in DDD (0.214 ± 0.05 m vs 0.196 ± 0.05 m, P < 0.01), while the patients with ARI > 270 ms demonstrated greater AFTVI under DDD compared to AAI(0.192 ± 0.03 m vs 0.166 ± 0.02 m, P < 0.01). At rate 90/min AFTVI was higher during DDD than AAI (0.183 ± 0.03 m vs 0.162 ± 0.03 m, P < 0.01). Mitral flow time velocity integral (MFTVI) at rate 70/min was higher in DDD than in AAI (0.189 ± 0.05 m vs 0.173 ± 0.05 mP < 0.01), while at rate 90/min the difference was not significant in favor of DDD (0.149 ± 0.05 m vs 0.158 ± 0.04 m). The results suggest that in patients with first-degree AV block the relative impact of DDD and AAI pacing modes on the systolic performance depends on the intrinsic AV conduction time and on pacing rate. [source]

    Synchronous Ventricular Pacing without Crossing the Tricuspid Valve or Entering the Coronary Sinus,Preliminary Results

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2009
    BENHUR D. HENZ M.D.
    Background: Right ventricular apical (RVA) pacing promotes tricuspid regurgitation (TR), electromechanical dyssynchrony, and ventricular dysfunction. We tested a novel intramyocardial bipolar lead to assess whether stimulation of the atrioventricular septum (AVS) produces synchronous ventricular activation without crossing the tricuspid valve (TV). Methods: A lead with an active external helix and central pin was placed on the AVS and the RVA in three dogs. High-density electroanatomic (EA) mapping was performed of both ventricles endocardially and epicardially. Intracardiac echocardiography was used to access ventricular synchrony. Results: The lead was successfully deployed into the AVS in all cases with consistent capture of the ventricular myocardium without atrial capture or sensing. The QRS duration was less with AVS compared with RVA pacing (89 ± 4 ms vs. 100 ± 11 ms [P < 0.0001, GEE P = 0.03]). There was decreased delay between color Doppler M-mode visualized peak contraction of the septum and the mid left ventricular free wall with AVS compared with RVA pacing (89 ± 91 ms vs. 250 ± 11 ms [P < 0.0001, GEE P = 0.006]). Activation time between the mid septum and mid free wall was shorter with AVS versus RVA pacing (20.4 ± 7.7 vs. 30.8 ± 11.6 [P = 0.01, GEE P = 0.07]). The interval between QRS onset to earliest free wall activation was shorter with AVS vs. RVA pacing (19.2 ± 6.4 ms vs. 31.1 ± 11.7 ms [P = 0.005, GEE P = 0.02]). Conclusion: The AVS was successfully paced in three dogs resulting in synchronous ventricular activation without crossing the TV. [source]

    Orthodromic Pacemaker-Mediated Tachycardia in a Biventricular System Without an Atrial Electrode

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2004
    ANTONIO BERRUEZO M.D.
    Pacemaker-mediated tachycardia is a well-known complication of dual-chamber devices. In this report, we describe for the first time a case of orthodromic pacemaker-mediated tachycardia in a patient in whom a biventricular system without an atrial electrode had been implanted. Retrograde atrial activation was directly produced by the dislodged coronary vein electrode in the AV groove, resulting in simultaneous capture of the left atrium and left ventricle. During tachycardia, AV nodal conduction was via the anterograde pathway of the circuit and limited the ventricular response. Subsequently, right ventricular activation was sensed by the right ventricular electrode that triggered biventricular pacing and left atrial capture, perpetuating the tachycardia. Because the left atrial threshold was higher than the left ventricular threshold, the problem could be resolved easily by lowering the output of the coronary vein electrode. [source]

    Evaluation of Myocardial Performance with Conventional Single-Site Ventricular Pacing and Biventricular Pacing in a Canine Model of Atrioventricular Block

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2003
    PATRICIO A. FRIAS M.D.
    Introduction: The aim of this study was to evaluate epicardial biventricular pacing as a means of maintaining synchronous ventricular activation in an acute canine model of AV block with normal ventricular anatomy and function. Chronic single-site ventricular pacing results in dyssynchronous ventricular activation and may contribute to ventricular dysfunction. Biventricular pacing has been used successfully in adult patients with congestive heart failure. Methods and Results: This was an acute study of open chest mongrel dogs (n = 13). ECG, left ventricular (LV), aortic, and pulmonary arterial pressures were measured. LV impedance catheters were used to assess cardiodynamics using instantaneous LV pressure-volume relations (PVR). Following radiofrequency ablation of the AV node, a temporary pacemaker was programmed 10 beats/min above the intrinsic atrial rate, with an AV interval similar to the baseline intrinsic PR interval. The pacing protocol consisted of 5-minute intervals with the following lead configurations: right atrium-right ventricular apex (RA-RVA), RA-LV apex (LVA), and RA-biventricular using combinations of four ventricular sites (RVA, RV outflow tract [RVOT], LVA, LV base [LVB]). RA-RVA was used as the experimental control. LV systolic mechanics, as measured by the slope of the end-systolic (Ees) PVR (ESPVR, mmHg/cc), was statistically greater (P < 0.05) with all modes of biventricular pacing (RA-RVA/LVA 20.0 ± 2.9, RA-RVA/LVB 18.4 ± 2.9, RA-RVOT/LVA 15.1 ± 1.8, RA-RVOT/LVB 17.6 ± 2.9) compared to single-site ventricular pacing (RA-RVA 12.8 ± 1.6). Concurrent with this improvement in myocardial performance was a shortening of the QRS duration (RA-RVA 97.7 ± 2.9 vs RA-RVA/LVA 75.7 ± 4.9, RA-RVA/LVB 70.3 ± 4.9, RA-RVOT/LVA 65.3 ± 4.4, and RA-RVOT/LVB 76.7 ± 5.9, P < 0.05). Conclusion: In this acute canine model of AV block, QRS duration shortened and LV performance improved with epicardial biventricular pacing compared to standard single-site ventricular pacing. (J Cardiovasc Electrophysiol, Vol. 14, pp. 996-1000, September 2003) [source]

    Arrhythmogenesis of T Wave Alternans Associated with Surface QRS Complex Alternans and the Role of Ventricular Prematurity: Observations from a Canine Model of LQT3 Syndrome

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2002
    MASAOMI CHINUSHI M.D.
    Intramural TWA and Its Arrhythmogenesis.Introduction: T wave alternans (TWA) is characterized by cycle-to-cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin-A model of long QT syndrome. Methods and Results: The cardiac cycle length was gradually shortened by interruption of vagal stimulation, and TWA was induced in six canine hearts. Transmural unipolar electrograms were recorded with plunge needle electrodes from endocardial (Endo), mid-myocardial (Mid), and epicardial (Epi) sites, along with the surface ECG and BP. The activation-recovery interval (ARI) was measured to estimate local refractoriness. During TWA, ARI alternans was greater at the Mid than the Epi/Endo sites, and it was associated with the development of marked spatial dispersion of ventricular repolarization. As TWA increased, ventricular activation of the cycles associated with shorter QT intervals displayed delayed conduction at the Mid sites as a result of a critically longer ARI of the preceding cycle and longer QT interval, while normal conduction was preserved at the Epi site. Delayed conduction at the Mid sites manifested as surface ECG QRS and BP waveform alternans, and spontaneous ventricular tachyarrhythmias developed in absence of ventricular prematurity. In other instances, in absence of delayed conduction during TWA, ventricular premature complexes infringed on a prominent spatial dispersion of ventricular repolarization of cycles with long QT intervals and initiated ventricular tachyarrhythmia. Conclusion: TWA accompanied by QRS alternans may signal a greater ventricular electrical instability, since it is associated with intramural delayed conduction, which can initiate ventricular tachyarrhythmia without ventricular premature complexes. [source]

    Right Ventricular Septal Pacing: A Comparative Study of Outflow Tract and Mid Ventricular Sites

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2010
    RAPHAEL ROSSO M.D.
    Background: Prolonged right ventricle (RV) apical pacing is associated with left ventricle (LV) dysfunction due to dysynchronous ventricular activation and contraction. Alternative RV pacing sites with a narrower QRS compared to RV pacing might reflect a more physiological and synchronous LV activation. The purpose of this study was to compare the QRS morphology, duration, and suitability of RV outflow tract (RVOT) septal and mid-RV septal pacing. Methods: Seventeen consecutive patients with indication for dual-chamber pacing were enrolled in the study. Two standard 58-cm active fixation leads were passed to the RV and positioned in the RVOT septum and mid-RV septum using a commercially available septal stylet (model 4140, St. Jude Medical, St. Paul, MN, USA). QRS duration, morphology, and pacing parameters were compared at the two sites. The RV lead with less-satisfactory electrical parameters was withdrawn and deployed in the right atrium. Results: Successful positioning of the pacing leads at the RVOT septum and mid-RV septum was achieved in 15 patients (88.2%). There were no significant differences in the mean stimulation threshold, R-wave sensing, and lead impedance between the two sites. The QRS duration in the RVOT septum was 151 ± 14 ms and in the mid-RV septum 145 ± 13 ms (P = 0.150). Conclusions: This prospective observational study shows that septal pacing can be reliably achieved both in the RVOT and mid-RV with active fixation leads using a specifically shaped stylet. There are no preferences in regard to acute lead performance or paced QRS duration with either position. (PACE 2010; 33:1169,1173) [source]

    Variability in Postpacing Intervals Predicts Global Ventricular Activation Pattern during Tachycardia

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2010
    ILYAS K. COLOMBOWALA M.D.
    Introduction: Assessment of ventricular activation pattern is critical to the successful ablation of ventricular tachycardia (VT). We have previously shown that the global atrial activation pattern during tachycardia can be rapidly and accurately assessed by calculating the postpacing interval variability (PPIV); PPIV was minimal in circuitous tachycardias and highly variable in centrifugal tachycardias. In the present study, we use the PPIV to determine the ventricular global activation pattern during VT. Methods: Patients with mappable VT were included. We defined global ventricular activation as either centrifugal (arising from a focus with radial expansion) or circuitous (gross macro-reentrant circuit), based on the findings of electroanatomic mapping. PPIV was calculated as the difference in postpacing interval with right ventricular apical overdrive pacing during tachycardia at cycle lengths (CL) 10 ms and 30-ms shorter than tachycardia, regardless of the origin of the tachycardia. We studied 20 patients with 23 VTs (11 centrifugal, mean CL 390 ± 36.1 ms; 12 circuitous, mean CL 418 ± 75.7 ms). Results: The mean PPIV was 45 ± 16 ms for patients with centrifugal VT and 6.7 ± 4.1 ms for patients with circuitous VT. Rank sum analysis of PPIV showed a significant difference between the two groups (P < 0.05). Conclusions: Our data suggest that the global ventricular activation pattern during VT can be rapidly and accurately defined by assessing the PPIV. This technique allows for a rapid confirmation of the tachycardia activation and significantly facilitates mapping and ablation. (PACE 2010; 33:129,134) [source]

    Real-time Integration of Intracardiac Echocardiography and Electroanatomic Mapping in PVCs Arising from the LV Anterior Papillary Muscle

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2009
    Ph.D., TAKUMI YAMADA M.D.
    A 54-year-old woman with idiopathic premature ventricular contractions (PVCs) underwent electrophysiological testing. Three-dimensional (3D) geometries of the papillary muscles and chamber of the left ventricle (LV) were reconstructed using a CARTO-based 3D ultrasound imaging system (Biosense Webster Inc., Diamond Bar, CA, USA) during the PVCs. Activation mapping in the LV was then performed during the PVCs and the activation map revealed the earliest ventricular activation on the anterior papillary muscle. An irrigated radiofrequency current delivered at that site with guidance from that system eliminated the PVCs. This case may suggest that the guidance system may be feasible and useful for catheter ablation of PVCs arising from uncommon sites. [source]

    Activation Sequence Modification During Cardiac Resynchronization by Manipulation of Left Ventricular Epicardial Pacing Stimulus Strength

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2007
    USHA B. TEDROW M.D.
    Background: Success of cardiac resynchronization therapy (CRT) depends on altering electrical ventricular activation (VA) to achieve mechanical benefit. That increases in stimulus strength (SS) can affect VA has been demonstrated previously in cardiomyopathy patients undergoing ablation. Objective: To determine whether increasing SS can alter VA during CRT. Methods: In 71 patients with CRT devices, left ventricle (LV) pacing was performed at escalating SS. Timing from pacing stimulus to right ventricular (RV) electrogram, ECG morphology, and maximal QRS duration on 12 lead ECG were recorded. Results: Demographics: Baseline QRS duration 153 ± 25 ms, ischemic cardiomyopathy 48%, ejection fraction 24%± 7%. With increased SS, conduction time from LV to right ventricle (RV) decreased from 125 ± 56 ms to 111 ± 59 ms (P = 0.006). QRS duration decreased from 212 ± 46 ms to 194 ± 42 ms (P = 0.0002). A marked change in QRS morphology occurred in 11/71 patients (15%). The RV ring was the anode in 6, while the RV coil was the anode in 5. Sites with change in QRS morphology showed decrease in conduction time from LV to RV from 110 ± 60 ms to 64 ± 68 ms (P = 0.04). Twelve patients (16%) had diaphragmatic stimulation with increased SS. Conclusions: Increasing LV SS reduces QRS duration and conduction time from LV to RV. Recognition of significant QRS morphology change is likely clinically important during LV threshold programming to avoid unintended VA change. [source]

    Excitation of the Intrinsic Conduction System Through His and Interventricular Septal Pacing

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2006
    TIMOTHY G LASKE
    Background: Direct His bundle pacing results in rapid synchronous ventricular activation. However, clinical experiences with such pacing have been associated with long procedure times and compromised pacing and sensing performance. Methods: We evaluated myocardial activation sequences (AS) for pacing of the His bundle and peri-His region and assessed acute pacing performance using custom-designed plunge electrodes. Unipolar pacing was performed in isolated swine hearts (n = 10) using four quadripolar stimulation/sensing electrodes implanted into the interventricular septum and equally spaced between the membranous septum and the coronary sinus ostium (zones 1,4, respectively; electrode depth (ED) 1 = most distal, ED 4 = most proximal). Optimal pacing sites were defined as: pacing thresholds ,1.5 V, a P-R ratio of ,0.5, and ,50% occurrence of an intrinsic midseptal left ventricular (LV) endocardial electrical breakout (BO) and activation pattern. Results: Pacing thresholds improved with greater depth of electrode location within the septum (ED 1: 1.51 ± 0.8 V vs ED 4: 5.2 ± 3.8 V, P < 0.001), as did the P-R ratio (0.34 ± 0.6 vs 0.78 ± 1.0, P < 0.05). His potentials were only observed in zone 1 and 2 electrodes (0.12 and 0.02 mV, respectively). Only electrodes in zones 1 and 2 produced LV endocardial electrical BOs in the midseptal region that demonstrated an intrinsic-like endocardial AS. Depth 1 and 2 electrodes (11.75 and 8.75 mm, respectively) in zone 1 satisfied all three optimal pacing site requirements. Conclusions: This study has shown that LV activation patterns similar to sinus rhythm may be achieved without direct activation of the His bundle, while maintaining acceptable pacing and sensing performance. These data indicate that pacing systems designed to stimulate the tissues below the point at which the His bundle penetrates the central fibrous body may provide improved system efficiency and LV performance in comparison to both direct His bundle pacing and traditional pacing sites. [source]

    Reduction of RV Pacing by Continuous Optimization of the AV Interval

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2006
    GORAN MILASINOVIC
    Background: In patients requiring permanent pacing, preservation of intrinsic ventricular activation is preferred whenever possible. The Search AV+ (SAV+) algorithm in Medtronic EnPulseÔ dual-chamber pacemakers can increase atrioventricular (AV) intervals to 320 ms in patients with intact or intermittent AV conduction. This prospective, multicenter study compared the percentage of ventricular pacing with and without AV interval extension. Methods: Among 197 patients enrolled in the study, the percentage of ventricular-paced beats was evaluated via device diagnostics at the 1-month follow-up. Patient cohorts were defined by clinician assessment of conduction via a 1:1 AV conduction test at the 2-week follow-up. The observed percentage of ventricular pacing with SAV + ON and the predicted percentage of ventricular pacing with SAV + OFF were determined from the SAV + histogram data for the period between the 2-week and 1-month follow-up visits. Results: Of 197 patients, 110 (55.8%) had intact 1:1 AV conduction, of which 109 had 1-month data. SAV + remained ON in 99/109 patients; 10 patients had intrinsic A-V conduction intervals beyond SAV + nominal and therefore SAV + disabled. The mean percentage of ventricular pacing in the 109 patients was SAV+ ON = 23.1% (median 3.7%) versus SAV + OFF = 97.2% (median 99.7%). In 87 patients without 1:1 AV conduction, SAV + was programmed OFF in 6, automatically disabled in 52, and remained ON in 29. In 8 of these patients, 80,100% reduction in ventricular pacing was observed with SAV + ON. Conclusion: The Search AV+ algorithm in the EnPulse pacemaker effectively promotes intrinsic ventricular activation and substantially reduces unnecessary ventricular pacing. [source]

    Initial Experience with an Active-Fixation Defibrillation Electrode and the Presence of Nonphysiological Sensing

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2001
    RAHUL N. DOSHI
    DOSHI, R.N., et al.: Initial Experience with an Active-Fixation Defibrillation Electrode and the Presence of Nonphysiological Sensing. Nonphysiological sensing by a pacing and defibrillation electrode may result in inappropriate defibrillator discharges and/or inhibition of pacing. Active-fixation electrodes may be more likely to sense diaphragmatic myopotentials because of the protrusion of the screw for fixation. In addition, the movement of the fixation screw in an integrated bipolar lead system could also result in inappropriate sensing. This may be increasingly important in patients who are pacemaker dependent because the dynamic range of the autogain feature of these devices is much more narrow. Five of 15 consecutive patients who received a CPI model 0154 or 0155 active-fixation defibrillation electrode with an ICD system (CPI Ventak AV3DR model 1831 or CPI Ventak VR model 1774 defibrillator) are described. In 2 of the 15 patients, nonphysiological sensing appearing to be diaphragmatic myopotentials resulted in inappropriate defibrillator discharges. Both patients were pacemaker dependent. Changes in the sensitivity from nominal to less sensitive prevented inappropriate discharges. In one patient, discreet nonphysiological sensed events with the electrogram suggestive of ventricular activation was noted at the time of implantation. This was completely eliminated by redeployment of the active-fixation lead in the interventricular septum. In two other patients, discreet nonphysiological sensed events resulted in intermittent inhibition of ventricular pacing after implantation. These were still seen in the least sensitive autogain mode for ventricular amplitude. These were not seen on subsequent interrogation 1 month after implantation. Increased awareness of nonphysiological sensing is recommended. The CPI 0154 and 0155 leads seem to be particularly prone to this abnormality. Particular attention should be made when deploying an active-fixation screw for an integrated bipolar lead. This increased awareness is more important when a given individual is pacemaker dependent, which may warrant DFT testing in a least or less sensitive mode in these patients. [source]

    Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial Infarction

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2001
    PAULUS KIRCHHOF
    KIRCHHOF P., et al.: Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial Infarction. QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2,3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%,15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 ± 7 vs 78 ± 1 ms, JT disp 80 ± 6 vs 79 ± 2 ms, mean ± SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction. [source]

    T-Wave Variability Detects Abnormalities in Ventricular Repolarization: A Prospective Study Comparing Healthy Persons and Olympic Athletes

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009
    Lara Heinz M.D.
    Background: Sudden cardiac death in athletes is more common than in the general population. Routine screening procedures are performed to identify competitors at risk. A new Holter-based parameter analyzes variation of the ventricular repolarization (TVar). The aim of this study was to evaluate differences in electrocardiogram (ECG), Echo, and Holter (H) in competitive athletes compared to a healthy control group consisting of medical students (MS). Methods: A total of 40 athletes (19 females, Olympic team, Luxembourg) and 40 MS (22 females) were examined by means of a resting ECG, treadmill exercise (TE), echocardiogram (Echo), as well as H recordings during a routine screening visit. To analyze TVar, a 20-minute H recording at rest (sampling rate 1000 per second) was performed. Moreover, heart rate variability (HRV) as well as HR turbulence (HRT) was computed. Results: No differences in demographic variables were detected. Quantification of HRV detected a significant increase in the vagal component of autonomic cardiac modulation. In contrast, no differences for HRT were found. Echo parameter demonstrated a thicker septal wall without differences of the posterior wall. TVar values were normal in range, but did differ significantly between the two groups. No correlation between TVar and echo as well as Holter parameters was detected. Conclusions: TVar was able to demonstrate significant differences in terms of alterations of ventricular activation. This might indicate an early change of myocardial repolarization representing a substrate for life-threatening arrhythmia. Larger studies on the predictive value of TVar including follow-up are necessary to confirm this preliminary finding. [source]

    Ionic Mechanisms and Vectorial Model of Early Repolarization Pattern in the Surface Electrocardiogram of the Athlete

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2008
    Eduardo C. Barbosa M.D.
    Background: The electrocardiogram (ECG) of the athlete displays particular characteristics as a consequence of both electrophysiological and autonomic remodeling of the heart that follows continued physical training. However, doubts persist on how these changes directly interact during ventricular activation and repolarization ultimately affecting surface ECG waveforms in athletes. Objective: This article considers an in deep rationale for the electrocardiographic pattern known as early repolarization based on both electrophysiological mechanisms at cellular level and the vectorial theory of the cardiac activation. Methods: The mechanism by which the autonomic remodeling influences the cardiac electrical activation is reviewed and an insight model of the ventricular repolarization based on ionic models and the vectorial theory of the cardiac activation is proposed. Results: Considering the underlying processes related to ventricular electrical remodeling, we propose that, in athletes' heart: 1) vagal modulation increases regional electrophysiological differences in action potential phases 1 and 2 amplitudes, thus enhancing a voltage gradient between epicardial and endocardial fibers; 2) this gradient affects depolarization and repolarization timing sequences; 3) repolarization wave front starts earlier on ventricular wall and partially overcomes the end of depolarization causing an upward displacement of the J-point, ST segment elevation, and inscription of magnified T-waves amplitudes leading to characteristic surface ECG waveform patterns. Conclusions: In athletes, the association between epicardial to endocardial electrophysiological differences and early repolarization ECG pattern can be demonstrated by the vectorial theory of the ventricular activation and repolarization. [source]

    Lack of Impact of Myocardial Ischemia on the Signal-Averaged ECG Assessment by Time-Domain Analysis

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002
    Michael A. E. Schneider M.D.
    Background: Late potentials represent an arrhythmogenic substrate in chronically infarcted myocardium. It is hypothesized that acute transient ischemia enhances anisotropic electrical ventricular activation and facilitates reentry mechanisms. Study aim was the prospective assessment of the impact of dipyridamole-induced myocardial ischemia on the signal-averaged ECG. Methods: Dipyridamole stress thallium-201 SPECT imaging was utilized to avoid noise contamination of the signal-averaged ECG from exercise and to document evidence and localization of myocardial ischemia or persistent perfusion defects in 68 patients with suspected coronary artery disease. Before and during dipyridamole-induced vasodilatation serial signal-averaged ECG was performed to evaluate the influence of transient ischemia on the occurrence of late potentials. Results: There was a significant difference between heart rate at rest and heart rate under dipyridamole influence in patients with inducible ischemia (70 ± 13 vs. 87 ± 13; P < 0.0001) in contrast to patients without dipyridamole-induced ischemia (74 ± 20 vs. 80 ± 16; n.s.). The number of averaged beats and achieved noise level was comparable between both groups. Thirty-three of 68 patients (49%) revealed dipyridamole-induced ischemia; however, no changes of the SAECG parameters, such as QRS, RMS, LAS at 25,250 and 40,250 Hz bandpass filtering in the leads X, Y, Z and vector magnitude, respectively, were observed as a result of ischemia. Conclusion: These results suggest that transient myocardial ischemia does not affect the signal-averaged ECG. Clinically, the signal-averaged ECG analysis seems not to be helpful in identifying patients with silent ischemia. A.N.E. 2002;7(3):191,197 [source]

    Incessant Nonreentrant Tachycardia Due to Simultaneous Conduction Over Dual Atrioventricular Nodal Pathways Mimicking Atrial Fibrillation in Patients Referred for Pulmonary Vein Isolation

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2003
    Moussa Mansour M.D.
    It has been reported that conduction over the fast and slow pathways of the AV node can occur simultaneously, leading to a double ventricular response from each atrial beat. We report the cases of two patients referred to us for evaluation of symptomatic, incessant, and irregular narrow-complex tachycardia, misdiagnosed as atrial fibrillation, for consideration of pulmonary vein isolation. At presentation, careful evaluation of the electrograms revealed the presence of two ventricular activations for each atrial beat. At electrophysiologic study, both patients were found to have nonreentrant tachycardias arising from simultaneous conduction over the fast and slow pathways of the AV node. In one patient, the tachycardia had resulted in cardiomyopathy. Slow AV nodal pathway ablation performed in both patients resulted in cure of their tachycardias and recovery of ventricular function in the patient with cardiomyopathy. (J Cardiovasc Electrophysiol, Vol. 14, pp. 752-755, July 2003) [source]