bluuebunny/crossref_metadata_2025 huggingface dataset:
Recurrence and Late Block of Accessory Pathway Conduction Following Radiofrequency Catheter Ablation
Authors: CHEN XU , KOTTKAMP HANS , HINDRICKS GERHARD , WILLEMS STEPHAN , HAVERKAMP WILHELM , MARTINEZ‐RUBIO ANTONIO , ROTMAN BRIGITE , SHENASA MOHAMMAD , BREITHARDT GÜNTER , BORGGREFE MARTIN
Published: May 2007

Recurrence After RF Ablation of AP. Introduction: Many issues regarding the recurrence of accessory pathway conduction and the long‐term outcome of late block of accessory pathway conduction are still unknown or controversial.

Methods and Results: Data from 217 patients who underwent an initially successful radiofrequency ablation of accessory pathways and 7 patients with late block of accessory pathway conduction following an initially unsuccessful ablation were analyzed. During a mean follow‐up of 19 ± 11 months, accessory pathway conduction resumed in 21 (10%) of 217 patients following an initially successful ablation and in 6 (86%) of 7 patients with late block of accessory pathway conduction (P < 0.01). After initially successful ablations, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. A late electrophysiologic study at 6 months uncovered recurrence in only 1 of 124 asymptomatic patients, but failed to detect the late recurrence in 2 patients in whom the accessory pathway conduction resumed after more than 6 months. Multivariate analysis revealed that independent predictors for recurrence of accessory pathway conduction were concealed accessory pathway, presence of transient effect of radiofrequency pulse, and more than 5 pulses required for initial cure. Accessory pathway location, length of the tip electrode of the ablation catheter, and repeat radiofrequency pulses (“safety pulses”) after effective pulses did not predict resumption of accessory pathway conduction.

Conclusions: After initially successful ablation, the recurrence rates of accessory pathway conduction at 1, 3, and 6 months were 5.9%, 7.4%, and 11.3%, respectively. Late electrophysiologic testing had little prognostic value in asymptomatic patients following successful ablation. Application of “safety pulses” did not prevent recurrence. Late block of accessory pathway conduction did not predict long‐term efficacy.
Mechanism‐Specific Antiarrhythmic Effects of the Potassium Channel Activator Levcromakalim Against Repolarization‐Dependent Tachycardias
Authors: VOS MARC A. , GORGELS ANTON P.M. , LIPCSEI GYORGYI C. , de GROOT S.H. MARIEKE , LEUNISSEN JET D.M. , WELLENS HEIN J.J.
Published: May 2007

Mechanism‐Specific Action of Levcromakalim. Introduction: The hypothesis that levcromakalim. a potassium channel (IK‐ATP.) activator with antihypertensive properties, has a mechanism‐specific antiarrhythmic action against repolarization‐dependent ventricular tachycardias (VTs) was tested in dogs.

Methods and Results: A low dose of leveromakalim (0.01 mg/kg) was selected, which decreased blood pressure by 25% but had almost no electrophysiologic effect on AV nodal or ventricular conduction or effective refractory period. In dogs with chronic AV block, the antiarrhythmic action of this dose of levcromakalim was evaluated in three models of abnormal impulse formation: (I) dsotalol (2 mg/kg) induced torsades de pointes VT, initiated by early afterdepolarizations (EADs). (2) sustained ouabain‐induced VTs, which are dependent on delayed after depolarizations (DADs), and (3) VT occurring 24 hours after left anterior descending coronary artery occlusion, which are likely based on abnormal automaticity. Levcromakalim abolished d‐sotalol induced U waves, ventricular ectopic beats, and self‐terminating bouts of torsades de pointes. Induction of torsades de pointes by pacing was also completely prevented. The cycle length of the idioventricular rhythm, which was lengthened after d‐sotalol from 1490 ± 515 to 1700 ± 610 msec (P < 0.05), remained similar after levcromakalim (1655 ± 580 msec). The QT(U) duration, which was increased after d‐sotalol from 410 ± 55 to 550 ± 40 msec (P < 0.05), normalized to 405 ± 70 msec (P < 0.05). Lcvcromakulim did not suppress but rather enhanced ouabain‐induced VT by decreasing the cycle length slightly from 315 ± 35 to 290 ± 35 msec (P < 0.05). Pretreatment with a beta Mocker prevented this acceleration in rate. Finally, levcromakalim had no effect on VT 24 hours after infarction.

Conclusion: A low dose of levcromakalim has specific antiarrhythmic properties against repolarization‐dependent arrhythmias, but it does not affect VTs based on other mechanisms of abnormal impulse formation.
Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices
Authors: ECHT DEBRA S. , GREMILLION STEVEN T. , LEE JOHN T. , RODEN DAN M. , MURRAY KATHERINE T. , BORGANELLI MARK , CRAWFORD DIANE M. , STEWART JAMES R. , HAMMON JOHN W.
Published: May 2007

Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement.

Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N‐acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide.

Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration‐dependent effect of sodium channel blockade on defibrillation energy requirements in patients.
Independent Ablation of Retrograde and Anterograde Accessory Connection Conduction at the Atrial and Ventricular Insertion Sites:
Authors: VIJGEN JOHAN M. , CARLSON MARK D.
Published: May 2007

Impedance Mismatch Causes Conduction Block. Introduction: The impedance mismatch hypothesis has been proposed as one of the mechanisms responsible for accessory connection conduction block.

Methods and Results: We describe a case in which retrograde conduction across block posters accessory connection was ablated at the atrial insertion site in the coronary sinus of, whereas Anterograde conduction was ablated at the ventricular insertion site in the left ventricle.

Conclusion: The evidence supports the impedance mismatch concept as the cause of unidirectional conduction block and shows that the distal junction between the accessory connection and the myocardium is more vulnerable to ablation.
Effect of Stimulus Intensity on Atrial Refractoriness and Sinus Node Recovery
Authors: EHLERT FREDERICK A. , DAMLE ROGER S. , GOLDBERGER JEFFREY J. , KADISH ALAN H.
Published: May 2007

Stimulus Intensity Effect on SA Tissue. Introduction: Prior studies of sinus node function in man stated that the stimulus intensity of overdrive pacing has no effect on (he response of the sinus node to overdrive suppression; however, data documenting these statements were lacking. Previous studies have also suggested that drive train stimulus intensity can alter ventricular refractoriness, but similar studies have not been performed on the human atrium. The purpose of this study was to evaluate the effects of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time.

Methods and Results: The effect of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time was studied in 42 patients undergoing clinical electrophysiologic tests. The atrial effective refractory period was shorter at 10 mA (221 ± 20 msec) and 5 mA (232 ± 25 msec) than at a drive train stimulus intensity of 1.5 times late diastolic threshold (248 ± 24 msec, P < 0.05 for pairwise comparison). The sinus node recovery time did not demonstrate a similar effect in the baseline state, following beta‐adrenergic blockade, or following combined parasympathetic and beta‐adrenergic blockade. However, following isolated parasympathetic blockade with atropine, the corrected sinus node recovery time shortened from 88 ± 51 msec at 1.5 times late diastolic threshold to 48 ± 55 msec at 10 mA (P < 0.05). Significant variability was present in sinus node recovery time measurements a(baseline and following beta blockade; this variability decreased following parasympathetic blockade.

Conclusion: These data suggest that drive train stimulus intensity can affect the electrophysiologic properties of sinus node and atrial tissue. This effect appears to he mediated by local catecholamine and acetylcholine release and provides further evidence that the interaction between pacing stimuli and the cardiac autonomic system may need to be considered in evaluating electrophysiologic effects.
A Neural Network System for Detection of Atrial Fibrillation in Ambulatory Electrocardiograms
Authors: CUBANSKI DAVID , CYGANSKI DAVID , ANTMAN ELLIOTT M. , FELDMAN CHARLES L.
Published: May 2007

Neural Network for Detecting AF. Introduction: A neural network classifier has been designed, which is able to distinguish atrial fibrillation (AF) from other supraventricular arrhythmias in ambulatory (Holter) ECGs.

Method and Results: The classification algorithm uses a rhythm analysts that considers the ECG to be a time series of RR interval durations. This is combined with an analysis of baseline morphology that considers the morphological characteristics of the non‐QRS portions of the waveform. A back propagation‐based neural network has been used as part of the classifier implementation. When applied to a library consisting exclusively of 42,970 examples of AF and other supraventricular rhythm disturbances validated by an experienced cardiologist, the algorithm demonstrated a sensitivity of 82.4% for 10‐beat runs of paroxysmal atrial fibrillation (PAF) and a specificity of 96.6%. Since this system has been implemented as a postprocessor to a conventional automated Holter system, operating only on segments of ECG that are known to contain supraventricular arrhythmias rather than ventricular arrhythmias or sinus rhythm, it can be added to most existing Holter processing systems without significantly increasing the average time to process a tape.

Conclusion: A neural network system has been designed, which can potentially provide, for the first time, an accurate, quantitative technique to determine the natural history of PAF and to evaluate potential treatments for PAF.
Benefits and Lessons Learned From Stored Electrogram Information in Implantable Defibrillators
Authors: MARCHLINSKT FRANCIS E. , CALLANS DAVID J. , GOTTLIEB CHARLES D. , SCHWARTZMAN DAVID , PREMINGER MARK
Published: May 2007

Stored Electrograms. Implantable defibrillators have evolved from simple event counters to sophisticated diagnostic monitoring units capable of storing electrocardiographic information surrounding arrhythmia events and device therapy. In this review, the nature and characteristics of these stored electrocardiographic recordings are discussed and examples displayed. Potential benefits and limitation of stored electrogram analysis are described with respect to both clinical utility and the ability to enhance our understanding of ventricular arrhythmogenesis. Finally, future developments to improve data storage, retrieval, and analysis are identified.
Independent Autonomic Modulation of the Human Sinus and AV Nodes: Evidence From Beat‐to‐Beat Measurements of PR and PP Intervals During Sleep
Authors: KOWALLIK PETER , MEESMANN MALTE
Published: May 2007

Autonomic Modulation of Sinus and AV Nodes. Introduction: Evidence from animal experiments indicates that the autonomic nervous system may influence the sinus (SA) and atrioventricular (AV) nodes differently. We investigated, therefore, whether there are spontaneous functional differences in the innervation of the SA and AV nodes in man.

Methods and Results: This study was performed in 10 healthy males (ages 21 to 26 years) during strict bed rest from 10 pm to 6 am. Three ECG leads were digitized on‐line. PR and PP intervals were determined on a heat‐to‐beat basis off‐line using a correlation algorithm with an accuracy of ± 2 msec and were verified visually. During; major body movements, there were sudden decreases in PP intervals of 36 to 827 msec (mean 335) for periods of 6 to 265 seconds (mean 24), During these phases of heart rate (HR) acceleration, PR intervals showed either concomitant shortening (9 to 30 msec), no change, or lengthening (6 to 25 msec). Furthermore, tonic changes in the PR interval occurred over 15‐minute periods during which the range of PP intervals was constant. Additionally, recovery‐adjusted PR interval (PR ‐ b2/RP) and cycle length were negatively correlated for some periods, which confirmed independent autonomic effects on SA node and A V node.

Conclusion: Beat‐to‐beat measurement of PR intervals allows for evaluation of autonomic effects on the human AV node. The different patterns in PR intervals during sudden spontaneous increases in HR and the tonic changes in PR interval indicate that the autonomic inputs to the SA and AV nodes are, in principle, independent of each other.
Responses of the Transmembrane Potential of Myocardial Cells during a Shocks
Authors: ZHOU XIAOHONG , ROLLINS DENNIS L. , SMITH WILLIAM M. , IDEKER RAYMOND E.
Published: May 2007

Responses of Transmembrane Potential During a Shock. Introduction: The purpose of this investigation was to study the transmembrane potential changes (δVm) during extracellular electrical field stimulation.

Methods and Results: Vm was recorded in seven guinea pig papillary muscles in a tissue hath by a double‐barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 μm) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten SI stimuli, an S2 shock field created by a 10‐msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 ± 0.1, 2.9 ± 0.2, 6.1 ± 0.6. and 8.8 ± 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak δVm caused by the above four potential gradients were 21.1 ± 8.2, 33.6 ± 13.6, 49.9 ± 24.2, and 52.3 ± 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 ± 14.2,56.6 ± 16.4,83.1 ± 19.4. and 92.9 ± 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though δVm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 ± 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 ± 0.1 to 8.8 ± 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 ± 1.8 to 1.6 ± 0.7 msec for depolarizing shocks and from 6.0 ± 3.1 to 3.4 ± 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, then depolarization, followed again by hyperpolarization.

Conclusion: During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between aproximately 2 and 9 V/cm.
Temperature Measurement as a determinant of Tissue Heating During Radiofrequency Catheter ablation: An Examination of Electrode Thermistor Positioning for Measurement Accuracy
Authors: McRURY IAN D. , WHAYNE JAMES G. , HAINES DAVID E.
Published: May 2007

Thermometry and Radiofrequency Catheter Ablation. Introduction: Temperature monitoring has been proposed as a control for lesion occurrence and dimension during radiofrequency transcatheter ablation. Effective temperature measurement depends on thermistor positioning relative to the heated cardiac tissue and the convective cooling effects of the circulation. But the accuracy of a single tip thermistor as a measure of peak electrode‐tissue interface temperature is unknown.

Methods and Results: A standard 8‐French, 4‐mm electrode catheter with 5 thermistors (1 tip thermistor, 4 radial thermistors) was used to deliver radiofrequency energy in vitro to 3 porcine right ventricles and in vivo to 7 mongrel dogs. In vitro, the catheter orientation was varied. In vivo the catheter was positioned under fluoroscopy at a variety of atrial, tricuspid annular, and ventricular sites, with no attempt to adjust catheter orientation. In both cases varied discrete power levels were used so that a wide temperature range was attained. Lesions created in vivo with a standard, single thermistor tipped electrode were compared to those of a catheter with a thermistor extending 1 mm from the tip. Power was varied and tip thermistor temperatures recorded. All lesions were examined pathologically. Comparisons of radial thermistor temperature to tip thermistor temperature for 3 catheter orientations in vitro resulted in tip thermistor underestimation of peak electrode‐tissue interface temperature by a median of 0.5°C in 35% of the perpendicular orientations, 1.9°C in 82% of the 45 orientations, and 5°C in 83% of the parallel orientations. During in vivo trials, the tip thermistor underestimated the peak electrode‐tissue interface temperature during 2 of 51 lesions by 1.2°C and 7.6°C. There was a sudden rise in electrical impedance in 17 of 51 radiofrequency energy deliveries. Only one case was observed where the peak electrode‐tissue interface temperature was below 95°C. The normal to extended tip thermistor configurations analysis showed similar relationships between lesion size and temperature.

Conclusions: Accuracy of a single tip thermistor was found to be dependent upon catheterlissue orientation. With routine catheter positioning in vivo, the tip thermistor was a good indicator of peak electrode‐tissue interface temperature. Thus with power regulation to avoid temperatures greater than 90°C, a single flush‐mounted tip thermistor is probably adequate for temperature monitoring of lesion formation and avoidance of impedance rises.
Internal Defibrillation with Smaller Capacitors: A Prospective Randomized Cross‐Over Comparison of Defibrillation Efficacy Obtained with 90‐μF and 125‐μF Capacitors in Humans
Authors: BLOCK MICHAEL , HAMMEL DIETER , BÖCKER DIRK , BORGGREFE MARTIN , SEIFERT THOMAS , FASTENRATH CHRISTIAN , SCHELD HANS H. , BREITHARDT GÜNTER
Published: May 2007

Defibrillation with Small Capacitance. Introduction: The size of current implantable cardioverter defibrillators (ICD) is still large in comparison to pacemakers and thus not convenient for pectoral implantation. One way to reduce ICD size is to defibrillate with smaller capacitors. A trade‐off exists, however, since smaller capacitors may generate a lower maximum energy output.

Methods and Results: In a prospective randomized cross‐over study, the step‐down defibrillation threshold (DFT) of an experimental 90‐μF biphasic waveform was compared to a standard 125‐μF biphasic waveform. The 90‐μF capacitor delivered the same energy faster and with a higher peak voltage but provided only a maximum energy output of 20 instead of 34 J. DFTs were determined intraoperatively in 30 patients randomized to receive either an endocardial (n = 15) or an endocardial‐subcutaneous array (n = 15) defibrillation lead system. Independent of the lead system used, energy requirements did not differ at DFT for the experimental and the standard waveforms (10.3 ± 4.1 and 9.5 ± 4.9 J, respectively), but peak voltages were higher for the experimental waveform than for the standard waveform (411 ± 80 and 325 ± 81 V, respectively). For the experimental waveform the DFT was 10 J or less using an endocardial lead‐alone system in 10 (67%) of 15 patients and in 12 (80%) of 15 patients using an endocardial‐subcutaneous array lead system.

Conclusions: A shorter duration waveform delivered by smaller capacitors does not increase defibrillation energy requirements and might reduce device size. However, the smaller capacitance reduces the maximum energy output. If a 10‐J safety margin between DFT and maximum energy output of the ICD is required, only a subgroup of patients will benefit from 90‐μF ICDs with DFTs feasible using current defibrillation lead systems.
Electrophysiologic Determinants of Ventricuiar Rate in Human Atrial Fibriliation
Authors: ASANO YUKIO , SAITO JUNICHI , YAMAMOTO TOSHIO , UCHIDA MASATSUGU , YAMADA YUICHI , MATSUMOTO KAZUO , MATSUO HIROSHI
Published: May 2007

Ventricular Rate During AF. Introduction: The mechanisms of the ventricular response during atrial fibrillation (AF) remain uncertain. The parameters obtained during an electrophysiologic study, including atrial rates during AF, were analyzed to clarify further the determinants of the ventricular rate during AF.

Methods and Results: Thirty patients without manifest preexcitation in whom AF was induced during electrophysiologic study were divided into two groups, Group I consisted of 20 patients (ages 55 ± 10 years) without a dual AV nodal pathway. Group 2 consisted of 10 patients (ages 53 ± 13 years) having a dual AV nodal pathway. The correlation coefficient between the mean RR interval during AF (mRR) and the mean intra‐atrial potential interval during AF (mff) was positive (0.05 [P < 0.05] in group 1 and 0.37 [P = NS] in group 2). The correlation coefficient of the mRR against the functional refractory periods of the AV node (AVFRP) was 0.73 (P < 0.001) in group 1. The correlation coefficients between mRR and the fast AV nodal pathway functional refractory periods and the slow AV nodal pathway effective refractory periods (SPERP) were 0.58 (P = NS) and 0.7 (P < 0.05) in group 2, respectively. The correlation coefficients between mRR against (mff × AVFRP)1/2 in group 1 and (mff × SPERP)1/2 in group 2 were 0.8 (P < 0.001) and 0.72 (P < 0.05), respectively.

Conclusions: This clinical study did not indicate an inverse relation between the atrial and ventricular rates that had been reported by the previous experimental study. The ventricular rate during AF appeared to be quantitatively related to the atrial rate via AV node function. The importance of the slow pathway in determining the ventricular rate during AF was observed.
Circadian Variation of Heart Rate Variability in Postinfarction Patients With and Without Life‐Threatening Ventricular Tachyarrhythmias
Authors: KLINGENHEBEN THOMAS , RAPP ULI , HOHNLOSER STEFAN H.
Published: May 2007

Circadian Variation of HRV. Introduction: Determination of heart rate variability (HRV) is widely used for noninvasive assessment of cardiac autonomic tone. A decreased HRV is associated with an increased mortality in patients surviving an acute myocardial infarction. There are, however, only sparse data about the circadian variation of different components of HRV that may be linked to the well‐known circadian fluctuations in the occurrence of sudden death. In addition, the potential prognostic impact of circadian variations of HRV has not been examined.

Methods and Results: The present study compared the circadian variation of HRV from 14 postinfarction patients who had survived at least one episode of out‐of‐hospital cardiac arrest (cardiac arrest group) with that of 14 age‐ and sex‐matched patients without a history of malignant arrhythmias after their index infarct (control group). Several time‐ and frequency‐domain measures of HRV were assessed from 24‐hour Holter recordings. Circadian variations of high‐ (HF), low‐ (LF), and total‐frequency (TF) components were determined by calculating for each parameter the hourly difference from the day's mean. The average of these differences was calculated for every hour as well as for predefined day and night periods. There was no significant difference between the two groups with regard to HRV indices that predominantly reflect vagal tone, such as SDNN (78 ± 25 vs 96 ± 24 msec), pNN50 (2.7%± 4.6% vs 4.9%± 4.2%), or HF (6.3 ± 3.0 vs 7.8 ± 3.2 msec; cardiac arrest vs control group). There was also no significant difference in the circadian variation of LF or TF between the two groups during daytime and nighttime. However, a significant difference in circadian variation of HF was found during daytime (0.02 ± 0.5 vs ‐0.6 ± 0.5 msec; P = 0.006) and nighttime (0.19 ± 0.64 vs 1.5 ± 0.75 msec; P = 0.0002). In cardiac arrest survivors, there was no difference in the mean deviation of HF between the day‐and the nighttime periods.

Conclusions: These results show an almost complete abolition in circadian variation of parasympathetic tone in postinfarction patients surviving an episode of out‐of‐hospital cardiac arrest, whereas circadian variation of sympathetic tone is comparable to that of postinfarction patients without arrhythmic episodes. These findings indicate that determination of diurnal variation of HRV may add to the prognostic value of HRV with respect to identifying patients at high risk of sudden death.
The Effect of Cardiac Compression on Defibrillation Efficacy and the Upper Limit of Vulnerability
Authors: IDRISS SALIM F. , ANSTADT MARK P. , ANSTADT GEORGE L. , IDEKER RAYMOND E.
Published: May 2007

Compression Affects Defibrillation and ULV. Introduction: We determined the effects of decreasing the ventricular blood volume and altering cardiac geometry on defibrillation, the upper limit of vulnerability (ULV), and the relationship between them.

Methods and Results: In six pigs, fibrillation/defibrillalion trials were performed with a left ventricular apex patch to a superior vena cava catheter electrode configuration and a biphasic waveform. Thirty trials each were performed on a compressed versus noncompressed (normal) heart. Compression was achieved using direct mechanical ventricular actuation. Dose‐response curves were constructed, and the 50% probability points (KD50) were compared for leading edge voltage (LEV), leading edge current (LEI), and total energy (TE). In another 12 pigs, triplicate defibrillation thresholds (DFTs) and ULVs were determined for each heart state. The T wave was scanned with shocks in 10‐msec steps for determining the ULV. Compression resulted in decreased ED50s for LEV (δ= 138 ± 77 V, P < 0.05, mean ± SD), LEI (A = 1.57 ± 0.7 A, P < 0.05), and TE (δ= 4.9 ± 3.6 J, P < 0.05) compared to normal. In the second study, compression significantly reduced DFT (P < 0.02) and ULV (P < 0.02) for LEV, LEI, and TE compared to normal. The ULV tended to be lower than the DFT for the normal heart state (δ= 23 ± 46 V LEV; P = NS). However, the ULV was significantly greater than the DFT for the compressed heart state (A = 19 ± 25 V LEV; P < 0.03).

Conclusions: Shock delivery during cardiac compression improves defibrillation efficacy. Additionally, cardiac compression decreases both DFT and ULV, which supports the ULV hypothesis of defibrillation. Finally, maintaining the heart's geometric and volumetric state during ULV testing in paced rhythm and DFT testing in ventricular fibrillation moves the ULV higher than the DFT—the position predicted by the ULV hypothesis for defibrillation.
AV Nodal‐His‐Purkinje Reentry: A Novel Form of Tachycardia
Authors: MARKOWITZ STEVEN M. , STEIN KENNETH M. , ENGELSTEIN ERICA D. , LERMAN BRUCE B.
Published: May 2007

AV Nodal‐His‐Purkinje Reentry. Introduction: Bundle branch reentry (BBR) typically occurs in patients with dilated cardiomyopathy and infra‐Hisian conduction system disease. The macroreentrant circuit of BBR is confined to the His‐Purkinje system (HPS) and ventricular myocardium. As such, the atrioventricular (AV) node plays no role in the tachycardia circuit.

Methods and Results: In the present study, we identified a novel form of wide complex tachycardia in a patient with coronary disease and severe aortic regurgitation. The tachycardia morphology was right bundle branch block with a left superior axis. Ventriculoatrial block was present during tachycardia. An unusual feature of this rhythm was two sequential His‐bundle deflections (H and H′) for each ventricular beat of tachycardia. The H′V interval was identical to the HV interval during supraventricular rhythm. Changes in the ventricular cycle length (VV) preceded changes in the HH interval, consistent with retrograde activation of the first His‐bundle deflection. Changes in the H ‘H’interval preceded changes in the VV interval, consistent with anterograde activation of the second His‐bundle deflection. Tachycardia could be terminated with ventricular extrastimuli that did not capture the proximal HPS as well as with ventricular extrastimuli that advanced the His deflection, consistent with block in the HPS and in the AV node, respectively. Reproducible termination of the tachycardia following the first His deflection was demonstrated with adenosine, consistent with an upper pivot in the AV node.

Conclusions: We have identified a new form of reentrant tachycardia in which the AV node, HPS, and ventricular myocardium each obligatorily participates in the tachycardia circuit, with the left posterior fascicle and right bundle functioning as the anterograde and retrograde limbs, respectively. Unlike BBR, however, the His bundle is activated twice as the wavefront pivots in the AV node. This model requires longitudinal dissociation at the levels of the AV node and His bundle.
In Vivo and In Vitro Electrophysiologic Effects of Terodiline on Dog Myocardium
Authors: PRESSLER MILTON L. , WARNER MARGARET R. , RUBART MICHAEL , RARDON DAVID P. , ZIPES DOUGLAS P.
Published: May 2007

Electrophysiologic Effects of Terodiline. Introduction: Terodiline hydrochloride, widely prescribed for urinary incontinence, has been reported to cause bradycardia and torsades de pointes.

Methods and Results: In this study, we characterized the electrophysiologic effects of terodiline in dog cardiac tissues in vivo and in isolated canine cardiac Purkinje fibers. Terodiline (1 to 10 μM) resulted in dose‐dependent reduction of action potential amplitude and maximal upstroke velocity (Vmax). The threshold for these effects was ∼ 2 μM (0.6 mg/L), and the changes were cycle‐length dependent. Terodiline (≥ 2 μM) also depressed the action potential plateau but did not significantly alter action potential duration at concentrations ≤ 10 μM. In vivo studies demonstrated that high doses of terodiline (3 mg/kg) lengthened AH and HV intervals, slowed spontaneous sinus rate, prolonged ventricular refractoriness, and inhibited vagally induced slowing of the sinus node. Sympathetic effects on spontaneous sinus rate were unchanged. In both isolated canine Purkinje fibers and anesthetized dogs, terodiline did not evoke afterdepolarizations, repetitive firing, or ventricular tachyarrhythmias under normal or hypokalemic conditions.

Conclusion: Our findings suggest that terodiline (≤ 1 to 2 μM) leads to blockade of sodium and calcium channels as well as muscarinic receptors in canine cardiac tissues.
The Clinical Spectrum of Neurocardiogenic Syncope
Authors: SUTTON RICHARD , PETERSEN MARK E.V.
Published: May 2007

Neurocardiogenic Syncope. Neurocardiogenic syncope is a collective term used to describe the clinical syndromes of syncope that result from inappropriate, and often excessive, autonomic reflex activity, and manifest as abnormalities in the control of vascular tone and heart rate. These include carotid sinus syndrome, vasovagal syncope, and the syndromes of cough, deglutition, and micturition syncope. Orthostatic hypotension, which, in contrast, results from a failure of autonomic reflexes, is not considered part of this family of closely related syndromes. This review will focus on vasovagal and carotid sinus syndromes.
Electrophysiologic Characteristics of M Cells in the Canine Left Ventricular Free Wall
Authors: SICOURI SERGE , ANTZELEVITCH CHARLES
Published: May 2007

Characteristics of M Cells. Introduction: Recent studies have described the existence of M cells in the deep structures of the canine and human ventricle. The present study was designed to further characterize the M cell with respect to its distribution across the canine left ventricular free wall and the dependence of its action potential on [K+]0.

Methods and Results: We used standard microelectrode techniques to record transmembrane activity from deep subepicardial or transmural strips isolated from the canine left ventricular free wall near the base as well as subendocardial Purkinje fibers. M cell behavior (steep APD‐rate relation) was observed at depths of 1 to 7 mm from the epicardial surface (deep subepicardium to mid‐myocardium). M cells were found to be distributed uniformly in the deep subepicardium and did not appear in discrete bundles. We observed transitional behavior throughout the wall. The maximum rate of rise of the action potential upstroke, Vmax, increased sharply between epicardium and deep subepicardium (176 ± 13 to 332 ± 61 V/sec), remained high throughout the mid‐myocardium and deep subendocardium, and returned to lower values only in the superficial layers of the endocardium (205 ± 21 V/sec). The relationship between Vmax and takeoff potential in the M cell was fit by a Boltzmann equation with a V V0.5 of ‐68.6 ± 1.5 mV and k of 3.4 ± 0.5. The relationship between resting membrane potential (RMP) and [K+]0 in the M cell was exponential from 8 to 20 mmol/L (58 mV change in RMP per 10‐fold change in [K+]0), deviating from K+ electrode behavior at [K+]0, < 8 mmol/L. RMP in M cells continued to hyperpolarize at [K+]0 < 2.5 mmol/L, reaching potentials of approximately ‐110 mV at I+]0, of 1 mmol/L. In contrast, subendocardial Purkinje fibers depolarized at these low levels of [K+]0. Unlike endocardium and epicardium, M cells developed early afterdepolarizations at low [K+]0 and slow rates.

Conclusions: Our data indicate that the M cells are widely distributed in the intramural layers of the canine left ventricular free wall. M cells and transitional cells occupy 30% to 40% of the left ventricular wall and an estimated 20% to 40% of the mass of the ventricles of the normal canine heart. They display characteristics common to both myocardial and specialized conducting cells. Like Purkinje fibers, M cells exhibit a relatively large Vmax and steep APD‐rute relations that are modulated by [K+]0. Unlike Purkinje fibers, M cells do not appear in bundles, they do not depolarize at [K+]0 < 2.5 mmol/L, nor do they exhibit phase 4 depolarization.
Comparison of Atrial‐His Intervals During Tachycardia and Atrial Pacing in Patients with Long RP Tachycardia
Authors: MAN K. CHING , NIEBAUER MARK , DAOUD EMILE , STRICKBERGER S. ADAM , KOU WILLIAM , WILLIAMSON BRIAN D. , MORADY FRED
Published: May 2007

Long RP Tachycardia. Introduction: The purpose of this study is to describe a simple and reliable diagnostic maneuver that allows for the rapid differentiation of atypical AV nodal reentrant tachycardia (AVNRT) from other causes of long KP tachycardia. Long RP tachycardias may he caused by atypical AVNRT, orthodromic reciprocating tachycardia (ORT) involving a slowly conducting retrograde accessory pathway, or atrial tachycardia. The differentiation of atypical AVNRT from ORT or atrial tachycardia may be difficult, especially when the differential diagnosis includes a posteroseptal accessory pathway or an atrial tachycardia arising in the posteroseptal right atrium.

Methods and Results: Twelve patients with atypical AVNRT, 21 with ORT, and 12 with an atrial tachycardia diagnosed using conventional criteria were enrolled In this study. The atrial‐His (AH) interval was measured at the His‐bundle position during the tachycardia and during atrial pacing from the high right atrium at the tachycardia cycle length in the setting of sinus rhythm. In patients with atypical AVNRT, the mean AH interval was 69 msec ± 50 msec (± SD) longer during high right atrial pacing than during the tachycardia (P < 0.001). In 10 of 12 patients with atypical AVNRT, the AH interval during atrial pacing was more than 40 msec longer than the AH interval measured during the tachycardia. In contrast, in patients with ORT or atrial tachycardia, the differences in AH interval between atrial pacing and tachycardia were never more than 20 and 10 msec, respectively.

Conclusion: The difference in the AH interval between atrial pacing and the tachycardia allows a simple and rapid means of differentiating atypical AVNRT from other types of long RP tachycardias.
Effects of Optical Enantiomers CK‐4000(S) and CK 4001(R) on Defibrillation and Enhancement of Shock‐ Induced Extension of Action Potential Duration
Authors: BEATCH GREGORY N. , DICKENSON DAVID R. , TANG ANTHONY S.‐L.
Published: May 2007

Antiarrhythmic Drugs and DFT. Introduction: Class III antiarrhythmics have been reported to lower defibrillation threshold (DFT); however, the mechanism(s) of this effect is unknown. Recent evidence suggests that DFT strength DC shocks may terminate reentrant arrhythmias through prolongation of action potential duration and refractory periods. Since Class III antiarrhythmic drugs prolong repolarization, we examined the hypothesis that these drugs enhance shock‐induced action potential duration extension (APDE), which might contribute to lowering of DFT.

Methods and Results: In order to investigate the specificity of drug effects on action potential repolarization following a shock, an optical enantiomer with mixed β‐blocking and Class III effects (CK‐4000) and its enantiomer with “pure” Class III antiarrhythmic effects (CK‐4001) were compared against placebo in a canine defibrillation model (n = 8 per group). At the 3 mg/kg dose, the enantiomers nonstereoselectively lowered DFT voltage by 19 ± 15% (CK‐4000, P < 0.05 compared to placebo) and 25 ± 12% (CK‐4001, P < 0.05 compared to placebo), indicating that Class III antiarrhythmic actions alone were sufficient for this effect. Similarly, CK‐4000 and CK‐4001 at 3 mg/kg enhanced APDE (P < 0.01 compared to placebo) by 20 ± 11% and 24 ± 17%, respectively. APDF prolongation significantly correlated with reduction in DFT voltage for both CK‐4000 (r = ‐0.55, P < 0.03) and CK4001 (r = ‐0.63, P < 0.01). At 3 mg/kg, the enantiomers stereoselectively prolonged action potential duration (APD75) by an average of 37 ± 14% (CK‐4000, P < 0.001) and 23 ± 14% (CK‐4001, P < 0.001), and ventricular effective refractory period (VERP) by 38 ± 15% (CK‐4000, P < 0.01) and 27 ± 13% (CK‐4001, P < 0.05). Prolongations of APD75 and VERP did not correlate with reductions of DFT in individual dogs.

Conclusions: These results show that Class III antiarrhythmics and DFT strength shocks additively delay repolarization, which suggests that drug enhancement of APDE may contribute to their effects on DFT.
Serial Defibrillation Threshold Measures in Man: A Prospective Controlled Study
Authors: POOLE JEANNE E. , BARDY GUST H. , LEE DOLACK G. , KUDENCHUK PETER J. , ANDERSON JILL , JOHNSON GEORGE
Published: May 2007

Serial DFT Measures in Man. Introduction; The defibrillation threshold (DFT) may change throughout the first year following implantation of a cardioverter defibrillator, but it remains uncertain if changes are a consequence of changes in clinical condition or are related to fundamental alterations at the electrode‐tissue interface. The purpose of this study was to evaluate the extent and time course of DFT changes over the first year following implantable cardioverter defibrillator (ICD) surgery when extraneous clinical and device variables potentially affecting the DFT were excluded.

Methods and Results.: We prospectively enrolled 61 patients undergoing epicardial or non‐thoracotomy/transvenous ICD therapy into a series of follow‐up studies where the DFT was measured at implant and at 1, 6,12, and 52 weeks following implantation in a uniform manner. Stored energy DFT was measured and recorded for all patients. Patient exclusion criteria were: (1) inability to complete all five measures of the DFT; (2) institution of Class I or Class III antiarrhythmic drugs at any time during the study; (3) lead system changes (relocation or new leads) or programming changes in pulse width or current pathway; or (4) development of a significant change in their clinical status, such as decompensated congestive heart failure or acute ischemia. Only 20 of the 61 patients satisfied the criteria required to complete the study. Two of the excluded patients developed high DFTs, which required reprogramming of the current pathway. Eight patients had an epicardial lead system, and 12 had a nonthoracotomy lead system. The rise in DFT over the first 12 weeks was significant for the eight epicardial lead system patients (P = 0.05) and for the 12 nonthoracotomy lead system patients (P = 0.004). The peak rise in DFT occurred at 1 week for the patients with an epicardial lead system (3.4 ± 1.8 J to 7.9 ± 3.8 J) and at 12 weeks for the patients with a transvenous lead system (10.3 ± 5.3 J to 16.1 ± 7.4 J).

Conclusions: This study confirms a transient significant rise in the DFT in the first 12 weeks following ICD surgery that partially returns to the implant value over the remainder of the year. Because specific clinical and technical variables were excluded from this study, the observations made in this patient population suggest that the rise in DFT may be a consequence of changes at the electrode‐tissue interface.
The Vulnerable Window for Unidirectional Block in Cardiac Tissue:
Authors: SHAW ROBIN M. , RUDY YORAM
Published: May 2007

Vulnerable Window of Unidirectional Block. Introduction: Unidirectional block is a requisite event in the initiation of reentry in cardiac tissue, but its initiation and behavior in the presence of tissue pathologies remain poorly understood. Previous experimental and theoretical reports on vulnerability to unidirectional block under conditions of reduced cellular coupling and reduced membrane excitability have varied due to differences in experimental and simulation protocols.

Methods and Results: We have addressed the issue of vulnerability to unidirectional block using the recent Luo‐Rudy membrane model and computer simulations of propagation in a one‐dimensional cardiac fiber. The vulnerable window (VW) of unidirectional block from premature stimulation is expressed in units of time, VWtime, and as a range of membrane potentials at the stimulus site, VWpot VWpot and VWtime, were quantified over a range of membrane excitability and gap junction resistances (intercellular coupling). With normal membrane excitability and intercellular coupling, VWpot, and VWtime, were small (VWPot, = 0.44 mV, VWtime, = 0.39 msec). A uniform reduction (0.25 ×) in the degree of intercellular coupling increased VWtime, and VWpot, by factors of 3.6 and 4.7, respectively, whereas a uniform decrease (0.25 ×) in membrane excitability (same resulting velocity) increased VWtime, by only a factor of 0.4 and decreased VWpot, to negligible levels. When inhomogeneities in fiber properties were introduced (intercellular coupling and membrane excitability), VWtime, increased more due to inhomogeneity in membrane excitability (VWtime= 4.5 msec) than to inhomogeneity in intercellular coupling (VWtime, = 1.5 msec). The simulations also clarify the dependence of the VW on the dimensions of the stimulating electrode. The length of the stimulating electrode added a factor, equal to the propagation time across the eiectrode length, to the intrinsic VW of the fiber.

Conclusions: VWpot, and VWtime, are both important parameters for quantifying vulnerability to unidirectional block. In an environment with uniform distribution of fiber and membrane properties, reduced intercellular coupling bas a greater effect on the VW than reduced membrane excitability. Inhomogeneous reduction of membrane excitability can significantly enhance vulnerability to unidirectional block, much more so than inhomogeneous reduction of intercellular coupling. Theoretically, stimulation at a point should be used to define the VW. Finite electrode dimensions introduce a geometrical factor that affects the measurement of the VW.
Kinetics of Cycle Length Dependence of Ventricular Repolarization:
Authors: RAEDER ERNST A. , ALBRECHT PAUL , PERROTT MICHAEL , COHEN RICHARD J.
Published: May 2007

Cycle Length Dependence of Repolarization. Introduction: Beat‐to‐beat adaptation of ventricular repolarization duration to cardiac cycle length and autonomic activity has not been previously characterized in the spontaneously beating human heart.

Methods and Results: The ECG of 14 healthy subjects was recorded from the supine and upright positions. Autonomic blockade was accomplished by atropine and propranolol. RR and RT intervals were measured by a computer algorithm, and the impulse response (h) from RR to RT computed. In the supine position the maximal adjustment of the RT interval occurred in the first beat following a change in cycle length (hpeak= 17.8 ± 1.6 msec/sec), but continued to be detectable for 3.8 seconds (2.9–4.7 sec). Propranolol attenuated the peak impulse response to 15.8 ± 4.0 msec/sec (P = NS). In the standing position the peak impulse response was increased to 25.2 ± 5.0 msec/sec (P = 0.004 vs supine), and the impulse response duration (hdur) shortened to 1.4 seconds (1.3–1.6). This was reversed by beta blockade (hpeak= 10.7 ± 3.6 [P = 0.005 vs standing]; hdur= 5.5 sec [4.8–6.1]). Parasympathetic and combined autonomic blockade resulted in too little residual heart rate variability to estimate the impulse response accurately. The slope of the regression of δRT and δRR in the supine position was 0.0177 ± 0.0016, which was closely correlated with the peak impulse response (r = 0.91).

Conclusions: System identification techniques can assist in characterizing the cycle dependence of veritricular repolarization and may provide new insights into conditions associated with abnormal repolarization.