bluuebunny/crossref_metadata_2025 huggingface dataset:
Quantitative Comparison of Temporal and Spatial High‐Resolution Recordings of Terminal QRS
Authors: YANG WEIQUN , HORAN LEO G. , WYLDS ANITA C. , FLOWERS NANCY C.
Published: May 2007

Beat‐by‐Beat Recording of Terminal QRS. Introduction: Beat‐by‐beat recordings of quasiorthogonal leads were performed in 82 normal subjects (35 male and 47 female) with normal standard electrocardiograms (ECGs) in order to: (1) establish normal values for parameters that were similar to those used in signal‐averaged ECG; (2) compare these data with the signal‐averaged ECG; and (3) assess the noise level in beat‐by‐beat recording.

Methods and Results: Low‐noise recordings were achieved by special instrumentation, preparation of subjects, and screening recording sites for an optimal magnetic field at 60 Hz or its harmonics without using a shielded room. Using a 40‐Hz bidirectional high‐pass filter, 95% of normal subjects had a beat‐by‐beat duration of vector magnitude complex ≤ 107 msec, a duration of low‐amplitude signal under 40 μV ≤ 37 msec, and a root mean square (RMS) voltage of last 40 msec ≥ 24.1 μV. Significant difference was found in duration of vector magnitude complex (P < 0.0001) between gender groups; this difference disappeared after normalization for height (P > 0.3). Although the beat‐by‐beat and signal‐averaged data were highly correlated in all three parameters, the beat‐by‐beat recordings exhibited a shorter duration of low‐amplitude signal (P < 0.0004) and a higher RMS voltage of last 40 msec (P < 0.002), and no significant variation in duration of vector magnitude complex (P > 0.2). The mean RMS noise in the vector magnitude lead from the normal group was 1.52 ± 0.65 μV (mean ± SD) while over 80% of the subjects had RMS noise under 1 μV in an individual lead.

Conclusion: The normal values from beat‐by‐beat recordings are correlated to but different from those of signal‐averaged ECGs. Every‐beat high‐resolution recordings of terminal QRS are stable and reproducible in normal subjects. Also, the use of individual lead (s) with lower noise is recommended for better detection of low‐level terminal QRS. (J Cardiovasc Electrophysiol, Vol. 3, pp. 109–118, April 1992)
Rapid Inward Current in Ischemically‐Injured Subepicardial Myocytes Bordering Myocardial Infarction
Authors: PATTERSON EUGENE , SCHERLAG BENJAMIN J. , LAZZARA RALPH
Published: May 2007

Ischemically‐Injured Myocytes. Introduction: To determine if collagenase‐dispersed epicardial myocytes overlying myocardial infarction reproduce the same altered electrophysiology observed in intact epicardiuma, multicellular tissue preparations and enzymatically‐dispersed myocytes from ischemically‐injured canine subepicardium were examined 1 and 4 days after myocardial infarction.

Methods and Results: The electrophysiologica changes observed with alchemic injury in enzymatic ally‐dispersed myocytes were not different from changes observed in multicellular tissue preparations at I and 4 days post infarction. Is chemically‐injured myocytes were depolarized versus normal myocytes at [K0] (2.5 to 40 mM) with reduced membrane potentials also observed in injured subepicardial tissue preparations [K] (4 to 24 mM). On day 1, the reduced Vmax and the prolonged recovery of Vmax from inactivation were consistent with the reduced membrane potentials observed at each [K]+. The half‐maximal Vmax, maximal Vmax and Boltzmann constant (k) in injured myocytes were unchanged versus normal myocytes. On day 4 postinfarction, the half‐maximal Vmax was shifted to a more negative membrane potential, the maximal Vmax. was reduced, and k was increased in injured versus normal myocytes. Prolonged recovery from inactivation was observed with depressed membrane potentials in injured myocytes on day 4.

Conclusion: Enzymatically‐dispersed myocytes from ischemically‐injured subepicardium closely reproduce altered cellular properties observed in multicellular tissue preparations. The data suggest that 1 day postinfarction, altered conduction and refractoriness largely result from a reduced membrane potential. At 4 days, a reduced maximal Vmax a shift in the inactivation curve to more negative voltages, and prolonged recovery of Vmax, from inactivation also contribute to slowed conduction and prolonged refractoriness.
Electrophysiologic Spectrum of Atrioventricular Nodal Behavior in Patients with Atrioventricular Nodal Reentrant Tachycardia Undergoing Selective Fast or Slow Pathway Ablation
Authors: JAZAYERI MOHAMMAD R. , SRA JASBIR S. , DESHPANDE SANJAY S. , BLANCK ZALMAN , DHALA ANWER A. , KRUM DAVID P. , AVITALL BOAZ , AKHTAR MASOOD
Published: May 2007

AV Nodal Behavior After Ablation. Introduction; The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT).

Methods and Results: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty‐two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty‐one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His‐bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety‐six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation.

Conclusion: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT: and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.
Drug Therapy For Torsade de Pointes
Authors: BANAI SHMUEL , TZIVONI DAN
Published: May 2007

Torsade de Pointes. Torsade de pointes is an uncommon and unique type of ventricular tachycardia. It differs from other forms of ventricular tachycardia by its morphological features, underlying mechanism, and modes of therapy. Recognizing torsade de pointes is of major clinical importance, as standard antiarrhythmic regimens might not only be ineffective in abolishing this life‐threatening arrhythmia but may aggravate it. Torsade de pointes is most commonly precipitated by QT prolonging drugs, mainly type IA antiarrhythmic therapy such as quinidine and disopyramide, and other antiarrhythmic agents are reported to cause torsade de pointes as well. Predisposing factors known to increase the likelihood of developing torsade de pointes are: electrolyte imbalance (hypokalemia, hypomagnesemia, or both) and slow heart rate induced either by sinus bradycardia or heart block. Treatment of torsade de pointes is aimed at shortening the QT interval. By acceleration of the heart rate, the QT interval is shortened, thus preventing the recurrence of the arrhythmia. Treatment of torsade de pointes includes: isoproterenol infusion, cardiac pacing, and intravenous atropine. Intravenous magnesium sulfate, a relatively new mode of therapy for torsade de pointes, was proven to be extremely effective and is now regarded as the treatment of choice for this arrhythmia.(Cardiovasc Electrophysiol, Vol. 4, pp. 206–210, April 1993)
Cardiac Arrhythmias and the Autonomic Nervous System
Authors: COUMEL PHILIPPE
Published: May 2007

Cardiac Arrhythmias and the Autonomic Nervous System. The multiple facets of cardiac arrhythmias and their relationship with the autonomic nervous system can be investigated by studying the spontaneous heart rate behavior through ambulatory ECG recordins, an approach that complements the limitations of invasive electrophysiologic investigations. Information obtained from heart rate behavior is more reliable in the absence of structural heart disease and ventricular hypertrophy/failure, during which compensatory mechanisms involving the autonomic nervous system tend to limit reflex changes in heart rate. Thus, in such situations, less marked sinus rhythm variations preceding the arrhythmia onset do not imply a more limited influence of the autonomic nervous system, and the sensitivity of the electrophysiologic substrate may otherwise vary. These two factors may combine to form the basis of the adrenergic paradox11 that implies that the more marked the autonomic nervous system dependence of tachyarrhythmias, the less obvious its evidence. Assessment of the QT interval dynamicity may also allow one to evaluate the modulation of autonomic neural effects on the ventricular tissues. Finally, it may be difficult to distinguish clearly autonomic nervous system dependence from rate dependence: the latter frequently conditions the behavior of the trigger whereas the former mainly concerns the electrophysiologic substrate. There are many examples of the importance of the autonomic nervous system as a determinant of cardiac arrhythmias. In the atrium, either limb of the autonomic nervous system, particularly the parasympathetic limb, can generate atrial fibrillation. The absence of structural heart disease defines pure electrophysiologic substrates responsible for benign forms of ventricular tachycardia as welt as potentially lethal tachyarrhythmias of the long QT syndrome and its variants. In both, the role of the autonomic nervous system is essential, although the therapeutic consequences are crucial only in the latter. In the presence of heart disease and, in particular, heart failure, the autonomic nervous system behavior is more difficult to assess than in the absence of structural heart disease. This does not mean that its role is less crucial. In this situation the beneficial effects of beta blockers may be as important as in normal hearts although physicians should be more cautious when heart failure is present.
“AV Nodal” Reentry:
Authors: McGUIRE MARK A. , JANSE MICHIEL J. , L DAVID
Published: May 2007

AV Nodal Reentry. The classical model of “atrioventricular (AV) nodal” reentrant tachycardia suggests that the reentrant circuit is entirely within the compact AV node and that AVnodal tissue is present proximal and distal to the circuit. Recent evidence from mapping studiesand from examination of the effects of curative procedures, however, suggests that the upperend of the circuit uses perinodal atrial or transitional tissue. Moreover, the anatomical suhstrate of dual “AV nodal” pathways is likely to be the multiple connections between compactAV node and atrium rather than discrete intranodal pathways. The antegrade slow pathwayappears to he situated at the posteroinferior approaches to the AV node in the region betweenthe coronary sinus orifice and the tricuspid annulus, The retrograde fast pathway appears lobe situated in the anterior atrionodal connections at the apex of Koch's triangle, close tothe His bundle. The lower turnaround point of the circuit is likely to be within the AV node.
Signal Averaging in Patients withCoronary Artery Disease:
Authors: SHENASA MOHAMMAD , FETSCH THOMAS , MARTINEZ‐RUBIO ANTONI , BORGGREEE MARTIN , BREITHARDT GUNTER
Published: May 2007

Late Potentials in CAD. In patients who have survived acute myocardial infarction, thepresence of ventricular late potentials using the high resolution signal‐averaged KCG indicatesareas of slow conduction and delayed activation that may potentially serve as a substrate lormalignant ventricular arrhythmias. Although detection of late potentials is technique specific, signal‐averaged analysis in the time or frequency domain may he a useful index for riskstratification with regard to ventricular tachycardia or sudden cardiac death. The sensitivityand specificity of late potentials for this purpose may he enhanced by comhination with othervariables, such as left ventricular ejection fraction and presence of complex ventricular ectopy, Therefore, the presence of ventricular late potentials in postmyocardial infarction patients, particularly in those patients with impaired left ventricular function, identifies those patienlswho are at high risk of malignant ventricular tachyarrhythmias, However., (he strategies forprevention of serious arrhythmia complications during follow‐up need to be established, Thenegative predictive value of late potentials is very high. Thus, the absence of late potentialsindicates a low propensity to sustained ventricular tachycardia or sudden death, even in thepresence of complex ventricular ectopy. Interventions may therefore not be necessary orshould even he avoided, The incidence of late potentials in patients with spontaneous orinduced ventricular fibrillation is lower and, if present, less pronounced than in those with sustained monomorphic ventricular tachycardia. This presumably is due to a lower degree of conduction delay, which serves as a substrate for reentry. Therefore, the ability of the signal‐aver‐aged ECG to predict a propensity to ventricular fibrillation is limited, Despite these limitations, the signal‐averaged ECG may be used as a risk predictor in evaluation of patients aftermyocardial infarction. Unfortunately, at least as far as time domain analysis is concerned, itcannot be used as an efficacy predictor for response to pbarniacologic interventions, Furtherstudies will determine whether other modes of signal‐averaged analysis can predict theresponse to drugs.
Modification of Sodium Channel Inactivation by α‐chymotrypsin in Canine Cardiac Purkinje Cells
Authors: SHEETS MICHAEL F. , HANCK DOROTby A.
Published: May 2007

Modification of Cardiac INa by α‐chymotrypsin. Introduction: Studies of tetrodotoxinsensitivc sodium current (INa) after modification of inactivation by intracellular enzymes in mammalian cells have demonstrated a markid increase in peak INa at test potentials near current threshold causing a large, negative shift of the peak INa conductance‐voltage relationship by approximately ‐20 mV. These findings support a kinetic model in which the unmodified Na channel has rapid and voltage‐independent inactivation from the open state. However, the kinetics of cardiac Na channels differ from those of mammalian nenronal Na channels. In particular, inactivation of cardiac Na channels has been proposed to be more voltage dependent than that of tetrodotoxin‐sensitive Na channels. To help understand the role of inactivation in cardiac Na channel kinetic hehavior, we studied Na currents before and after modification of inactivution by the proteolytic enzyme, α‐chymotrypsin.

Methods and Results: Whole cell INa was measured in single canine cardiac Purkinje cells that were voltage clamped and internally perfused with a large‐bore suction pipette. The decay of INa in response to step depolarizations was dramatically slowed after perfusion with intracellular α‐chyniotrypsin consistent with modification of inactivation. In contrast to mammalian tetrodotoxin‐sen‐sitive Na current, Boltzmann distribution fits to peak INa conductance‐voltage (GNa‐V) relationships after α‐chymotrypsin showed no change in either the potential at half maximum conductance (V1/2), after correction for the spontaneous background shift of INa kinetics, or in the voltage‐dependence of conductance (i.e., slope factor of GNa‐V relationships). Maximal peak INa conductance increased by 18%. INa tail‐current relaxations at potentials ≤−110 mV, after correction for spontaneous shifts in Na channel kinetics, were also similar before and after modification by α‐chymotrypsin.

Conclusion:α‐chymotrypsin modified inactivation of cardiac INa with little or no change in activation, and cardiac Na channel inactivation was slow near threshold and played little role in determining V1/2 for peak INa conductance‐voltage relationships.
Unexpected Emergence of Manifest Preexcitation Following Transcatheter Ablation of Concealed Accessory Pathways
Authors: WILLEMS STEPHAN , SHENASA MOHAMMAD , BORGGREFE MARTIN , SEIDL KARLHEINZ , CHEN XU , HINDRICKS GERHARD , HAVERKAMP WILHELM , BREITHARDT GÜNTER
Published: May 2007

Preexcitation After Catheter Ablation. Introduction: The basis for anterograde or retrograde unidirectional block of accessory pathways still remains a controversial issue.

Methods and Results: Four of 19 consecutive patients (1 mule, 3 Female; ages 27 to 34 years) who underwent transcatheter ablation of concealed accessory pathways developed manifest preexcitation after the ablation. The location of the concealed accessory pathways in these four patients were right lateral, left posteroseptal, left posterolateral, and left lateral. Radiofrequency current was used in three of the four patients and high energy direct current in one patient. After ablation, manifest preexcitation was observed in these four patients for the first time. Manifest preexcitation developed immediately after ablation in two of the four patients and after 4 and 14 days in the other two. Detailed endocardial mapping revealed that the manifest preexcitation originated from the same location as the concealed pathways. Subsequently, catheter ablation was successfully performed in three of the four patients using radiofrequency current. One patient underwent successful surgical ablation. No recurrence of preexcitation was observed during a follow‐up period of 9 to 38 months. All patients remained free of arrhythmias.

Conclusion: The basis for this unexpected emergence of preexcitation in these patients with only retrograde conducting accessory pathways deserves further investigation. Although not compared in the present study, this phenomenon has not been reported in patients who underwent surgical interruption of accessory pathways. We postulate that a lesion at the site of insertion of the accessory pathway had modified the anterograde conduction capacity.
The Value of Electrophysiologic Testing in Patients Resuscitated From Documented Ventricular Fibrillation
Authors: LI HUAGUI G. , THAKUR RANJAN K. , YEE RAYMOND , KLEIN GEORGE J.
Published: May 2007

EP Study and Ventricular Fibrillation. Introduction: Electrophysiologic testing is performed in patients resuscitated from ventricular fibrillation (VF) on the assumption that sustained monomorphic ventricular tachycardia (VT) may be a precursor to VF, with the former amenable to assessment by serial drug testing.

Methods and Results: We assessed the usefulness of this strategy by analyzing clinical and electrophysiologic data of 42 survivors (29 men and 13 women; mean age 54 ± 14 years) of VF without a reversible cause. All patients had VF documented on ECG and required defibrillation. Underlying heart diseases included coronary disease in 28, dilated cardiomyopathy in 3, arrhythmogenic right ventricular dysplasia in 1, and no apparent structural heart disease in 10 patients. Only 2 (4.7%) patients had a prior history of documented VT. The electrophysiologic study was performed 7 to 30 days after VF. Programmed stimulation at the right ventricular apex using at least two drive cycle lengths and up to three extrastimuli induced sustained monomorphic VT in 4 (9.5%), sustained polymorphic VT in 3 (7.1%), nonsustained monomorphic VT in 1 (2.3%), nonsustained polymorphic VT in 5 (11.9%), and VF in 13 (30.9%) patients. Two patients with documented prior VT and coronary disease had sustained VT induced during the electrophysiologic study. On the other hand, sustained monomorphic VT was induced in 53 of the 59 (90%) patients (45 men and 14 women; mean age 57 ± 16 years) with clinically documented VT concurrently studied using the same stimulation protocol.

Conclusion: We conclude that reproducible induction of sustained monomorphic VT in survivors of documented VF is uncommon. It may be more cost effective to proceed directly to treatment with implantable cardioverter defibrillators in these patients.
Involvement of a Nodofascicular Connection in Supraventricular Tachycardia with VA Dissociation
Authors: HAÏSSAGUERRE MICHEL , CAMPOS JULIO , MARCUS FRANK I. , PAPOUIN GÉRARD , CLÉMENTY JACQUES
Published: May 2007

Nodofascicular Connection in SVT. We present the case of a patient with episodes of supraventricular tachycardia and atrial dissociation that were terminated by either adenosine or verapamil. Involvement of an accessory pathway was shown by ventricular extrastimuli, elicited during His‐bundle refractoriness, that interrupted the tachycardia or advanced the next His potential. The tachycardia circuit was demonstrated to he confined to the nodofascicular region based on the exclusion of surrounding tissues. Atrial activity, including that in the perinodal region, was totally dissociated during tachycardia. The lowest part of the circuit was determined to be located above the Hisian bifurcation, as multiple episodes with either a right or left bundle branch configuration during tachycardia did not modify the HH cycle. The ventricular septum summit was determined not to be involved, as no preexcitation was present during tachycardia or atrial pacing, and the right bundle branch was not part of the circuit. Radiofrequency current applied beneath the tricuspid valve at the His region successfully eliminated the nodofascicular connection with preservation of 1:1 AV conduction. The anatomical substrate underlying the abnormal connection may be either nodofasciculoventricular Mahaim fibers or a duality or dispersion of the nodo‐Hisian conducting system.
Insights into the Electrophysiology of Ventricular Tachycardia Gained by the Catheter Ablation Experience:
Authors: CALLANS DAVID J. , SCHWARTZMAN DAVID , GOTTLIEB CHARLES D. , MARCHLINSKI FRANCIS E.
Published: May 2007

VT Catheter Ablation. The success of catheter ablation has significantly improved the treatment of patients with cardiac arrhythmias and has established electrophysiology as an increasingly interventional subspecialty. Some members of the electrophysiology community have expressed concern that this success has been purchased at the cost of undermining what had been our primary concern: understanding the anatomic and physiologic basis of arrhythmia syndromes. In many laboratories, endpoints such as case load and primary success have eclipsed physiologic investigation. Despite these trends, however, catheter ablation is not inherently at odds with investigation and education. On the contrary, because the lesions delivered with current techniques are much more discrete than the effects of antiarrhythmic agents or surgical ablation, catheter ablation can be used as a research tool directed toward a more precise understanding of arrhythmia substrates. Conscious attempts at “learning while burning” have already provided important and unique information about arrhythmia pathogenesis.
Role of Na+:Ca2+ Exchange Current in Cs+‐Induced Early Afterdepolarizations in Purkinje Fibers
Authors: SZABO BELA , SWEIDAN RAED , RAJAGOPALAN CADATHUR V. , LAZZARA RALPH
Published: May 2007

Na+:Ca2+ Exchanger and EADs. Introduction: The ionic mechanisms for early afterdepolarizations (EADs) have not been fully clarified. It has been suggested that L‐type Ca2+ current (IcaL) is the primary current generating EADs that occur near the plateau level (E‐EADs) of the membrane potential (Vm) when IcaL is enhanced. The purpose of these studies was to determine accurately the range of Vm at which EADs occur in Purkinje fibers with K+ currents blocked by Cs+ and to investigate the importance of Na+:Ca2+ exchange current (INa:ca) as opposed to lCaL and other currents in the generation of EADs occurring later during repolarization (L‐EADs).

Methods and Results: Shortened Purkinje strands from dogs and guinea pigs were superfused with physiologic solution containing Cs+ (3.6 mM) and a low [K+]o (3.0 or 2.0 mM) to induce EADs. The Vm of origin of EADs and their evolution were measured with the aid of phase plane plots of the rate of repolarization against Vm. L‐EADs occurred over a wide range of Vm (−35 to −90 mV), generally more negative in guinea pig than in dog. Elevation of [Ca2+]o, from 1.8 to 3.6 mM suppressed L‐EADs within a few cycles, and they returned with continued exposure. After repeated exposures to high [Ca:2+]0, L‐EADs migrated toward less negative Vm when |Ca2+]0, was reestablished to 1.8 mM in the presence of Cs+. Reduction of [Na+]0 from 147.5 to 112.5 mM by substitution with Li+ or sucrose also rapidly depressed L‐EADs.

Conclusions: The observation of Cs+‐induced L‐EADs over a wide range of Vm indicates that there is not a single inward gated current as a common ionic mechanism for L‐EADs but does not exclude an important role for INa:Ca, which can operate over a wide range of Vm. The rapid suppression of L‐EADs with elevated [Ca2+]o, and reduced [Na+]o, and the migration of EADs to more positive Vm after exposures to high |Ca2+]o, are compatible with INc:Ca as the major charge carrier for L‐EADs.
Implantable Cardioverter Defibrillator Patch Erosion Presenting as Hemoptysis
Authors: VERHEYDEN CHARLES N. , PRICE LARRY , LYNCH DENNIS J. , KNIGHT WADE L.
Published: May 2007

ICD Patch Erosion. Although the internal cardioverter defibrillator has prevented many premature deaths from lethal ventricular arrhythmias, some complications have occurred with its use. We present a patient who developed a fistula between the left ventricle and a bronchus, caused by erosion of the ventricular patch. The patient's presenting symptom was hemoptysis. Physicians caring for patients with these devices should be aware of this potential problem.
Effects of Acute Volume Changes on P Wave Characteristics:
Authors: VAINER JINDRICH , CHERIEX EMILE C. , van der STELD BERT , DASSEN WILLEM R.M. , SMEETS JOEP L.R.M. , WELLENS HEIN J.J.
Published: May 2007

Effects of Acute Volume Changes on P Wave. Introduction: This study was performed to determine the effect on the P wave of different hemodynamic loads to the heart.

Methods and Results: Signal–averaged P wave ECC and atrial echocardiographic measurements were obtained from eight healthy male volunteers at rest and after infusion of 1000 mL of plasma expander (Haemaccel®) over 15 minutes. These measurements were repeated 24 hours later at rest and after 0.8 mg of nitroglycerin given sublingually. The effect of positional changes was also studied. At rest the amplitude of the P wave and the time of the maximal the P wave amplitude were reproducible. Sitting increased heart rate variability; no significant changes of the P wave were found. Volume overload decreased the heart rate and increased the atrial size on echocardiography with changes in lead V, (earlier appearance of the first positive deflection). Nitro–glycerin administration increased heart rate and decreased the echocardiographic size of the atria, the latter not reaching statistical significance. Administration of nitroglycerin induced P wave amplitude rise in leads 1 and II. The maximal power in fast Fourier transformation for calculated orthogonal leads X and Y increased as well.

Conclusions: Amplitude behavior in leads I, II, and V, appears to correlate with load conditions, particularly with volume redistribution. In healthy men subtle changes in the P wave morphology after volume changes can be detected by the signal–averaged ECU. Application of these findings in patients following acute changes in circulation needs further investigation.
Immunohistochemical Localization of Gap Junction Protein Channels in Hamster Sinoatrial Node in Correlation with Electrophysiologic Mapping of the Pacemaker Region
Authors: TRABKA‐JANIK ELIZABETH , COOMBS WANDA , LEMANSKI LARRY F. , DELMAR MARIO , JALIFE JOSE
Published: May 2007

Gap Junction Proteins in the Sinoatrial Node. Introduction: Gap junction proteins are thought to form the low resistance pathways that connect neighboring cells within the sinoatrial node, and to mediate pacemaker synchronization.

Methods and Results: We have carried out microelectrode mapping experiments of the hamster sinoatrial region to localize the primary pacemaker area for subsequent light, electron, and immunofluorescence microscopic studies aimed at testing the hypothesis that the major cardiac gap junction protein (connexin43) is present in such an area. The site of earliest activation is unifocal and the pattern of activation, obtained In multiple sequential microelectrode recordings of the Sinoatrial region, is qualitatively similar to that previously described for other species. However, quantitatively, the impulse transmission time from the primary pacemaker area to the crista (sulcus) terminal's in the hamster sinoatrial node is about 50% briefer than that of the guinea pig and five times faster than that of the rabbit. Immunolocalization studies in the hamster sinoatrial node using anti‐connexin43 antisera demonstrated specific staining at the areas of cell‐to‐cell apposition and suggested that the apparently high degree of electrical coupling in this tissue is the result of abundant connexin43 expression. The immunofluorescence data were supported by light microscopic studies, which demonstrated the typical morphologic characteristics of sinus nodal cells in the pacemaker area. In addition, an electron microscopic study of the sinoatrial region revealed the presence of gap junctions in the junctional complex at areas of cell‐to‐cell contact.

Conclusion: Our results demonstrate that cells in the sinoatrial region of the hamster heart are electrically well coupled and strongly suggest that such coupling is mediated by gap junctional channels formed by connexin43.
Bipolar Stimulation of Cardiac Tissue Using an Anisotropic Bidomain Model
Authors: SEPULVEDA NESTOR G. , WIKSWO JOHN P.
Published: May 2007

Bipolar Stimulation of the Cardiac Bidomain. Introduction: One of the fundamental electrophysiologic problems that has not yet been completely elucidated is the response of cardiac tissue to externally applied electric currents. A limited number of theoretical and experimental techniques has been used to study the electric behavior of cardiac tissue in the presence of stimulating currents, and to demonstrate that the anisotropy in the passive electrical properties of the tissue plays an important role in the genesis and propagation of the activation wave‐front and the resulting potential distributions.

Methods and Results: In this work we have applied the finite element method to study the electric and magnetic fields produced by cardiac tissue in response to bipolar current injection, using a linear bidomain model to represent the tissue. We found that the transmembrane potential distribution close to the stimulus electrode has a rather complex geometrical pattern, with adjacent hyperpolarized and depolarized regions.

Conclusion: This behavior is consistent with previous theoretical and experimental results and may have implications in the study of electrical stimulation of cardiac tissue that are not apparent using other models.
The Conduction System Findings in Sudden Cardiac Death
Authors: BHARATI SAROJA , LEV MAURICE
Published: May 2007

Conduction System in Sudden Death. This is a brief review of the findings in the conduction system in cases of sudden death victims who were living “normal” active lives. Twenty–two representative samples from more than 100 cases of sudden cardiac death, especially in young and asymptomatic individuals, revealed a plethora of findings that varied from normal to congenital and acquired changes, in most cases either at the gross or microscopic level, especially in the conduction system to a varying degree. Despite these changes, the individuals were living normal, symptom–free lives and were not clinically diagnosed to have lethal cardiac problems. This suggests that these individuals might have experienced lethal arrhythmias in the past, which might have been “silent” in nature. Innovative new methodologies must be developed to detect the silent lethal arrhythmic focus that may lead to sudden cardiac death.
Radiofrequency Ablation of a Mahaim Fiber Following Localization of Mahaim Pathway Potentials
Authors: MOUNSEY J. PAUL , GRIFFITH MICHAEL J. , McComb JANET M.
Published: May 2007

Mahaim Fiber Ablation. We report radiotfrequency ablation of a Mahaim fiber in a patient with wide complex supraventricular tachycardia. Pathway potentials from the lateral aspect of the right AV groove were recorded, which were distinct from the His potential. During atrial pacing, decremental properties of the fiber were demonstrated, which resulted in prolongation of the interval between the atrial electrogram and the Mahaim pathway potential. The pathway potentials, preexcitation, and tachycardia disappeared after a single application of radiofrequency energy, after which the patient has remained free of palpitations. Mapping of a Mahaim fiber by identifying pathway potentials thus allowed accurate localization and successful ablation with minimal energy. We therefore suggest that, where possible, recording of such Mahaim potentials may be the optimal technique for Mahaim liber localization.
Bridging the Gap Between Basic and Clinical Electrophysiology:
Authors: FRANZ MICHAEL R.
Published: May 2007

Monophasic Action Potentials. With rapid advances occuring in both basic and clinical electrophysiology, the gap between the two disciplines appears to be widening rather than narrowing. In most instances, we cannot apply the knowledge derived from cellular studies directly to clinical practice. Monophasic action potential (MAP) recording by contact electrode technique allows us in measure basic electrophysiological phenomena in the human heart and thus provides an important bridge between basic and clinical electrophysiology. MAP recordings produce the lime course of cellular repolarization during cycle length changes and antiarrhythmic drug administration, lending insights into use dependency and reverse use dependency of antiarrhythmic drug effects in the clinical electrophsiology laboratory. The ability to deliver electrical stimuli at the MAI recording site further allows one to investigate drug‐induced postrepolarization refractoriness. MAP recordings provide precise local activation times, important for mapping of abnormal ventricular activation, and detect areas of abnormal repolarization due to ischemia or scarring. MAP recordings are uniquely suited to detect early and delayed afterdepolarizations in the human heart, thereby helping to unravel the arrhythmia mechanisms in the long QT syndrome. By embedding the MAP electrode in a radiofrequency electrode, arrhythmogenic foci may be both detected and ablated. In many instances, MAP recordings are more accurate than KCG tracings in defining and distinguishing ventricular fibrillation and ventricular tachycardia. This can he of clinical importance during testing of the implantable cardioverler/delibrillator. An area of growing interest is stretch‐activated arrhythmias. Here, MAP recordings are of particular value because no other method is available to record mechanically induced electrophysiological changes in the vigorously beating heart. It can be expected that MAP recordings will, in the future, provide this important bridge between “cell and bedside” also in atrial tachyarrhythmias, such as in atrial fibrillation and flutter.
A Prospective Randomized Comparison of Defibrillation Efficacy of Truncated Pulses and Damped Sine Wave Pulses in Humans
Authors: BARDY GUST H. , ZAGHI HEDAYATOLLAH , GARTMAN DAVID , E JEANNE , KUDENCHUK PETER K. , LEE DOLACK G. , JOHNSON GEORGE , TROUTMAN CHARLES
Published: May 2007

Damped Sine Wave Defibrillation Pulses. Introduction: Damped sine wave pulses have been used for nearly 50 years in transthoracic defibrillation systems. The purpose of this study was to determine whether damped sine wave pulses have a role in implantable defibrillators.

Methods and Results: In 21 survivors of cardiac arrest, we prospectively compared defibrillation efficacy of a standard truncated capacitor (RC) monophasic pulse with a damped sine wave inductor‐capacitor (LRC) pulse using a right ventricular‐left ventricular epicardial patch‐patch electrode system. The RC pulse was a standard 65% tilt monophasic waveform generated from a 120μF capacitor. The LRC pulse was designed to simulate the waveform currently used in transthoracic defibrillators and was generated by passing the charge stored on a 40μF capacitor through a 37‐mH inductor. Capacitor voltage, peak delivered voltage, peak delivered current, discharge pathway resistance, delivered energy, and stored energy were compared for the two waveforms at the defibrillation threshold. There was no difference in defibrillation efficacy for the two waveforms. Peak delivered voltage was similar at the defibrillation threshold: 313 ± 101 V for the RC pulse and 342 ± 119 V for the LRC pulse (P = 0.16). Similarly, no differences were found in defibrillation threshold peak delivered current: 8.6 ± 2.5 (RC) versus 9.3 ± 2.7 (LRC) amperes (A) (P = 0.20); discharge pathway resistance: 37 ± 11 (RC) versus 38 ± 13 (LRC) O (P = 0.71); delivered energy: 7.0 ± 4.5 (RC) versus 7.0 ± 4.0 (LRC) joules (J) (P = 0.88); and stored energy: 8.7 ± 5.7 (RC) versus 9.8 ± 5.4 (LRC) J (P = 0.35). Although both waveforms performed the same, it was necessary to use substantially higher stored voltages with the damped sine wave delivery system than with the truncated waveform delivery system: 356 ± 110 V for the RC pulse and 675 ± 192 V for the LRC pulse (P < 0.0001).

Conclusion: This study demonstrates that RC monophasic pulses provide equally effective epicardial defibrillation as LRC pulses with respect to delivered voltage and current and stored and delivered energy. However, in order for LRC pulses to provide comparable delivered voltage, current, and energy to that of RC pulses, nearly twice the voltage must be stored on the capacitor to accomplish the same task. These findings suggest that despite the nearly 50‐year experience with damped sine wave pulses with transthoracic defibrilliitors, there is no need to begin using damped sine wave pulses for implantabte defibrillators. Moreover, these data raise a question regarding the need for inductors in transthoracic defibrillators.
Radio frequency Catheter Ablation of Sustained Intraatrial Reentrant Tachycardia in a Patient With Mirror‐Image Dextrocardia
Authors: WU TSU‐JUEY , CHEN SHIH‐ANN , CHIANG CHERN‐EN , YANG CHIN‐JUEY , CHENG CHEN‐CHUAN , WANG SHIH‐PU , CHIANG BENJAMIN N. , CHANG MAU‐SONG
Published: May 2007

RF Catheter Ablation in Dextrocardia. Introduction: There has been limited experience with radio frequency catheter ablation in patients with Dextrocardia. This report describes a 37‐year‐oid man who had corundum type Atrial septal defect, mirror‐image Dextrocardia, and drug‐refractory Atrial tachycardia, in whom catheter‐mediated radio frequency energy successfully eliminated the tachycardia without complication.

Methods and Results: On electrophysiologica study, the Atrial tachycardia could be induced and terminated by Atrial extra stimulation or rapid Atrial pacing. Mixed resetting response pattern and manifest entrainment were also demonstrated. These findings suggested that the mechanism of atrial tachycardia might be related to reentry with an excitable gap. Because of the mirrorimage dextrocardia, biplane fluoroscopy was adjusted to the right anterior oblique (RAO) 60°G and left anterior oblique (LAO) 30° positions. Inducibility of the tachycardia was completely abolished after the sixth application of radiofrequency current (30 W). It was noted that the successful electrogram preceded the onset of P wave during Atrial tachycardia by about 40 msec.

Conclusion: This report presents another case in which radiofrequency catheter ablation was used in a patient with Dextrocardia. Atrial tachycardia in patients with congenital heart disease may be difficult to control pharmacologically; however, the use of radiofrequency catheter ablation could be recommended as an alternative to medication and surgery.
Wide Complex Bigeminy:
Authors: KANTER RONALD J. , SABA ZIAD , GARSON ARTHUR
Published: May 2007

Bigeminal Rhythm Using Atriofascicular Fiber. Ventricular bigeminy in children is regarded as a benign arrhythmia in the absence of coexisting heart disease. We present the case of a patient with an atriofascicular fiber that electrocardiographically presented as wide complex bigeminy and wide complex tachycardia. At electrophysiologic study, the mechanism for the wide complex extrasystoles was reentry within the atriofascicular fiber or at its atrial insertion. Retrograde conduction within the fiber was also demonstrated under the influence of verapamil and ventricular extrastimulus testing. We conclude that conduction through an atriofascicular fiber should be included in the differential diagnosis of wide complex bigeminy having left bundle branch block morphology.
Spatial and Temporal Inhomogeneity of Adenosine's Effect on Atrial Refractoriness in Humans:
Authors: BOTTERON GREGORY W. , SMITH JOSEPH M.
Published: May 2007

Adenosine's Effects on Atrial Refractoriness. Introduction: Adenosine is an antiarrhythmic agent widely used for the diagnosis and treatment of supraventricular tachyarrhythmias. Bolus administration of adenosine has been associated with transient atrial fibrillation, but the underlying mechanisms have not yet been delineated, due in part to the technical limitations resulting from adenosine's short half‐life. In this study, the rapid, repetitive activation of atrial tissue during atrial fibrillation was exploited to yield a nearly continuous estimate of atrial refractoriness, enabling a description of adenosine's action on atrial refractoriness in humans.

Methods and Results: Simultaneous right and left atrial, narrow‐spaced, bipolar electro‐grams were recorded in 15 patients before, during, and after bolus administration of 12 mg of adenosine during atrial fibrillation. By estimating the local cycle length of excitation from the atrial activation frequency, a refractory period index (RPI) of local tissue was obtained. Adenosine dramatically increased the activation frequency from 6.4 ± 0.7 to 12.2 ± 12.2 Hz in the right atrium and from 6.1 ± 0.6 to 8.7 ± 1.2 Hz in the left atrium, corresponding to a decrease in the RPI from 156 to 82 msec (P < 0.0001) and from 163 to 116 msec (P < 0.0001), respectively. The magnitude of adenosine's effect was greater (47% vs 29% shortening) (P < 0.001) and the duration of adenosine's effect longer (28 vs 19 sec) (P < 0.05) in the right compared to the left atrium.

Conclusion: Adenosine, at doses routinely used clinically, produces a transient, but spatially and temporally inhomogeneous, shortening of atrial refractoriness, which may explain the increased propensity toward atrial fibrillation associated with its use.
Role of Calcium Loading in Early Afterdepolarizations Generated by Cs+ in Canine and Guinea Pig Purkinje Fibers
Authors: SZABO BELA , KOVACS TIBOR , LAZZARA RALPH
Published: May 2007

Ca2+‐Loading and EAD. introduction: Our previous observations indicate that the Na2+:Ca2+ exchange current (INa:Ca) plays an important role in early afterdepolarizations occurring at more negative Vm (L‐EAD). The purpose of these studies was to examine the role of Ca2+‐loading, which stimulates INa:Ca, in generation of L‐EAD.

Methods and Results: Purkinje strands and preparations of ventricular myocardium from dogs and guinea pigs were superfused with oxygenated physiologic buffer solutions at 37°C, To induce EADs, [K+]0 was reduced to 2.0 to 3.0 mM and [Cs+]0, (3.6 to 4.0 mM) was added at slow rates of ≤ 0.3 Hz. Isometric contraction in canine Purkinje strands and guinea pig papillary muscles doubled in 1‐hour exposure to Cs+ and low [K+]0 at slow rates, and the uptake of 45Ca2+ was approximately doubled after 30 minutes. Forty‐three percent of Purkinje fibers developed L‐EAD after a latent period of 17 to 123 minutes of exposure. Ouabain (0.2 μM) suppressed LEAD within 10 minutes reversibly. Ca2+‐loading (low [Na+]0 or high [Ca2+]0 for 5 to 10 minutes before exposure to Cs+, low [K+]0, and slow rates resulted in rapid development of L‐EAD in all preparations during subsequent exposure. In Ca2+‐loaded preparations, delayed afterdepolarizations (DADs) as well as L‐EADs developed.

Conclusion: Reduction of K+ currents with Cs+, low [K+]0, and slow rates induced L‐EAD in a fraction of Purkinje fibers after a latent period during which Ca2+‐loading of the sarcoplasmic reticulum occurred, while fibers preloaded with Ca2+ developed L‐EAD rapidly and uniformly. These findings indicate that Ca2+‐loading is a critical condition for the development of L‐EAD. Early suppression of L‐EAD by ouabain suggests a dependence of L‐EAD on low [Na+]1. These findings implicate INa:Ca in the generation of L‐EAD.
Expanding Indications for the Use of Class III Agents in Patients at High Risk for Sudden Death
Authors: SINGH BRAMAH N.
Published: May 2007

Expanding Indications of Class III Agents. The evidence that antiarrhythmic compounds that act by slowing conduction velocity increase mortality in patients with cardiac disease is now compelling. Emphasis is now shifting to agents that act by lengthening repolarization and have additional antiadrenergic properties. There is preliminary evidence that pure Class III agents devoid of antisympathetic activity may also increase rather than decrease mortality in certain patients. Thus, in recent years, sotalol and amiodarone have emerged as the preferred agents for the control of most ventricular arrhythmias occurring in the setting of significant heart disease. Sotalol has not been widely studied in postinfarct patients; one trial indicated that the drug did reduce total mortality but the difference did not reach statistical significance. A number of studies with amiodarone in the postmyocardial infarction patients have revealed benefit, but these were from nonblinded studies. Two blinded, placebo‐controlled studies are currently ongoing. A potential new indication of amiodarone is in patients with arrhythmias in heart failure in whom amiodarone markedly increased left ventricular ejection fraction, with a pronounced suppressant effect on premature ventricular complexes and nonsustained ventricular tachycardia and a trend for a decrease in mortality in patients with nonischemic cardiomyopathy. The most promising Indication of amiodarone in low doses is in the maintenance of sinus rhythm in patients with atrial flutter and fibrillation. For the present, amiodarone appears to be the best prototype of a desirable complex antiarrhythmic compound, if its variegated side effect profile can be favorably modified from knowledge of structure‐activity relationships.
Drugs Versus Devices: Contemporary Practice in Light of Contemporary Trials
Authors: EPSTEIN ANDREW E.
Published: May 2007

Antiarrhythmic Drugs Versus Devices. In years past, the secondary prevention of life‐threatening ventricular arrhythmias was limited to empiric drug therapy. In close temporal proximity to the birth of electrophysiologic study‐guided treatment strategies to manage these arrhythmias, devices to convert arrhythmias were envisioned and designed. Now, advanced generation implantable defibrillators provide synchronized, low‐energy cardioversion, anti‐tachycardia pacing, and pacing support for bradycardia. Over the past decade and a half, this technology that was once applied as a therapy of last resort has evolved and emerged as a therapy of first choice. Recently, however, enthusiasm for drug treatment strategies has also increased, especially the use of amiodarone. Most experts now agree that drug therapy chosen by electrophysiologic study guidance provides superior survival compared to the empiric use of Class I drugs, as long as a drug that suppresses arrhythmia inducibility is found. The empiric use of amiodarone and beta blockers may also improve outcome. This review examines some of the recent clinical trials utilizing pharmacologic and nonpharmacologic methods. The importance of ongoing and future clinical trials is emphasized.