bluuebunny/crossref_metadata_2025 huggingface dataset:
“Supernormal” Conduction and Excitability
Authors: MOORE E. NEIL , SPEAR JOSEPH F. , FISCH CHARLES
Published: May 2007

“Supernormal” Conduction and Excitability. Electrocardiograph manifestation of “supernormal” conduction is defined as conduction that is more rapid than expected or presence of conduction when block is anticipated. It is not supernormal in the sense of being more rapid than normal. Therefore, the term relative supernormality or “supernormality” is more appropriate. The mechanism of “supernormal” conduction is conduction during a period of supernormal excitability and conduction associated with altered membrane potential. Some of the more common phenomena that are not dependent on conduction during the supernormal period but manifest better than expected conduction, thus simulating “supernormal” conduction, include dual AV nodal conduction, the “gap” phenomenon, “peeling back” of the refractory period, summation of subthreshold responses, diastolic phase 4 depolarization, and phasic autonomic influences.
Inducibility of Atrial Fibrillation Before and After Radiofrequency Catheter Ablation of Accessory Atrioventricular Connections
Authors: KALBFLEISCH STEVEN J. , El‐ATASSI RAFEL , CALKINS HUGH , LANGBERG JONATHAN J. , MORADY FRED
Published: May 2007

Inducibility of Atrial Fibrillation. Introduction: The purpose of this study was to evaluate the inducihility of atrial fibrillation in patients with an accessory atriovcentricular connection (AAVC) and to determine if the inducibility of atrial fibrillation is altered after successfulradiofrequency catheter ablation of the AAVC.

Methods and Results: Thirty‐seven patients with an AAVC and 36 control patients wereprospectively evaluated using a standardized atrial pacing protocol. The high right atrium waspaced using a 25‐beat drive train, 1.5‐second intertrain pause, 10‐mA pulse amplitude, and 2‐msec pulse duration at cycle lengths of 250 to 100 msec, in 10‐msec decrements. Pacing wasperformed twice at each cycle length. Thirty patients with an AAVC underwent repeat atrialoverdrive pacing after successful radiofrequency ablation of the AAVC. Atrial fibrillation wasinduced in 26 (70%) patients with an AAVC and 22 (61 %) controls (P = NS). Atrial flutter wasinduced in 26 (70%) patients with an AAVC and 22 (61%) controls (P = NS). The cumulativepercentage of patients with atrial fibrillation/flutter induced at each pacing cycle length was thesame in each group. There was no difference in the duration of atrial fibrillation/flutterbetween control patients and patients with an AAVC. Among the 30 patients who underwentrepeat atrial overdrive pacing after radiofrequency ablation of an AAVC, there was no difference in the inducibility or duration of atrial fibrillation/atrial flutter after ablation compared tobaseline.

Conclusion: These findings indicate that the vulnerability of the atrium to fibrillate inresponse to atrial pacing is independent of the presence of an AAVC.
Radiofrequency Catheter Ablation of AtypicalAtrioventricular Nodal Reentrant Tachycardia
Authors: STRTCKBERGER S. ADAM , KALBFLBISCH STEVEN J. , WILLIAMSON BRIAN , MAN K. CHING , VORPERIAN VICKEN , HUMMEL JOHN D. , LANGBERG JONATHAN J. , MORADY FRED
Published: May 2007

Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia, Introduction: Published reports of radiofrequency ablation of atypical atrioventricular nodal reentranttacbycardia (AVNRT) have been limited. We present our experience in 10 consecutive patientswith atypical AVNRT wbo underwent radiofrequency ablation of the “slow” AV nodal pathway.

Methods and Resttlts: there were 9 females and 1 male; their mean age was 44 ± 19 years (± SD), the mean AVNRT cycle length and ventriculoatrial (VA) interval at the His positionduring AVNRT were 340 ± 50 msec and 200 ± 70 msec, respectively. the slow pathway wassuccessfully ablated in all patients with a mean of 10 ± 7 radiofrequency energy applications inthe posteroseptal right atritim near the coronary sinus os. The mean procedure duration was 100 ± 35 minutes. There were no complications. In 4 patients, target sites were identified during sinus rhythm by mapping for possible slow pathway potentials, In the other 6 patients, target sites were identified by mapping retrograde atrial activation during AVNRT or ventricularpacing, The VA times at successful target sites were a mean of 45 ± 30 msec less tban the VAtime at the His cathetcr during AVNRT, There were no differences in success rate, number ofradiofrequency energy applications, or procedure duration between patients in whom mappingwas guided by possible slow pathway potentials or by retrograde atrial activation, During 6 ± 3 months of followup, 1 patient bad a recurrence of atypical AVNRT and underwent a secondablation procedure, which was successful.

Conclusion: Radiofrequency ablation of atypical AVNRT can be safely and effectivelyaccomplisbed when target sites are identified based either on possible slow pathway potentialsduring sinus rbytbm or retrograde atrial activation times during tachycardia.
A Quantitative Measurement of Spatial Orderin Ventricular Fibrillation
Authors: BAYLY PHILIP V. , JOHNSON ERIC E. , WOLF PATRICK D. , GREENSIDB HENRY S. , SMITH WILLIAM M. , IDEKER RAYMOND E.
Published: May 2007

Quantifying Spatial Order in Fibrillation. Introduction: The degree of organization in ventricular fibrillation (V F) is not known. As an objective measurement of spatial order, spatial correlation functions and their characteristic lengths were estimated from epicardial electrograms of pigs in VF.

Methods and Results: VF was induced by premature stimulation in five pigs, EIectroj;raniswere simultaneously recorded with a 22 × 23 array of unipolar electrodes spaced 1.12 mmapart, Data were obtained by sampling the signals at 2000 Hz for 20 minutes immediately afterthe initiation of VF. Correlations between all pairs of signals were computed at various times.Correlation lengths were estimated from the decay of average correlation as a function of electrode separation. The correlation length of the VF in pigs was found to be approximately 4 to 10 mM. varying as fihrillation progressed. The degree of correlation decreased in the first 4 seconds after fibrillation then increased over the next minute.

Conclusion: The correlation length is much smaller than the scale of the heart, suggestingthat many independent regions of activity exist on the epicardium at any one time. On theother hand, the correlation length is 4 to 10 times the interelectrode spacing, indicating thatsome coherence is present. These results imply that the heart behaves during VF as a highdimensional, but not random, system involving many spatial degrees of freedom, which mayexplain the lack of convergence of fractal dimension estimates reported in the literature.Changes in the correlation length also suggest that VF reorganizes slightly in the first minuteafter an initial breakdown in structure.
Cardiac Arrhythmias in Chagas’Heart Disease
Authors: ELIZARI MARCELO V. , CHIALE PABLO A.
Published: May 2007

Chagas’ Heart Disease. Chagas’ disease is a chronic parasitosis affecting most LatinAmerican countries, Its most important clinical manifestation is a late developing chronicmyocarditis and, much less frequently, an early acute myocarditis, Chagasic myocardial damage is microfocal and disseminated throughout the heart, In most cases, the coexistence ofareas of myocytic degeneration, inflammatory infiltration, and fibrosis suggests a permanentevolving process. Commonly, chronic chagasic myocarditis resemhies a dilated cardiomyopa–thy, with characteristic ECG abnormalities (atrial and ventricular extrasystoles, intraventricular and/or AV conduction disturbances, and primary ST‐T wave changes), Since myocardialdamage is scattered throughout the heart, the ECG abnormalities (arrhythmias, conductiondisturbances, and repolarization changes) are also representative of the widespread cardiacinvolvement. Thus, sick sinus syndrome, atrial extrasystoles, intraatrial conduction disturbances, and atrial fibrillation or flutter are common findings in different stages of the disease, At the ventricular level, both conduction disturbances and arrhythmias are conspicuousexpressions of the myocardial damage. Right bundle branch block alone or in combinationwith left anterior hemiblock are the most common conduction defects, Further compromise ofthe conduction system can lead to different degrees of AV block, Chagas’ disease is the maincause of bundle branch block and AV block in endemic areas, In advanced cases of Chagas'heart disease, ventricular premature contractions are extremely frequent, multiforM. andrepetitive (couplets and runs of ventricular tachycardia), and show R on T phenomenon, Thesearrhythmias are usually aggravated by increased sympathetic tone, implying an enbanced riskof cardiac sudden death among chagasic patients, which is sometimes the first manifestation ofthe illness, Chronic chagasic myocarditis is the leading cause of cardiovascular death, mostly asa consequence of heart failure and sudden death, in areas where the disease is endemic.
Endocardial Mapping of Reentry Around an Anatomical Barrier in the Canine Right Atrium:
Authors: PINTO JUDITH M.B. , GRAZIANO JOSEPH N. , BOYDEN PENELOPE A.
Published: May 2007

Flecainide and Atrial Reentry. Introduction: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y‐shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier.

Methods and Results: To investigate the mechanism of flecainide‐induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 ± 24 msec) by 89% to 309 ± 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In flve episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (± 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long‐short cycle length oscillations led to return reexcitation by the impulse within the primary path and suhsequent termination.

Conclusion: In summary, similar to our previous findings with the Class III agent, d‐sotalol, two different modes of termination of atrial reentry were observed with flecainide.
Congenital Disorders of Cardiac Rhythm and Conduction
Authors: JAMES THOMAS N.
Published: May 2007

Congenital Arrhythmias and Heart Block. Electrical instability of the heart has numerous congenital origins. This review approaches the problems from a morphological standpoint, utilizing selected examples from my own studies of the human cardiac conduction system performed during the last three decades. Subjects discussed include multifocal Purkinje cell tumors, benign congenital polycystic tumors of the AV node, several types of congenital heart hlock, postnatal morphogenesis of the AV node and His bundle (including considerations of persistent fetal dispersion and crib death), the Wolff‐Parkinson‐White syndrome, left superior vena cava, focal fibromuscular dysplasia of small coronary arteries, hereditary neuromus‐cular or musculoskeletal diseases, familial atrial fibrillation, long QT syndrome, and apoptosis of the heart. In many congenital disorders of cardiac electrical activity, both arrbythmias and conduction disturbances may occur. How the abnormal anatomy may relate to cardiac electrical instahility is discussed, including certain clinical matters to he considered.
Influence of ANP on Sympathetic Nerve Activity and Chronotropic Regulation of the Heart
Authors: IMAIZUMI TSUTOMU , TAKESHITA AKIRA
Published: May 2007

Physiological Effects of ANP. hypotension caused by atrial natriuretic peptide (ANP) is often not accompanied by the anticipated increases in beart rate or sympathetic nerve activity. the sympathetic inhibitory action of ANP occurs in cardiac and noncardiac sympathetic nerves, and has been demonstrated in conscious or anesthetized animals as well as in humans. The sympathetic inhibition by ANP occurs after atropinization but is abolisbed after va‐gotomy. Thus, ANP alters sympathetic nerve activity by influencing cardiopulmonary barore‐ceptors, wbich in turn is mediated by vagal afferents. In addition to the effects of ANP on cardiopulmonary baroreceptors, ANP affects arterial baroreceptors. ANP dilates the ascending aorta where some of the arterial baroreceptors are located, causing resetting of these arterial baroreceptors. When ANP is microinjected into the cerebroventricle or nucleus tractus soli‐tarii, it causes inhibition of sympathetic nerve activity. It has been shown tbat ANP inhibits sympathetic ganglionic transmission and augments cardiac parasympathetic effects on heart rate. Thus., ANP may play important roles in cardiovascular regulation by influencing sympathetic nerve activity and beart rate in addition to the direct vasodilating and renal effects.
Spontaneous Myocardial Calcium Oscillations:
Authors: LAKATTA EDWARD G. , GUARNIERI THOMAS
Published: May 2007

Spontaneous Myocardial Calcium Oscillations. The physiological oscillation of cytosolic that underlies each heart heat is generated by the sarcoplasmic reticulum (SK) in response to an action potential (AP) and occurs relatively synchronously within and among cells. When the myocardial cell and SR loading become sufficiently high, the SK can also generate spontaneous, i.e., not triggered by sarcolemmal depolarization, oscillations The purpose of this review is to describe properties of S‐CaOs in individual cells, myocardial tissue, and the intact heart, and to examine the evidence that may link S‐CaOs to the initiation or maintenance of ventricular fibrillation (VF). The SR Ca2+ release that generates S‐CaOs occurs locally within cells and spreads within the cell via Ca2+‐induced Ca2+ release. The localized increase in cytosolic [Ca2+] due to S‐CaOs may equal that induced by an AP and causes oscillatory sarcolemmal depolarizations of cells in which it occurs. These oscillatory depolarizations are due to activation of the Na/Ca exchanger and of nonspecific cation channels. Asynchronous occurrence of diastolic S‐CaCs among cells within the myocardium causes inhomogencity of diastolic SR loading; this leads lo inhomogeneity of the systolic cytosolic [Ca2+] transient levels in response to a subsequent AP, which leads to heterogeneity of AP repolarization, due to heterogeneous modulation of the exchanger, nonspecific cation channels, and of the L‐type channel. In a tissue in which asynchronous S‐CaOs are occurring in diastole, the subsequent AP temporarily synchronizes SR Ca2+ loading and release within and among cells. Varying extents of synchronized S‐Caos then begin to occur during the subsequent diastole. The partial synchronization of this diastolic S‐CaOs among celts within myocardial tissue produces after contractions and diastolic depolarizations. When S‐CaOs are sufficiently synchronized, the resultant depolarizations summate and can be sufficient to trigger a spontaneous AP. S‐CaOs occurrence within some cells during a long AP plateau also modulates the removal of voltage inactivation of L‐type channels and increases the likelihood for “early after depoializations” to occur in myocardial tissue. S‐CaOs have an apparent modulatory role in the initiation at VF in the CV+ overload model and in the reflow period following ischemia. Likewise, in non‐a priori Ca2+ overloaded hearts, S‐CaOs modulate the threshold for VF induction (induced typically by alternating current) but may not be essential for VF induction. The role of S‐CaOs in maintenance of VF in these VF models is less clear: to date there is no evidence that inhibition of S‐CaOs can abolish VF once it has been established. The precise definition of the role of S‐CaOs in the initiation and mechanisms of VF merits further study.
Rate‐Related and Autonomic Effects on Atrioventricular Conduction Assessed Through Beat‐to‐Beat PR Interval and Cycle Length Variability
Authors: LEFFLER CHRISTOPHER T. , SAUL J. PHILIP , COHEN RICHARD J.
Published: May 2007

Atrioventricular Conduction Variability. Introduction: Atrioventricular AV) conduction time varies on a beat‐by‐beat basis in response to the influences of cardiac efferent autonomic activity and rate‐dependent electrical recovery processes. The goals of this study were to distinguish these effects on AV conduction time and to compare the variability in sinoatrial and AV nodal function.

Methods and Results: The PR interval on the surface ECG served as an index of AV conduction time in this study of 14 adult human subjects undergoing a random interval breathing protocol. P and R waves were located by a template‐matching algorithm. Spectral analysis allowed frequency‐domain comparisons between PR and RR interval variability. Spectra of PR and RR intervals had similar power distributions, although the power of the RR interval spectra was much greater. Autonomic blockade with atropine plus propranolol reduced the power of both spectra. Standing significantly decreased the spectral power from 0.15 to 0.5 Hz for PR and RR spectra, and introduced a peak near 0.1 Hz in the mean PR and RR spectra, although the latter finding was significant only for the RR interval spectra. Propranolol had no significant effects on the PR and RR interval spectra. Linear regression analysis allowed quantification of the autonomic and recovery effects on AV conduction and showed which effect predominated. Simple linear regression confirmed in adults a previous finding in children that conduction time may be either positively or negatively correlated with cycle length. By multiple regression and transfer function analysis, the inverse relation seen in some subjects was attributed to the effect of recovery from the preceding cycle. With the preceding recovery period accounted for, the conduction time and cycle length of the current beat were positively correlated, presumably due to the parallel autonomic effects on the sinoatrial and AV nodes. The magnitude of the recovery effect predicted by the regression analysis was similar to published values.

Conclusion: A noninvasive evaluation of the surface ECG can be used to compare variability in AV conduction time and cycle length and characterize the effects of autonomic efferent activity and rate‐related recovery on AV nodal function.
Dynamic Behavior of the Atrioventricular Node:
Authors: BILLETTE JACQUES , NATTEL STANLEY
Published: May 2007

AV Nodal Memory. The wide variety of delays that the atrioventricular node can generate in response to an increased rate are explained by dynamic interactions between the three intrinsic properties of recovery, facilitation, and fatigue. The functional model presented suggests that any deviation of nodal conduction time from its minimum basal value represents, at any given time, the net sum of the effects produced by these properties. When a constant fast atrial rate is suddenly initiated, the node first “sees” a shortening in recovery time and responds by an increase in conduction time. This increase further shortens the recovery time of the ensuing beat, which is accordingly further delayed, and so on until a steady state is reached or a block occurs. However, these events do not occur alone. The second heat al the fast rate is conducted with a shorter conduction time than expected from the recovery time alone, and is therefore facilitated. These facilitatory effects develop within one short cycle and dissipate within one long cycle. They affect increasingly the conduction time of beats occurring with shorter cycle lengths. While steady‐state effects of recovery and facilitation occur within seconds, nodal conduction time continues to increase slowly over several minutes when a rapid rate is maintained. This effect is attributed to fatigue, which develops and dissipates with a slow, symmetric time course. The dynamics of these properties can now be directly studied with selective stimulation protocols, and have many implications for the understanding of nodal behavior in the context of supraventricular tachyarrhythmias.
Ultrastructural Observations in the Myocardium Beyond the Region of Acute Coagulation Necrosis Following Radiofrequency Catheter Ablation
Authors: NATH SUNIL , REDICK JAN A. , WHAYNE JAMES G. , HAINES DAVID E.
Published: May 2007

Ultrastructural Findings After RF Ablation. Introduction: We hypothesized that myocardial injury following radiofrequency (KF) catheter ablation may extend beyond the region of acute coagulation necrosis as defined by histochemical staining.

Methods and Results: Five RF lesions were created in vivo in the left ventricle of two dogs using a 4‐inm tipped ablation electrode in which RF power was adjusted to maintain an electrode‐tissue interface temperature of 85°C for 60 seconds. The lesions were bisected; one half of the lesions were stained with nitroblue tetrazolium (NBT) and the other half processed for electron microscopy. Three zones of interest were identified extending 0–3 mm, 3–6 mm, and > 6 mm from the visible pathologic lesion border. The degree of Ultrastructural injury to the myocardium was scored for each zone. Electron microscopy demonstrated the presence of significant abnormalities of the plasma membrane, mitochondria, sarcomeres, sarcoplasmic reticuluni, and gap junctions of myocytes, as well as damage to the microvasculature extending up to 6 mm beyond the pathologic lesion edge. The plasma membrane and gap junctions of myocytes and the microvasculalure appeared particularly sensitive to thermal injury, whereas the intercalated discs were relatively thermally resistant.

Conclusion: RF catheter ablation results in Ultrastructural damage to the myocardium extending up to 6 mm beyond the acute pathologic RF lesion border as denned by NBT histochemical staining.
Heart Rate and Heart Rate Variability in Normal Young Adults
Authors: COUMEL PHILIPPE , MAISON‐BLANCHE PIERRE , CATULI DIDIER
Published: May 2007

Heart Rate and Heart Rate Variability. Introduction: The relationships between heart rate (HR) and HR variability (HRV) are not simple. Because both depend on the autonomic nervous system (ANS), they are not independent variables. Technically, the quantification of HRV is influenced by the duration of the cardiac cycles. The complexity of these relationships does not justify ignoring HK when studying HRV, as frequently occurs.

Methods and Results: Using spectral and nonspectral methods, the HR and various normalized and non‐normalized indices of HRV were studied in 24‐hour recordings of a homogeneous cohort of seventeen 20‐year‐old healthy males. The HR‐HRV relationships were appraised by analyzing the same data in two different ways. The 24 mean hourly values provide consistent information on the circadian behavior of the indices, while the average 24‐hour individual data show a wide spectrum of normality. Combined approaches allow assessment of the direct impact of RR interval on HRV evaluation. The correlations between HR and normalized indices of HRV arc weaker in 24‐hour individual data than in pooled hourly data of the same individuals. These correlations are close to 1 in the latter case, which does not mean that measuring HRV is simply another method of evaluating HR, but that normal physiology supposes a harmonious behavior of the various indices. When considered individually without normalization, the specific indices of vagal modulation (high‐frequency band of the spectrum, short‐term HR oscillations of the nonspectral analysis) consistently increase at night and diminish during the day. However, the low‐frequency power, which supposedly reflects sympathetic influences, also increases at night, whereas more logically the longer HR oscillations would predominate during the day. Moreover, the selective analysis of HR oscillations during HR acceleration or decrease indicates that their behavior differs accordingly.

Conclusion: We recommend that closer attention be paid to the complex relationships between HR and HRV. The strong correlations found in healthy subjects may reflect either the physiological harmony of ANS functions or simple redundancy. Their tendency to deteriorate in diseased hearts suggests that redundancy is not the cause and that abnormalities of ANS functions are not demonstrated by HRV analysis alone.
Trans venous‐Subcutaneous Defibrillation Leads:
Authors: BLOCK MICHAEL , HAMMEL DIETER , BÖCKER DIRK , BORGGREFE MARTIN , BUDDE THOMAS , ISBRUCH FRANK , SCHELD HANS H. , BREITHARDT GUNTER
Published: May 2007

Effect of Transvenous Electrode Polarity on DFT. Introduction: The defibrillation threshold (DFT) of a transvenous‐subcutaneous electrode configuration is sometimes unacceptably high. To obtain a DFT with a sufficient safety margin, the defibrillation field can be modified by repositioning the electrodes or more easily by a change of electrode polarity. In a prospective randomized cross‐over study, the effect of transvenous electrode polarity on DFT was evaluated.

Methods and Results: In 21 patients receiving transvenous‐subcutaneous defibrillation leads, the DFT was determined intraoperatively for two electrode configurations. Two monophasic defibrillation pulses were delivered in sequential mode between either the right ventricular (RV) electrode as common cathode and the superior vena cava (SVC) and subcutaneous electrodes as anodes (configuration I) or the SVC electrode as common cathode and the RV and subcutaneous electrodes as anodes (configuration II). In each patient, both electrode configurations were used alternately with declining energies (25, 15, 10, 5, 2 J) until failure of defibrillation occurred. The DFT did not differ between both configurations (18.3 ± 8.2 J vs 18.9 ± 8.9 J; P = 0.72). Eleven patients had the same DFT with both electrode configurations, 5 patients a lower DFT with the RV electrode as cathode, and 5 patients a lower DFT with the SVC as cathode. Four patients had a sufficiently low DFT (≤ 25 J) with only 1 of the 2 configurations.

Conclusion: A change of electrode polarity of transvenous‐subcutaneous defibrillation electrodes may result in effective defibrillation if the first electrode polarity tested fails to defibrillate. In general, neither the RV electrode nor the SVC electrode is superior if used as a common cathode in combination with a subcutaneous anodal chest patch.
Flecainide
Authors: FALK RODNEY H. , FOGEL RICHARD I.
Published: May 2007

Flecainide. Flecainide is a Class IC antiarrhythmic agent whose primary electrophysiologic effect is a slowing of conduction in a wide range of cardiac tissues. It is well absorbed and effective in suppressing isolated premature ventricular contractions (PVCs) or nonsustained ventricular arrhythmia but has only a modest efficacy when electrophysiologic testing is used as an endpoint. Us adverse effect on mortality in the CAST trial suggested a propensity to proarrhythmia‐a phenomenon to which the Class IC agents appear particularly prone. Despite the applicability of the CAST study only to patients with a prior myocardial infarction, there has been a shift away from flecainide in ventricular arrhythmia, but the low noncardiac side effect profile of the agent allows for its continued use in a wide variety of supraventricular arrhythmias. (J Cardiovasc Electrophysiol, Vol. 5, pp. 964–981. November 1994)
Is There Any Indication for an Intracardiac Defibrillator for the Treatment of Atrial Fibrillation?
Authors: LÉVY SAMUEL , RICHARD PHILIPPE
Published: May 2007

ICD for Treatment of AF. The experience gained using intracardiac cardioverter defibrillators for the treatment of ventricular arrhythmias has prompted the development of an automatic atrial defibrillator capable of detecting and automatically terminating atrial fibrillation (AF). Experimental studies in sheep have shown that it is possible to terminate AF with energies ranging from < 1 to 7 joules [J], using biphasic shocks. The best electrode configuration using intracardiac catheters and/or a subcutaneous patch was two catheters, one in the right atrium and the other in the coronary sinus. Current studies in man focus on the answers to three questions. First, can the experimental results of atrial defibrillation derived from healthy anesthetized sheep without spontaneous AF be extrapolated to AF in man with areas of fibrosis within the atria and/or underlying heart disease in 80% of cases? Preliminary studies in man suggest that cardioversion of AF of short duration is feasible using a mean energy of 2 J. Second, are these energies well tolerated in an awake nonsedated patient? Energies < 1 J were well tolerated, but pain resulting from higher energies needs further investigation. Third, is low‐energy atrial defibrillation safe, i.e., is there a risk of ventricular arrhythmias induced by an atrial shock? Experimental results in sheep have shown that the risk of R wave synchronized shock to induce ventricular arrhythmias was only present when the preceding RR interval was shorter than 300 msec. The risk of proarrhythmia in man is undergoing evaluation and must be sufficiently low (< 0.1) before sanctioning implantation of a stand‐alone (without associated ventricular defibrillator) automatic atrial defibrillator. Preliminary data on 1212 shocks showed no proarrhythmia. There is definitely a significant group of patients with attacks of AF (Class IIIB or IIIC) that are resistant to antiar‐rhythmic therapy. Another group of symptomatic patients may have infrequent attacks, or poorly tolerated (syncope or heart failure) or long‐lasting attacks requiring medical intervention and/or hospitalization (Class IB, IIB), for whom an automatic atrial defibrillator may be a valuable option. The alternative therapies could be either catheter ablation of the AV node with implantation of a pacemaker or selective surgery. Most of the technical problems related to AF detection and reliable atrial defibrillation have been solved. However, clinical investigations are needed to evaluate the efficacy and safety of this new and exciting therapeutic modality.
Cesium Abolishes the Barium‐Induced Pacemaker Potential and Current in Guinea Pig Ventricular Myocytes
Authors: SHEN JIAN‐BING , VASSALLE MARIO
Published: May 2007

Cesium Abolishes Barium‐Induced PM Current. Introduction: The ability of cesium to block barium‐induced diastolic depolarization (“Ba‐DD”) and pacemaker current was tested in isolated ventricular myocytes. Because Ba‐DD is due to decreasing k conductance and there is no If at the resting potential, this approach permits verification of whether Cs+ is a specific blocker of I, or if it instead also blocks a K+ pacemaker current.

Methods and Results: Guinea pig isolated ventricular myocytes were studied by a discontinuous, single electrode, voltage clamp method. During hyperpolarizing voltage clamp steps from ‐80 up to ‐140 mV in Tyrode's solution, the inward current increased as a function of voltage but did not change us a function of time (no If or K+ depletion). Cesium (4mM) reduced the current size during the hyperpolarizing steps hut did not induce or unmask time‐dependent currents. Barium (0.05 to 0.1 mM) induced diastolic depolarization, and, in its presence, depolarizing voltage clamp steps were followed by an outward tail current that reversed at ‐92.0 ± 1.3 mV. Outward tail currents were larger at ‐50 mV than at the resting potential, and inward tail currents decayed more rapidly and to a larger extent during larger hyperpolarizing steps. In the presence of Ba2+, Cs+ (4 mM) had little effect on the steady‐state current but markedly reduced or abolished undershoot, Ba‐DD, and time‐dependent tail currents at potentials both positive and negative to the resting potential. Cs+ had a smaller effect on the steady‐state current‐voltage (I‐V) relation in the presence than in the absence of Ba2+, as part of the Ikl channels were already blocked by Ba2+ and the time‐dependent changes induced by Ba2+ were not present. Both Ba2+ and Cs+ had little blocking effect on the steady‐state current positive to the negative slope region of the I‐V relation.

Conclusion: In ventricular myocytes, Cs+ abolishes the Ba2+‐induced pacemaker current by blocking the time‐dependent change in K+ conductance, not by blocking If. Because Cs+ can also block a decaying K+ pacemaker current, the abolition of a pacemaker current by Cs+ in other cardiac tissues cannot be taken as unequivocal proof that the blocked current is If
Successful Catheter Ablation of Atrial Fibrillation
Authors: HAÏSSAGUERRE MICHEL , GENCEL LAURENT , FISCHER BRUNO , LE MÉTAYER PHILIPPE , POQUET FRANCK , MARCUS FRANK I. , CLEMÉNTY JACQUES
Published: May 2007

Catheter Ablation of AF. Introduction: Catheter ablation of a case of incessant atrial fibrillation was attempted using linear right atrial lesions created by sequential applications of radiofrequency energy.

Methods and Results: A 46‐year‐old patient had incessant episodes of atrial fibrillation. He had previously undergone successful radiofrequency catheter ablation of a common atrial flutter. Antiarrhythmic drugs including amiodarone and various drug combinations were ineffective. A 7‐French specially designed 14‐polar catheter with interelectrode distance of 3 mm was used to create linear lesions in the right atrium. Each electrode was 4 mm in length and able to transmit radiofrequency energy. Three linear lesions, two longitudinal and one transverse that connected the two longitudinal lesions, were created using 30 radiofrequency applications of 10 to 40 W. The final application interrupted an atrial fibrillation that had been persistent for 55 minutes. No sustained atrial fibrillation was inducible despite repeated pacing maneuvers. There was no complication. In short‐term follow‐up of 3 months, the patient has been free of arrhythmias without antiarrhythmic medication.

Conclusion: Successful catheter ablation of human atrial fibrillation is feasible using linear atrial lesions created by radiofrequency energy delivery. Further studies are mandatory to ascertain the efficacy and safety of this procedure, as well as to assess different catheter techniques.
Electrocardiographic and Electrophysiologic Properties of Cardiac Allografts
Authors: BABUTY DOMINIQUE , AUPART MICHEL , COSNAY PIERRE , SIRINELLI AGNES , ROUCHET SERGE , MARCHAND MICHEL , FAUCHIER JEAN PAUL
Published: May 2007

Electrophysiology and Cardiac Allografts. The increasing number of heart transplant patients requires that physicians be able to recognize the electrocardiographic (ECG) and electrophysiologic properties of cardiac allografts. Cardiac allografts are characterized by modifications of resting ECGs and frequent arrhythmias in the postoperative period, and the loss of autonomic nervous control illustrated by permanent tachycardia and loss of heart rate variability during 24‐hour ambulatory ECG recording. Some clinical and experimental observations suggest a mid‐term reinnervation of the cardiac allograft, but this requires histologic confirmation. The electrophysiologic characteristics of the denervated myocardium are similar to those of the innervated myocardium at rest. However, supersensitivit v to circulating cate‐cholamines has been observed in cardiac allografts as in experimentally denervated hearts, which is responsible for a progressive increase in heart rate during exercise and a slow decrease during recovery. Supersensitivity of the denervated heart to acetylcholine may explain the high prevalence of donor sinus dysfunction due to impairment of its automaticity. More often, the sinus node dysfunction is transient and can be treated with an adenosine antagonist, such as theophylline, before permanent implantation of a pacemaker. In the case of pacemaker implantation, synchronization of the donor atria with the recipient atria is desirable, and an endocardial lead implantation is preferred. Several electrophysiologic changt‐s have been observed during acute cardiac allograft rejection. From experimental studies, the most important of these are the disturbance of conduction in the atria and the atrioventricular node and a decrease in the amplitude of the ventricular potential. Initial studies on isolated myocytes show profound changes in membrane conductance during experimental cardiac rejection. The development of new noninvasive detection methods of cardiac allograft rejection, such as intramyocardial voltage electrogram monitoring and high‐resolution ECG, could help early diagnosis.
The Dynamic Range of Neonatal Heart Rate Variability
Authors: GRIFFIN M. PAMELA , SCOLLAN DAVID F. , MOORMAN J. RANDALL
Published: May 2007

Neonatal Heart Rate Variability. Introduction: Although it is generally appreciated that heart rate variability is low during severe illness, the extent, time course, and mathematical characteristics of heart rate variability during transitions between health and illness have not been systematically examined. The purpose of this study was to analyze heart rate variability in newborn infants during a rapid recovery from severe respiratory and circulatory failure.

Methods and Results: From prolonged ECG recordings, we evaluated heart rate variability in the time domain (mean, relative change, and coefficient of variation of RR intervals), in the frequency domain (using power spectra of the time series of RR intervals), and using a neural network. Qualitatively, RR interval plots showed little heart rate variability during severe illness but became “noisier” during recovery. Quantitatively, recovery was marked by twofold to threefold increases in time‐domain parameters, by eightfold increases in frequency‐domain parameters, and by more than 20‐fold increases in a neural network measure. Time‐domain and frequency‐domain measures were correlated, but not strongly. Heart rate variability reached stable levels by 4 to 5 days. Heart rate did not change dramatically.

Conclusion: Recovery from severe neonatal illness is accompanied by large and rapid increases in heart rate variability, but not by large changes in heart rate. This increase can be effectively assessed in the time domain, in the frequency domain, and by using a neural network.
Ablation of Left Free‐Wall Accessory Pathways Using Radiofrequency Energy at the Atrial Insertion Site:
Authors: DESHPANDE SANJAY S. , BREMNER SIOBHAN , SRA JASBIR S. , DHALA ANWER A. , BLANCK ZALMEN , BAJWA TANVIR K. , AL‐BITAR ISSAM , GAL RAMI , SARNOSKI JOSEPH S. , AKHTAR MASOOD , JAZAYERI MOHAMMAD R.
Published: May 2007

Transseptal versus Transaortic Ablation. Introduction: Transcatheter ablation of the left free‐wall atrioventricular accessory pathways (AP) by delivery of radiofrequency current at the ventricular insertion site has been shown to be effective. The efficacy of such a technique targeting the atrial insertion site of the AP was evaluated.

Methods and Results: One hundred consecutive patients with left free‐wall APs and symptomatic supraventricular tachyarrhythmias were included. APs were manifest in 55 patients and concealed in 45. There were 55 men and 45 women with a mean age of 35 years. A total of 107 left free‐wall APs were identified in these patients. In these 100 patients, successful ablation was accomplished in all by using a transseptal (45 patients) or transaortic (54 patients) technique. In one patient, ablation was accomplished from within the coronary sinus. Seven patients required a repeat ablative procedure, which was performed successfully. During 107 ablative procedures, six were associated with nonfatal complications including pericardial effusion (hemopericardium) in two patients, mild mitral regurgitation in two patients, swelling of the left arm in one patient, and staphylococcal bacteremia in one patient. Eighty‐two (82%) patients underwent a repeat electrophysiologic study 6 to 8 weeks after successful ablation and were found to have no functioning AP or inducible supraventricular tachycardia. During a mean follow‐up of 20 ± 8 months, none of the 100 patients had a recurrence of tachyarrhythmias.

Conclusion: These data indicate that the atrial insertion site of the AP can be successfully ablated in the majority of patients with left free‐wall APs by using cither a transseptal or transaortic approach. Furthermore, both techniques are associated with minimal morbidity and no mortality.
Abnormal Automaticity as Mechanism of Atrial Tachycardia in the Human Heart—Electrophysiologic and Histologic Correlation:
Authors: DE BARKER JACQUES M.T. , HAUER RICHARD N.W. , BAKKER PATRICIA F.A. , BECKER ANTON E. , JANSE MICHIEL J. , DE MEDINA ETIENNE O. ROBLES
Published: May 2007

Abnormal Automaticity in Human Atrium, introduction: A 32‐year‐old woman was operated upon because of drug refractory atrial tachycardia.

Methods and Results: Electrophysiologic study was performed prior to operation. During surgery, epicardial mapping of the electrical activity of the left atrium was performed. The left atrial appendage was resected and studied in a tissue bath. Thereafter, histologic examination was performed. Polarity of the P wave in the surface ECG suggested that the tachycardia originated high in the left atrium. Epicardial mapping disclosed earliest activation in the apex of the left atrial appendage. Intracellular recordings from surgical specimen made at the site of origin, which was marked during surgery, revealed cells with phase 4 depolarization at cycle lengths ranging from 360 to 540 msec. Exit block prevented spread of activation from the spontaneously firing cells to surrounding tissue. Histology showed that spontaneous activity arose in an area with abnormal cells‐characterized by an amorphous, pale eosinophilic staining cytoplasm and absence of nuclei‐surrounded by normal myocytes.

Conclusion: The observations indicate that the mechanism of the atrial tachycardia was based on abnormal automaticity in an area consisting of a conglomeration of normal and abnormal myocytes.
Pleomorphic Ventricular Tachycardia with Antegrade His‐Bundle Activation:
Authors: TAI YAU‐TING , LEE KATHY LAI‐FUN
Published: May 2007

His‐Bundle Activation During VT. The use of multiple His bundle‐right hundle branch recordings in electrophysiologic studies has facilitated definition of the mechanism and elucidation of the direction of impulse propagation in bundle branch reentrant tachycardia, “Mahaim” fiber reciprocating tacbycardia, and retrograde His depolarization in fascieular or ventricular tacbycardias. This report details the electrophysiologic evaluation of pleomorphic ventricular tachycardia in a patient with advanced coronary heart disease. The ventricular tachycardia at baseline revealed variation in the QRS duration without alteration of the elec‐trocardiographic (ECG) morphology. Following flecainide administration, a ventricular tachycardia with close resemblance of tbe ECG morpbology to sinus rbytbm was induced. Proximal and distal His‐bundle recordings revealed early antegrade His‐bundle activation during tbis tacbycardia. Programmed stimulation converted this tachycardia back to tbe clinical ventricular tacbycardia witb intermittent narrowing of the QRS complexes. Early His activation was evident only during the narrower complexes but not in tbe tacbycardia beats witb wide complex. Penetration of the His bundle by ventricular tacbycardia, witb resultant fusion from intramyocardial ventricular activation and His‐Purkinje activation, could have accounted for tbe near normalization of tbe QRS morphology during the ventricular tachycardia.
Electrophysiologic Basis for T Wave Alternans as an Index of Vulnerability to Ventricular Fibrillation
Authors: VERRIER RICHARD L. , NEARING BRUCE D.
Published: May 2007

Electrophysiologic Basis for T Wave Alternans. Substantial evidence indicates that T wave alternans is an intrinsic property of ischemic myocardium. The electrophysiologic basis appears to be spatial and temporal heterogeneity of repolarization resulting from changes in action potential morphology rather than in activation sequence. Ischemia‐induced changes in postrepolarization refractoriness and depressed electrical restitution of action potential duration have also been implicated. The main underlying ionic basis for T‐wave alternans during coronary occlusion appears to be derangements in intracellular cycling of calcium. Accumulation of potassium in the extracellular space adjoining ischemic cells and disruption in electro‐genie sodium‐calcium exchange may also be involved. In humans, T wave alternans has been observed in Prinzmetal's and classical angina, angioplasty, and bypass graft occlusion. Under these conditions associated with acute myocardial ischemia, alternans is restricted to the ischemic zone, and alternation in action potential morphology is an underlying factor. Recently, repolarization alternans has been shown to be a statistically significant predictor of the results of electro physiologic testing and arrhythmia‐free survival in individuals with and without organic heart disease. Collectively, these observations provide a rationale for quantitation of T‐wave alternans magnitude for assessment of vulnerability to life‐threatening ventricular arrhythmias both in response to and independent of the effects of myocardial ischemia.
Resting and Action Potentials of Nonischemic and Chronically Ischemic Human Ventricular Muscle
Authors: MUBAGWA KANIGULA , FLAMENG WILLEM , CARMELIET EDWARD
Published: May 2007

Membrane Potentials in Human Ventricle. Introduction: The effect of chronic ischemia on the electrical properties of human cardiac tissue is not well understood.

Methods and Results: Membrane potentials were studied using microelectrode techniques in isolated human ventricular tissues obtained from nonischemic (n = 17) or chronically ischemic (n = 71 myocardium. In normal Tyrode's solution, resting potential (Vr) was lower in ischemic (−70.1 · 2.12 mV) than in nonischemic muscles (−77.6 · 0.93 mV; mean · SKM; P < 0.051. In high [K]0 (> 10 mM) media, V, was of similar magnitude in both types of tissue (in 21.6 mM [K]0 Vr was −53.1 · 2.24 mV in nonischcmic and −49.6 · 2.03 mV in ischemic preparations; n = 7 each; P > 0.05). Lowering [K]0. caused persistent Hyperpolarization in nonischemic muscles, but caused depolarization in chronically ischemic preparations (in 2,7 mM [K]0 Vr was −84.9 · 2.74 mV and –61.7 · 7.72 mV, respectively; n = 7; P < 0.05). Pinacidil (100 μM) normalized the response of chronically ischemic preparations to [K]0. Action potentials (APs) from nonischemic tissues varied in shape and could show aberrations. Kpinephrine (1.5 μM) and 4‐aminopyridine (3 mM) increased the AP duration, while butanedione monoxime (20 mM) and tetrodotoxin (1 μM) shortened it. In chronically ischemic muscles, the AP was characterized by the absence of a plateau and the presence of a slow phase of final repolarization.

Conclusion: The differential effect of tow [K]0 on the resting membrane potential of nonischemic and chronically ischemic tissues suggests a change in the properties or the regulation of background K+ channels during chronic ischemia.