bluuebunny/crossref_metadata_2025 huggingface dataset:
Rossby Solitary Waves in the Presence of a Critical Layer
Authors: Caillol P. , Grimshaw R. H.
Published: April 2007

This study considers the evolution of weakly nonlinear long Rossby waves in a horizontally sheared zonal current. We consider a stable flow so that the nonlinear time scale is long. These assumptions enable the flow to organize itself into a large‐scale coherent structure in the régime where a competition sets in between weak nonlinearity and weak dispersion. This balance is often described by a Korteweg‐de‐Vries equation. The traditional assumption of a weak amplitude breaks down when the wave speed equals the mean flow velocity at a certain latitude, due to the appearance of a singularity in the leading‐order equation, which strongly modifies the flow in a critical layer. Here, nonlinear effects are invoked to resolve this singularity, because the relevant geophysical flows have high Reynolds numbers. Viscosity is introduced in order to render the nonlinear‐critical‐layer solution unique, but the inviscid limit is eventually taken. By the method of matched asymptotic expansions, this inner flow is matched at the edges of the critical layer with the outer flow. We will show that the critical‐layer–induced flow leads to a strong rearrangement of the related streamlines and consequently of the potential‐vorticity contours, particularly in the neighborhood of the separatrices between the open and closed streamlines. The symmetry of the critical layer vis‐à‐vis the critical level is also broken. This theory is relevant for the phenomenon of Rossby wave breaking and eventual saturation into a nonlinear wave. Spatially localized solutions are described by a Korteweg‐de‐Vries equation, modified by new nonlinear terms; depending on the critical‐layer shape, this leads to depression or elevation waves. The additional terms are made necessary at a certain order of the asymptotic expansion while matching the inner flow on the dividing streamlines. The new evolution equation supports a family of solitary waves. In this paper we describe in detail the case of a depression wave, and postpone for further discussion the more complex case of an elevation wave.
The experience of wind in early and medieval Chinese medicine
Authors: Hsu Elisabeth
Published: April 2007

Two terms for wind prevail in Chinese medical texts and practice:qiandfeng. Shigehisa Kuriyama noted thatqiusually referred to regular andfengto unruly winds. This is not contested in this paper, but it considers these connotations of wind a characteristic ofqiandfengin late imperial China in particular, and calls for an account that is more sensitive to historical change. Based on a study of twenty‐five medical case histories in the 105th chapter of theRecords of the Historian(Shi ji,c.86 BCE) and related texts, it suggests that in the third and second century BCEqigenerally designated internal andfengexternal winds. Both alluded to the spirit world:qi‐breaths tended to be associated withshen‐spirits,feng‐winds withgui‐ghosts, although there were overlaps. Breathing techniques, with their emphasis on regularity, were developed for stabilizing the mind and appeasing the emotions, whilefeng‐winds, associated with the fecundity‐enhancing weather conditions of wind and rain, were a generative principle of procreation. By medieval times, the violent and unruly aspects of wind, and their destructive potential, started to be emphasized. Accordingly,feng‐winds became the main aetiology of madness, which in early texts had been rising heat and hot bloodedness.
The bodily winds in ancient India revisited
Authors: Zysk Kenneth G.
Published: April 2007

This paper examines the historical development of the doctrine of the five bodily winds (prāas) in the early Sanskrit literature of Yoga and Āyurveda. Special attention is paid to the Indian's understanding of the connection between atmospheric wind and bodily breath and the role of wind in the human body. The paper traces the evolution of the Indian concept of breath. Originally, wind and breath were used metaphorically to indicate life. Breath was subsequently classified into five types by early ascetics who used breath‐control in their practice of Yoga; and these same five breaths were eventually utilized by the Āyurvedic medical thinkers to establish a sophisticated doctrine of wind and its function in the body.
Bat diversity and abundance associated with the degree of secondary succession in a tropical forest mosaic in south‐eastern Mexico
Authors: Castro‐Luna A. A. , Sosa V. J. , Castillo‐Campos G.
Published: April 2007

Under the hypothesis that bat diversity would be lower in the early stages of secondary succession and that species affected negatively by habitat modification would be more frequent in later successional stages, we evaluated how bats use 12 vegetation stands representing four stages of secondary succession, following disturbance caused by slash‐and‐burn agriculture and selective logging. We compared bat richness, abundance and diversity, and found that none of these variables was different among stages or rainy seasons. However, of the 10 most common bat species, two were significantly more abundant in stands at the early stages of secondary succession, while the opposite was true for three other species. Canopy cover mainly explains these patterns. Rainy season had no effect on the abundance of the common species. The results of this study indicate that although some frugivorous species were very abundant in the younger stands, the majority of the rare species were captured in older stands. The absence of rare and habitat‐specialized species from young successional stages close to primary forest suggests that, for effective bat conservation in landscapes modified by human activity, areas with original vegetation should be maintained to ensure the survivorship of sensitive‐to‐deforestation species.
Manipulating sex ratio to increase population growth: the example of the Lesser Kestrel
Authors: Lenz T. L. , Jacob A. , Wedekind C.
Published: April 2007

Small or decreasing populations call for emergency actions like, for example, captive breeding programs. Such programs aim at rapidly increasing population sizes in order to reduce the loss of genetic variability and to avoid possible Allee effects. The Lesser Kestrel Falco naumanni is one of the species that is currently supported in several captive breeding programs at various locations. Here, we model the demographic and genetic consequences of potential management strategies that are based on offspring sex ratio manipulation. Increased population growth could be achieved by manipulating female conditions and/or male attractiveness in the captive breeders and consequently shifting the offspring sex ratio towards more female offspring, which are then used for reintroduction. Fragmenting populations into wild‐breeding and captive‐breeding demes and manipulating population sex ratio both immediately increase the inbreeding coefficient in the next generation (i.e. decrease Ne) but may, in the long term, reduce the loss of genetic variability if population growth is restricted by the number of females. We use the Lesser Kestrel and the wealth of information that is available on this species to predict the long‐term consequences of various kinds of sex‐ratio manipulation. We find that, in our example and possibly in many other cases, a sex‐ratio manipulation that seems realistic could have a beneficial effect on the captive breeding program. However, the possible long‐term costs and benefits of such measures need to be carefully optimized.
Malignant Sustained Ventricular Tachyarrhythmias in Women:
Authors: KUDENCHUK PETER J. , BARDY GUST H. , POOLE JEANNE E. , LEE DOLACK G. , GLEVA MARYE J. , REDDY RAMU , JONES GREGORY K. , TROUTMAN CHARLES , ANDERSON JILL , JOHNSON GEORGE
Published: April 2007

Implantable Defibrillators in Women. Clinical rhythm, heart disease, ejection fraction, defibrillation threshold, recurrent arrhythmias, and mortality were compared in 268 consecutive recipients (213 men and 55 women) of their first implantable cardioverter defibrillator for life‐threatening ventricular tachycardia or fibrillation. Women were younger than men, less likely to have structural heart disease, and more likely to have clinical ventricular fibrillation, a higher ejection fraction, and a lower defibrillation threshold. Complications of defibrillator placement were similar in both sexes. Unadjusted survival tended to be higher in women than in men (97% vs 90%, respectively, at 2 years, P = 0.08), largely due to fewer deaths from noncardiac causes or cardiac causes other than arrhythmia (P = 0.04). Women also tended to be at lower, albeit still substantial, risk for recurrent arrhythmias during follow‐up (37% vs 52% in men at 2 years, P = 0.11). After adjustment for baseline differences, overall survival, arrhythmia death‐free survival, nouarrhythmia death‐free survival, and frequency of recurrent arrhythmias were not found to be gender related. Despite their apparent “lower risk” status on initial presentation, women remained at substantial risk for recurrent arrhythmias. This underscores the need to avoid being unduly biased by the “appearance” of health in managing women with malignant arrhythmias. That survival and other clinical endpoints were all ultimately independent of gender emphasizes the importance of other clinical variables in assessing risk from ventricular tachyarrhythmias.
Chemical Cardiac Sympathetic Denervation Hampers Defibrillation in the Dog
Authors: RUFFY RODOLPHE , LEONARD MICHAEL
Published: April 2007

Cardiac Sympathetic Denervation and Defibrillation. Introduction: Cardiac defibrillation is influenced by several physical and nonphysical factors. Previous animal studies have shown that beta‐adrenergic stimulation facilitates the process of defibrillation. The purpose of this study was to examine the effects of chemical sympathetic denervation on the ability to defibrillate the canine heart.

Methods and Results: Twelve chronically instrumented dogs underwent serial measurements of the energy required to defibrillate the heart, ten before and after treatment with 50 mg/kg 6‐hydroxydopaniine (6‐OHDA). Two of the animals received 1% ascorbic acid in 0.9% saline solution (the vehicle) only, and three dogs received the vehicle followed several weeks later by 6‐OHDA. Following treatment with 6‐OHDA, the energy to defibrillate the heart rose from 11.9 ± 7.4 J (baseline 1) and 14.3 ± 8.7 J (baseline 2) to 23.3 ± 10.8 J (P < 0.01 and < 0.05, respectively). In contrast, following saline administration, no significant change was measured in the energy required to defibrillate the heart. After 6‐OHDA, 5 of the 10 animals could not he defibrillated versus none of 5 after saline treatment (Chi square 3.750, P = 0.053). In surviving animals, a return of measurements to, or toward, baseline was measured after active treatment.

Conclusions: In this chronically instrumented, closed chest animal model, chemical sympathetic denervation with 6‐OHDA hampered the process of cardiac defibrillation. These results support previous observations of a modulating effect of this process by adrenergic activity.
Congestive Heart Failure and Arrhythmias:
Authors: SINGH STEVEN N.
Published: April 2007

Congestive Heart Failure. Congestive heart failure affects millions of Americans, and thousands of new cases are reported each year. The prognosis continues to be grim. Most deaths in heart failure patients can be attributed to low‐output states (pump failure) and arrhythmias (sudden). Attempts have been made to decrease the incidence of pump failure deaths by using contractility agents that, in most cases, have been shown to be detrimental. The results of trials using beta blockers are encouraging. Vasodilators have made a positive impact on outcome. However, the use of pharmacologic antiarrhythmic agents to decrease sudden death has failed to improve survival. Studies with implantable devices are ongoing and will provide an answer to the question of whether a reduction in sudden death will translate into a reduction of all‐cause mortality. Antiplatelet and antithrombotic agents appear to be favorable, and revascularization is recommended when feasible.
Tissue Magnesium Levels and the Arrhythmic Substrate in Humans
Authors: HAIGNEY MARK CP. , BERGER RONALD , SCHULMAN STEVEN , GERSTENBLITH GARY , TUNIN CAROL , SILVER BURTON , SILVERMAN HOWARD S. , TOMASELLI GORDON , CALKINS HUGH
Published: April 2007

Magnesium and Arrhythmias. Introduction: Magnesium deficiency has been implicated in the pathogenesis of sudden death, but the investigation of arrhythmic mechanisms has been hindered by difficulties in measuring cellular tissue magnesium stores.

Methods and Results: To see if magnesium deficiency is associated with a propensity toward triggered arrhythmias, we measured tissue magnesium levels and QT interval dispersion (as an index of repolarization dispersion) in 40 patients with arrhythmic complaints. Magnesium was measured in sublingual epithelium using X‐ray dispersive analysis. QT interval dispersion was assessed on 12‐lead surface F‐XCs in all patients, and programmed stimulation was performed in 28. The sublingual epithelial magnesium level ([Mg]i), but the not the serum level, correlated Inversely with QT interval dispersion in 40 patients (r = 0.58, P < 0.0.5); in 12 patients undergoing repeat testing on therapy, the change in magnesium also correlated inversely with the change in QT dispersion (r = 0.61, P < 0.05). Patients with left ventricular ejection fractions > 40% had significantly higher tissue magnesium and lower QT dispersion (34.5 ± 0.5 mEq/L, 81 ± 8 msec) than those with left ventricular ejection fractious < 40% (32.7 ± 0.5 mEq/L, P < 0.01, and 114 ± 9 msec, P < 0.05). There was no difference in either [Mg]i, or QT dispersion in the 16 patients with inducible monomorphic ventricular tachycardia versus the 12 noninducible patients.

Conclusion: Reduced tissue magnesium stores may represent a significant risk factor for arrhythmias associated with abnormal repolarization, particularly in patients with poor left ventricular systolic function, but may not represent a risk for excitable gap arrhythmias associated with a fixed anatomic substrate (e.g., monomorphic ventricular tachycardia).
Effect of Ventricular Dilatation on Defibrillation Threshold in the Isolated Perfused Rabbit Heart
Authors: OTT PETER , REITER MICHAEL J.
Published: April 2007

Ventricular Dilatation and DFT. Introduction: Ventricular dilatation has Important electrophysiologic effects, but its effect on ventricular defibrillation threshold (DFT) is unknown.

Methods and Results: A fluid‐filled, latex balloon was placed in the left ventricular cavity of 19 isolated rabbit hearts. In each experiment, an undilated volume (equivalent to a left ventricular end‐diastolic pressure of approximately 0 mmHg) was compared to a dilated volume achieved by adding 1.0 mL of saline (n = 10) or 5% dextrose (n = 9) to the intracavitary balloon. Left ventricular effective refractory period (ERP) and DFT were determined at each volume. Defibrillation was attempted with a monophasic shock delivered between a patch electrode positioned over the posterior left ventricle (cathode) and a metallic aortic cannula (anode). DFT was determined using a modified “down/up” protocol with 10‐V steps. Ventricular dilatation increased the left ventricular end‐diastolic pressure from 0 ± 0.5 mmHg to 35 ± 3 mmHg (P < 0.001), decreased the average left ventricular ERP 15% (from 116 ± 3 msec to 99 ± 3 msec; P < 0.001), and increased the average DFT 30% (from 96 ± 4 V to 125 ± 7 V; P < 0.001). In one third of experiments, the dilated DFT was ≥ 150% of the DFT at zero volume. The mechanism of the observed increase in DFT is unknown but may be related to the decrease in refractoriness observed with ventricular dilatation.

Conclusion: Acute ventricular dilatation in this model increased DFT an average of 30%, an effect not previously described. This observation may have implications for patients with implantable cardioverter defibrillators.
Transmembrane Voltage Changes Produced by Real and Virtual Electrodes During Monophasic Defibrillation Shock Delivered by an Implantable Electrode
Authors: EFIMOV IGOR R. , CHENG YUANNA N. , BIERMANN MARTIN , Van WAGONER DAVID R. , MAZGALEV TODOR N. , TCHOU PATRICK J.
Published: April 2007

Defibrillation Shock‐Induced Virtual Electrodes. Introduction: Epicardial point stimulation produces nonuniform changes in the trans membrane voltage of surrounding cells with simultaneous occurrence of areas of transient positive and negative polarization. This is the phenomenon of virtual electrode. We sought to characterize the responses of epicardial ventricular tissue to the application of monophasic electric shocks from an internal transvenous implantable cardioverter defibrillator (ICD) lead.

Methods and Results: Langendorff‐perfused rabbit hearts (n = 12) were stained with di‐4‐ANEPPS. A 9‐mm‐long distal electrode was placed in the right ventricle. A 6‐cm proximal electrode was positioned horizontally 3 cm posteriorly and 1 cm superiorly with respect to the heart. Monophasic anodal and cathodal pulses were produced by discharging a 150‐μF capacitor. Shocks were applied either during the plateau phase of an action potential (AP) or during ventricular fibrillation. Leading‐edge voltage of the pulse was 50 to 150 V, and the pulse duration was 10 msec. Transmembrane voltage was optically recorded during application of the shock, simultaneously from 256 sites on a 11 × 11 mm area of the anterior right ventricular epicardium directly transmural to the distal electrode. The shock effect was evaluated by determining the difference between the AP affected by the shock and the normal AP. During cathodal stimulation an area of depolarization near the electrode was observed, surrounded by areas of hyperpolarization. The amplitude of polarization gradually decreased in areas far from the electrode. Inverting shock polarity reversed this effect.

Conclusion: ICD monophasic defibrillation shocks create large dynamically interacting areas of both negative and positive polarization.
Electrocardiographic and Electrophysiologic Characterization of Atypical Atrial Flutter in Man:
Authors: KALMAN JONATHAN M. , OLGIN JEFFREY E. , SAXON LESLIE A. , LEE RANDALL J. , SCHEINMAN MELVIN M. , LESH MICHAEL D.
Published: April 2007

Atypical Atrial Flutter. Introduction: Although the circuit in typical counterclockwise atrial flutter has been clearly delineated, the mechanisms of “atypical atrial flutters” have been less well characterized. The purpose of this study was to investigate the ECG and electrophysiologic (EP) characteristics of atypical atrial flutter.

Methods and Results: Thirty‐three patients with at least one form of atypical atrial flutter underwent EP evaluation with multipolar atrial activation and entrainment mapping. Nineteen patients with clockwise flutter had: (1) stereotypic ECG morphology; (2) same cycle length as counterclockwise flutter; (3) clockwise activation around the tricuspid annulus; (4) recording of discrete split potentials along the length of the crista terminalis, suggesting the presence of conduction block; (5) concealed entrainment from the low right atrial isthmus; (6) successful ablation in this isthmus. Twenty patients with atypical flutter not consistent with a clockwise mechanism (“true atypical flutter”) showed: (1) heterogeneous ECG morphology; (2) cycle length shorter than that of clockwise flutter; (3) frequent transitions from and to atrial fibrillation; (4) could be entrained in only six patients and, when accomplished, demonstrated surface fusion when entraining from the low right atrial isthmus.

Conclusions: Atypical flutter falls into two broad categories. Clockwise flutter uses the same circuit with the same endocardial barriers as its counterclockwise counterpart and is best con sidered a form of typical flutter. True atypical flutter induced in the EP laboratory is a hetero geneous group of arrhythmias that are transitional to atrial fibrillation. Although it may superficially resemble clockwise or counterclockwise flutter based on the 12‐lead ECG alone, the distinction can be readily made from a combined evaluation including activation and entrainment mapping.
The Zone of Vulnerability to T Wave Shocks in Humans
Authors: SWERDLOW CHARLES D. , MARTIN DAVID J. , KASS ROBERT M. , DAVIE SCOTT , MANDEL WILLIAM J. , GANG ELI S. , CHEN PENG‐SHENG
Published: April 2007

Vulnerability to VF in Humans. Introduction: Shocks during the vulnerable period of the cardiac cycle induce ventricular fibrillation (VF) if their strength is above the VF threshold (VFT) and less than the upper limit of vulnerability (ULV). However, the range of shock strengths that constitutes the vulnerable zone and the corresponding range of coupling intervals have not been defined in humans. The ULV has been proposed as a measure of defibrillation because it correlates with the defibrillation threshold (DFT), but the optimal coupling interval for identifying it is unknown.

Methods and Results: We studied 14 patients at implants of transvenous cardioverter defibrillators. The DFT was defined as the weakest shock that defibrillated after 10 seconds of VF. The ULV was defined as the weakest shock that did not induce VF when given at 0, 20, and 40 msec before the peak of the T wave or 20 msec after the peak in ventricular paced rhythm at a cycle length of 500 msec. The VFT was defined as the weakest shock that induced VF at any of the same four intervals. To identify the upper and lower boundaries of the vulnerable zone, we determined the shock strengths required to induce VF at all four intervals for weak shocks near the VFT and strong shocks near the ULV. The VFT was 72 ± 42 V, and the ULV was 411 ± 88 V. In all patients, a shock strength of 200 V exceeded the VFT and was less than the ULV. The coupling interval at the ULV was 19 ± 11 msec shorter than the coupling interval at the VFT (P < 0.001). The vulnerable zone showed a sharp peak at the ULV and a less distinct nadir at the VFT. A 20‐msec error in the interval at which the ULV was measured could have resulted in underestimating it by a maximum of 95 ± 31 V. The weakest shock that did not induce VF was greater for the shortest interval tested than for the longest interval at both the upper boundary (356 ± 108 V vs 280 ± 78 V; P < 0.01) and lower boundary (136 ± 68 msec vs 100 ± 65 msec; P < 0.05).

Conclusions: The human vulnerable zone is not symmetric with respect to a single coupling interval, but slants from the upper left to lower right. Small differences in the coupling interval at which the ULV is determined or use of the coupling interval at the VFT to determine the ULV may result in significant variations in its measured value. An efficient strategy for inducing VF would begin by delivering a 200‐V shock at a coupling interval 10 msec before the peak of the T wave.
Mechanisms for Depolarization by I‐PalmitoyIcarnitine in Single Guinea Pig Ventricular Myocytes
Authors: SHEN JIAN‐BTNG , PAPPANO ACHILLES J
Published: April 2007

I‐PC Inhibits INa/K and IK1 in Heart. introduction: The changes of the resting potential (RP) and of the current‐voltage (I‐V) relationship induced by l‐palmitoylcarnitine (I‐PC) in the presence of the IK1 blocker, cesium, or in the presence of the INa/K blocker, ouabain, were tested in guinea pig ventricular myocytes to ascertain the relative contributions of IK1 and INa/k suppression to the membrane depolarization caused by this amphiphile.

Methods and Results: Ramp voltages were applied to myocytes with the whole cell, patch clamp technique. 1‐PC (10 μM) produced additional membrane depolarization in the presence of either 10 mM Cs+ or 30 μM ouabain. In the presence of Cs+ 1‐PC, like 3 μM ouabain, shifted current inward at potentials negative to ‐20 mV as a result of INa/K blockade. In the presence of 30 μM ouabain, 1‐PC, like Cs+, shifted current inward at potentials between ‐27 and ‐88 mV and outward at potentials negative to ‐88 mV. This is attributed to IK1 block because the current was inwardly rectifying, with a reversal potential near EK. When I‐PC or ouabain inhibited INa/K, the presence of an Ni2+‐sensitive component attributed to INa/ca distorted the membrane I‐V relationship, particularly in the presence of Cs+. The relative contributions of IK1 and INa/K block by 1‐PC were voltage dependent. At the RP, 1‐PC produced a greater block of INa/K than of IK1.

Conclusion: I‐PC depolarizes the resting membrane by inhibiting both IK1 and INa/K. It is concluded that suppression of INa/K by I‐PC predominates over block of IK, to depolarize the membrane at the RP.
Pathologic Findings Following Sudden Death in an Infant with Hypertrophic Cardiomyopathy and Supraventricular Tachycardia
Authors: KANTER RONALD J. , GRAVATT ANDREA , BHARATI SAROJA
Published: April 2007

Sudden Infant Death in Hypertrophic Cardiomyopathy. The cardiac conduction system from infants suddenly dying with hypertrophic cardiomyopathy has not been described. We studied by serial section examination the conduction system from a 13‐month old infant also known to have had supraventricular tachycardia. At autopsy, there was cardiomegaly with asymmetric septal hypertrophy. Microscopic examination revealed myofiber disarray around an abnormally formed central fibrous body, numerous nodoventricular fibers to both sides of the ventricular septum, and fibrosis of the left bundle branch. We postulate that supraventricular tachycardia utilized a concealed pathway or the malformed AV Junction. Death may have resulted from deranged hemodynamics secondary to supraventricular tachycardia.
Upper Limit of Vulnerability Predicts Chronic Defibrillation Threshold for Transvenous Implantable Defibrillators
Authors: MARTIN DAVID J. , CHEN PENG‐SHENG , HWANG CHUN , GANG ELI S. , MANDEL WILLIAM J. , PETER C. THOMA , SWERDLOW CHARLES D.
Published: April 2007

ULV Predicts Chronic DFT. Introduction: The upper limit of vulnerability (ULV) is the shock strength at or above which ventricular fibrillation cannot be induced when delivered in the vulnerable period. It correlates acutely with the acute defibrillation threshold (DFT) and can be determined with a single episode of fibrillation. The goal of this prospective study was to determine the relationship between the ULV and the chronic DFT.

Methods and Results: We studied 40 patients at, and 3 months after, implantation of transvenous cardioverter defibrillators. The ULV was defined as the weakest biphasic shock that failed to induce fibrillation when delivered 0,20, and 40 msec before the peak of the T wave. Patients were classified as clinically stable or unstable based on prospectively defined criteria. There were no significant differences between the group means for the acute and chronic determinations of ULV (13.5 ± 5.3 J vs 12.4 ± 6.8 J, P = 0.25) and DFT (10.1 ± 5.0 J vs 9.9 ± 5.7 J, P = 0.74). Five patients (15%) were classified as unstable. The strength of the correlation between acute ULV and acute DFT (r = 0.74, P < 0.001) was similar to that between the chronic ULV and chronic DFT (r = 0.82, P < 0.001). There was a correlation between the change in ULV from acute to chronic and the corresponding change in DFT (r = 0.67, P < 0.001). The chronic DFT was less than the acute ULV + 3 J in all 35 stable patients, but it was greater in 2 of 5 unstable patients (P = 0.04).

Conclusions: The strength of the correlation between the chronic ULV and the chronic DFT is comparable to that between the acute ULV and the acute DFT. Temporal changes in the ULV predict temporal changes in the DFT. In clinically stable patients, a defibrillation safety margin of 3 J above the acute ULV proved an adequate chronic safety margin.
Intra‐Atrial Reentrant Tachycardia After Palliation of Congenital Heart Disease:
Authors: TRIEDMAN JOHN K. , JENKINS KATHY J. , COLAN STEVEN D. , SAUL J. PHILI , WALSH EDWARD P.
Published: April 2007

Catheter Mapping of IART. introduction: The anatomic substrate of intra‐atrial reentrant tachycardia (IART) following congenital heart surgery is poorly understood, but is presumed to be different than common atrial flutter.

Methods and Results: To study the mechanisms of IART, we used a new technique for high‐density endocardial mapping using recordings from a multipolar basket recording catheter (25 bipolar pairs). For each recording, biplane fluorographic reference points were digitized to obtain the spatial locations of electrode pairs, and activation times were calculated using temporal reference points from the surface ECG. Using custom software, data were combined to create three‐dimensional atrial activation sequence maps, which were displayed as animated sequences. Using this technique, recordings were made in induced and/or spontaneous IART in 8 patients following congenital heart surgery (5 Fontan, 2 tetralogy of Fallot repair, 1 ventricular septal defect repair), and in 3 patients with normal intracardiac anatomy (I with type I atrial flutter). Ten discrete IART activation sequences were recorded; 2 patients had 2 sequences each. IART maps were constructed using a median of 108 electrode positions (range 27 to 197) from a median of 6 recordings/sequence (range 3 to 11). Sinus or paced atrial rhythms were also recorded, and maps were created in a similar fashion. Visual analysis of activation sequences of sinus and paced rhythm were anatomically concordant with known mechanisms of atrial activation. IART sequences revealed diverse mechanisms; only 1 IART circuit was similar to that associated with common atrial flutter. Activation wavefront emergence from presumed zones of slow conduction, lines of conduction block, and apparent bystander activation were observed.

Conclusions: High‐density atrial activation sequence maps demonstrate that IART following congenital heart surgery utilizes diverse circuits and is distinct from common atrial flutter. The technique used to create these three‐dimensional activation sequences may improve understanding of these complex atrial arrhythmias and assist in the development of ablative therapies.
High‐Resolution Fluorescent Imaging Does Not Reveal a Distinct Atrioventricular Nodal Anterior Input Channel (Fast Pathway) in the Rabbit Heart During Sinus Rhythm
Authors: EFIMOV IGOR R. , FAHY GERARD J. , CHENG YUANNA , VAN WAGONER DAVID R. , TCHOU PATRICK J. , MAZGALEV TODOR N.
Published: April 2007

Fluorescent Imaging of AVN. Introduction: We sought to determine the precise pathways of engagement of the AV node during sinus rhythm.

Methods and Results: Langendorff‐perfused rabbit hearts were stained with 20 μM of the voltage‐sensitive dye di‐4‐ANEPPS. Preparations containing the right atrium, sinoatrial (SA) and AV nodes, and interatrial septum were subsequently dissected and mapped in vitro using a 16 × 16 photodiode array with an adjustable resolution of 150 to 750 μm per diode. Motion artifacts were eliminated by using 15 mM 2,3‐butanedione monoxime (BDM). Activation time‐points were defined as (‐dF/dt)max, where F = fluorescence. Isochronal maps of activation were plotted using the triangulation method. In all preparations, spontaneous activation began at the SA node, rapidly spread along the crista terminalis (CrT), entered the AV nodal region via the posterior “slow” pathway, and retrogradely spread to the septal region with a smaller conduction velocity compared to that along the CrT. Collision of anterograde and retrograde wavefronts was frequently observed in the mid‐septum. Notably, there was no evidence for the presence of a distinct anterior entrance into the AV node.

Conclusion: Fast pathway conduction during sinus rhythm results from a broad posterior wavefront that envelops the AV node with subsequent retrograde atrial septal activation.
Lyme Myocarditis Presenting as Fascicular Tachycardia with Underlying Complete Heart Block
Authors: GREENBERG YISACHAR J. , BRENNAN JOSEPH J. , ROSENFELD LYNDA E.
Published: April 2007

Lyme Myocarditis with Fascicular Tachycardia. A case of Lyme myocarditis manifest as a fascicular tachycardia is presented. Subtle findings of heart block hi the presence of preserved ventricular function led to the correct diagnosis in this otherwise healthy patient. Treatment with ceftriaxone resolved both abnormalities.
Atrial Flutter:
Authors: WALDO ALBERT L.
Published: April 2007

Entrainment Characteristics. Entrainment was first described based on observations during rapid (overdrive) pacing of type I atrial flutter. Entrainment is capture of the reentrant circuit of a tachycardia without interrupting the tachycardia, so that with cessation of pacing, the spontaneous reentrant tachycardia is still present. During entrainment, the orthodromic wavefront from the pacing impulse resets the tachycardia to the pacing rate, while the antidromic wavefront either collides with the orthodromic wavefront of the previous beat (usual case) or is blocked by some other mechanism (refractoriness or another cause of block). Entrainment may be either manifest or concealed. The principles of entrainment during type I atrial flutter have permitted identification of targets for successful ablation, of mapping sites within or outside the reentrant circuit, and of appropriate pacing rates to successfully interrupt atrial flutter and restore sinus rhythm.
Atrial Flutter:
Authors: MARY‐RABINE LUC , MAHAUX VÉRONIQUE , WALEFFE ANDRÉ , KULBERTUS HENRI
Published: April 2007

Atrial Flutter. For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiologv in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified interiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.
Noncontact Endocardial Mapping: Reconstruction of Electrograms and Isochrones From Intracavitary Probe Potentials
Authors: LIU ZHIWEI W. , JIA PING , ERSHLER PHILIP R. , TACCARDI BRUNO , LUX ROBERT L. , KHOURY DIRAR S. , RUDY YORAM
Published: April 2007

Noncontact Endocardial Mapping.Introduction: Mapping endocardial activation and repolarization processes is critical to the study of arrhythmias and selection of therapeutic procedures. Previously, we developed methodology for reconstructing endocardial potentials from potentials measured with a noncontact, intracavitary probe. This study further develops and evaluates the ability of the approach to provide detailed information on the spatiotemporal characteristics of the activation process. Specifically, we reconstructed endocardial electrograms and isochrones throughout the activation process over the entire endocardium during a single beat.

Methods and Results: Cavity potentials were measured with a 65‐electrode probe placed inside an isolated canine left ventricle. Endocardial potentials were measured simultaneously using 52 electrodes. Potentials were acquired during subendocardial pacing from different locations. Computed electrograms at various sites closely resemble the measured electrograms (correlation coefficient > 0.9 at 60% of the electrodes). Computed isochrones locate subendocardial pacing sites with 10‐mm accuracy. Two pacing sites, 17 mm apart, were resolved. Critical regions, such as areas of isochrone crowding, were accurately reconstructed.

Conclusions: Results indicate the applicability of the approach to mapping the cardiac excitation process on a beat‐by‐beat basis without occluding the ventricle. The ability of locating electrical events (e.g., single or multiple initiation sites) is demonstrated. Importantly, the method is shown to be capable of reconstructing electrograms over the entire endocardium and determining nonuniformities of activation spread (e.g., areas of slow conduction). These capabilities are important to clinical application in the electrophysiology laboratory and experimental studies of arrhythmias in the intact animal.
Ablation of Ventricular Tachycardia Associated with Tetralogy of Fallot: Demonstration of Bidirectional Block
Authors: HORTON RODNEY P. , CANBY ROBERT C. , KESSLER DAVID J. , JOGLAR JOSE A. , HUME ANDREW , JESSEN MICHAEL E. , SCOTT WILLIAM P. , PAGE RICHARD L.
Published: April 2007

Ablation of VT in Tetralogy of Fallot. Introduction: Ventricular tachycardia is commonly seen in patients following surgical repair for tetralogy of Fallot. The technique of ablation for this arrhythmia is not well defined.

Methods and Results: In two patients with ventricular tachycardia following surgical repair of tetralogy of Fallot, the traditional indicators for a site for ventricular tachycardia ablation did not yield cure. Based on careful mapping, the circuit was found to involve the isthmus between the outflow tract patch and the tricuspid annulus; linear radiofrequency lesions across this isthmus resulted in cure of ventricular tachycardia. Not only was the tachycardia no longer inducible, but bidirectional block at the line of ablation confirmed interruption of the reentrant circuit.

Conclusion: A linear radiofrequency lesion was effective in eliminating ventricular tachycardia in both patients. The demonstration of bidirectional block confirms a cure independent of inducibility of ventricular tachycardia.
Radiofrequency Catheter Ablation of the Anterosuperior and Posteroinferior Atrial Approaches to the AV Node for Treatment of AV Nodal Reentrant Tachycardia
Authors: KOTTKAMP HANS , HINDRICKS GERHARD , BORGGREFE MARTIN , BREITHARDT GÜNTER
Published: April 2007

Catheter Ablation Techniques in AVNRT. Radiofrequency catheter ablation has been established as a first‐line curative treatment modality in patients with symptomatic AV nodal reentrant tachycardia (AVNRT). The successful sites of stepwise catheter ablation approaches of the so‐called fast and slow pathways strongly suggest that AVNRT involves the atrial approaches to the AV node. The typical fast pathway ablation sites are located anterosuperior toward the apex of the triangle of Koch, which also contains the compact AV node, whereas the usual slow pathway ablation sites are located posteroinferior toward the base of the triangle of Koch at a greater distance to the compact AV node and bundle of His. Accordingly, ablation studies with large patient cohorts have demonstrated that fast pathway ablation carries a higher risk of inadvertent complete AV block. Thus, the slow pathway is clearly the primary target site, and fast pathway ablation is rarely necessary. Different approaches for slow pathway ablation have been elaborated: anatomically oriented stepwise techniques, ablation guided by double potentials recorded within the area of the slow pathway insertion, and combined techniques. The modern concept of AVNRT suggests that this arrhythmia involves the highly complex three‐dimensional nonuniform anisotropic AV junctional area. Accordingly, mapping and ablation studies demonstrated that the anterior approach is not identical with fast pathway ablation, and the posterior approach is not identical with slow pathway ablation. Therefore, it is essential for interventional electrophysiologists to familiarize themsdves with the anatomic and electrophysiologic details of this complex and variable specialized AV junctional region. In this review, the anatomic and pathophysiologic aspects of the AV junctional area as they relate to interventional therapy are summarized briefly, and the catheter techniques for ablation of the so‐called fast and slow AV nodal pathways for the treatment of AVNRT are described.
Insights into Mechanisms of Antiarrhythmic Drug Action From Experimental Models of Atrial Fibrillation
Authors: NATTEL STANLEY , BOURNE GERALD , TALAJIC MARIO
Published: April 2007

Antiarrhythmic Drugs in AF. Atrial fibrillation (AF) remains a challenge to medical therapy. Over the past several years, a variety of experimental models of AF have been developed. These have provided insights into mechanisms underlying AF and antiarrhythmic drug action against the arrhythmia. A variety of drugs effective against clinical AK, including flecainide. propafenone, procainamide, and sotalol, have been found to terminate experimental AF, All of these agents appear to act by prolonging the wavelength for atrial reentry at rapid rates, thereby increasing the size and decreasing the number of functional circuits maintaining the arrhythmia. While the ability to terminate AF is determined by refractoriness prolongation at rapid rates, refractoriness prolongation at slow rates (e.g., sinus rhythm) can prevent AF induction by premature beats. Thus, drugs with strong reverse use‐dependence (like sotalol) may be much more effective in preventing than in terminating AF. Spacial heterogeneity in refractoriness is an important contributor to AF occurrence in some models, particularly vagal AF, and is reduced by some (but not all) drugs that terminate AF, New insights are being gained into mechanisms of electrical remodeling, which promotes AF maintenance when rapid atrial rates are maintained, such as during AF, This electrical remodeling may be an interesting novel target for therapy of AF, Insights into AF mechanisms obtained in experimental models of AF should help in the development of new and improved therapeutic approaches.
Electrophysiologic Characteristics and Radiofrequency Catheter Ablation in Atrioventricular Node Reentrant Tachycardia with Second‐Degree Atrioventricular Block
Authors: LEE SHIH‐HUANG , CHEN SHIH‐ANN , TAI CHING‐TAI , CHIANG CHERN‐EN , WEN ZU‐CHI , UENG KWO‐CHANG , CHIOU CHUEN‐WANG , CHEN YI‐JBN , YU WEN‐CHUNG , HUANG JIN‐LONG , CHENG JUN‐JACK , CHANG MAU‐SONG
Published: April 2007

Second‐Degree AV Block During AVNRT. Introduction: Detailed electrophysiologic study of AV nodal reentrant tachycardia (AVNRT) with 2:1 AV block has been limited.

Methods and Results: Six hundred nine consecutive patients with AVNRT underwent electrophysiologic study and radiofrequency catheter ablation of the slow pathway. Twenty‐six patients with 2:1 AV block during AVNRT were designated as group I, und those without this particular finding were designated as group II. The major findings of the present study were: (1) group I patients had better anterograde and retrograde AV nodal function, shorter tachycardia cycle length (during tachycardia with 1:1 conduction) (307 ± 30 vs 360 ± 58 msec, P < 0.001), and higher incidence of transient bundle branch block during tachycardia (18/26 vs 43/609, P < 0.001) than group II patients: (2) 21 (80.8%) group I patients had alternans of AA intervals during AVNRT with 2:1 AV block. Longer AH intervals (264 ± 26 vs 253 ± 27 msec, P = 0.031) were associated with the blocked beats. However, similar HA intervals (51 ± 12 vs 50 ± 12 msec, P = 0.363) and similar HV intervals (53 ± 11 vs 52 ± 12, P = 0.834) were found in the blocked and conducted beats; (3) ventricular extrastimulation before or during the His‐bundle refractory period bundle could convert 2:1 AV block to 1:1 AV conduction.

Conclusions: Fast reentrant circuit, rather than underlying impaired conduction of the distal AV node or infranodal area, might account for second‐degree AV block during AVNRT. Slow pathway ablation is safe and effective in patients who have AVNRT with 2:1 AV block.
Paroxysmal Atrioventricular Block Induced During Head‐Up Tilt Testing in an Apparently Healthy Man
Authors: SUMIYOSHI MASATAKA , NAKATA YASURO , MINEDA YORIAKI
Published: April 2007

Paroxysmal AV Block During HUT Testing. Introduction: Prolonged asystole during head‐up tilt testing has been reported, but the occurrence of paroxysmal AV block appears to he rare.

Methods and Results: A 25‐year‐old man with no history of syncope underwent head‐up tilt testing. After 11 minutes of 80° tilting, he developed syncope with paroxysmal AV block and asystole lasting 10.5 seconds. However, this response was not reproduced during a subsequent tilt test 4 weeks later. Treadmill exercise testing and Holter monitoring showed no abnormalities. Power spectral analysis of heart rate variability revealed a marked increase in sympathetic activity several minutes before the induction of paroxysmal AV block.

Conclusion: We report a case of paroxysmal AV block that occurred during head‐up tilt testing but did not recur on a subsequent test in an apparently healthy young man.
Mechanisms of Idiopathic Left Ventricular Tachycardia
Authors: LERMAN BRUCE B. , STEIN KENNETH M. , MARKOWITZ STEVEN M.
Published: April 2007

Idiopathic Left Ventricular Tachycardia. Idiopathic left ventricular tachycardia (ILVT) differs from idiopathic right ventricular outflow tract (RVOT) tachycardia with respect to mechanism and pharmacologic sensitivity. ILVT can he categorized into three subgroups. The most prevalent form, verapamil‐sensitive intrafascicular tachycardia, originates in the region of left posterior fascicle of the left bundle. This tachycardia is adenosine insensitive, demonstrates entrainment, and is thought to he due to reentry. The tachycardia is most often ablated in the region of the posteroinferior interventricular septum. A second type of ILVT is a form analogous to adenosine‐sensitive RVOT tachycardia. This tachycardia appears to originate from deep within the interventricular septum and exits from the left side of the septum. This form of VT also responds to verapamil and is thought to he due to cAMP‐mediated triggered activity. A third form of ILVT is propranolol sensitive. It is neither initiated or terminated by programmed stimulation, does not terminate with verapamil, and is transiently suppressed by adenosine, responses consistent with an automatic mechanism. Recognition of the heterogeneity of ILVT and its unique characteristics should facilitate appropriate diagnosis and therapy in this group of patients.
Recent Advances in Cardiopulmonary Resuscitation
Authors: LURIE KEITH G. , UNDNER KARL H.
Published: April 2007

Recent Advances in CPR. Mechanical and pharmacologic measures intended to increase blood now to vital organs are the mainstay of therapy for patients in cardiac arrest. Several new cardiopilmonary resuscitation (CPR) techniques as well as novel devices and pharmacologic agents have been developed and tested since the first report of manual closed chested CPR over three decades ago. These recent mechanical and pharmacologic advances in the treatment of cardiac arrest are described. Some of these new techniques, devices, and drug therapies are presently undergoing clinical evaluation in patients in cardiac arrest. While many of these new methods and techniques have shown promise in small clinical trials in humans, none have yet lo be found to be conclusively superior to manual closed chested CPR and treatment with standard pharmacologic agents.