bluuebunny/crossref_metadata_2025 huggingface dataset:
Parenting Competence, Social Support, and Self‐Esteem in Teen Mothers Case Managed by Public Health Nurses
Authors: Herrmann Marilyn M. , Cleve Lois Van , Levisen Linda
Published: May 2007

ABSTRACT The purpose of this descriptive study was to determine whether self‐esteem, parenting competence, and social support for teenage mothers changed over the first 18 months of parenting when case managed by a public health nurse (PHN). A sample of 56 first‐time teen mothers from a health department parenting project agreed to participate in the study. PHN case managers collected data close to the birth of the infants and at 6, 12, and 18 months. Demographic findings of teen mothers showed that the majority were below expected grade level, over half lived with parents, and over half were children of teen mothers. Outcome findings related to the infants revealed no delays in development as measured on the Denver Development Screening Test, adequate follow‐up for identified health problems, and a high percentage of the children with up‐to‐date with immunizations. The research question findings showed a statistically significant drop in self esteem for the teens between birth and 6 months, and in social support between 6 and 18 months. No other findings were significant, but some trends appeared when the sample was divided by ethnicity, suggesting a need for closer follow‐up for certain groups. Implications for public health nursing and nursing education are included.
In vitro evaluation of prestorage pools consisting of mixed A and O platelet concentrates
Authors: Sweeney Joseph , Kouttab Nicola , Holme Stein , Cheves Tracey , Nelson Ed
Published: May 2007

BACKGROUND: Current FDA regulations allow the prestorage pooling of whole blood–derived platelet concentrates (PCs) of identical ABO type in a recently cleared platelet (PLT) pooling bag (Acrodose, Pall Medical). It is unclear how ABO‐mixed PC pools would store if pooled before storage.

STUDY DESIGN AND METHODS: Pools consisting of ABO‐identical PLTs and mixed A and O PLTs in varying proportions were evaluated on Days 1, 5, and 7 of storage with measures of the PLT storage lesion, lymphocyte activation, and activation of the complement and coagulation system. Data were analyzed by analysis of variance.

RESULTS: Pools did not differ on Day 7 in pH (p = 0.63), hypotonic shock response (p = 0.25), extent of shape change (p = 0.26), morphology score (p = 0.18), or white cell count (p = 0.79), but surface P‐selectin expression was more evident in the ABO‐mixed pools (p = 0.02). Small microscopic clumps of PLTs were observed in all pools, but were more prominent in the ABO‐mixed pools (p < 0.01). PLT counts, however, did not differ between pools (p = 0.93), indicating that only a small proportion of PLTs were clumped. Surface A‐antigen expression was proportional to the number of A PCs in each pool and did not vary between study days. Anti‐A1 titers were either unchanged or decreased by one dilution. Complement and coagulation activation markers did not differ between pools.

CONCLUSION: Pooling A and O PCs is associated with evidence of increased microscopic PLT clumping and activation, but these differences are not exacerbated with 7‐day storage. Other major measures of PLT quality do not differ, and there was no evidence of a mixed lymphocyte reaction.
Mobilization, collection, and immunomagnetic selection of peripheral blood CD34 cells in recovered aplastic anemia patients
Authors: Sloand Elaine M. , Read Elizabeth J. , Scheinberg Phillip , Tang Yong , More Kenneth , Leitman Susan F. , Maciejewski Jaroslaw , Young Neal S.
Published: May 2007

BACKGROUND: Most patients with severe aplastic anemia (sAA) respond to immunosuppression, but a significant number relapse or develop clonal abnormalities such as paroxysmal nocturnal hemoglobinuria, myelodysplasia, or leukemia. In principle, patients without matched sibling donors and older patients might benefit from transplantation of autologous hematopoietic peripheral blood progenitor cells (PBPCs) obtained during remission. Even patients who have clinically recovered from aplastic anemia have diminished hematopoietic progenitor cells, so the practicability of PBPC mobilization in these individuals is unknown.

STUDY DESIGN AND METHODS: The feasibility of PBPC mobilization in nine patients with a history of sAA was evaluated. Granulocyte–colony‐stimulating factor (10 µg/kg) was administered subcutaneously for 5 days and followed by a 12‐L leukapheresis procedure.

RESULTS: Only two of the nine patients had sufficient mobilization of CD34 cells to merit collection; in these cases sufficient CD34 cells were obtained for autologous transplantation should the need arise.

CONCLUSION: PBPC collection is feasible only in a fraction of recovered AA patients.
Effects of Milrinone on Atrioventricular Conduction in the Canine Heart Under Normal Conditions, During Atrial Flutter and After Ligation and Reperfusion of the Septal Artery
Authors: DAVIDENKO JORGE M. , FARAH ALFRED E. , ANTZELEVITCH CHARLES
Published: May 2007

Milrinone and AV Conduction. Milrinone, in addition to its vasodilatory and inotropic actions, has been shown to enhance or restore electrical activity in depolarized tissues and to improve conduction in isolated cardiac tissues depressed by exposure to an ischemic environment. These electrophysiological actions of the drug are thought to be secondary to milrinone's ability to enhance the transmembrane calcium current (ICa). The present study was designed to evaluate the effectiveness of milrinone (10–100 μg/kg, IV bolus) to modulate atrioventricular (AV) nodal conduction in anesthetized dogs under normal conditions, after ligation and reperfusion of the septal coronary arteries and during atrial flutter. All dosage regimens (10–100 μg/kg milrinone) produced a positive inotropic effect with no significant changes in blood pressure. Under normal conditions, 100 jig/kg of milrinone significantly reduced the PR interval, Wenckebach cycle length and AV nodal refractory period without causing a significant change in heart rate. The improvement in AV conduction and decrease in AV nodal refractoriness led to significant dose‐dependent increases in ventricular rate during atrial flutter. Low doses of milrinone also accelerated the flutter rate. Ligation of the septal coronary arteries for 2 to 6 hours produced stable atrioventricular conduction disturbances in six of the 11 dogs studied: complete AV block (n = 1), second‐degree AV block (n= 2) and first‐degree AV block (n= 3). Milrinone (100 μg/kg) improved AV conduction in five of the six dogs. Reperfusion of the septal arteries following 6 hours of ligation produced a sustained high degree AV block in two out of five dogs. Milrinone promptly restored 1:1 conduction in both cases. Our results suggest that milrinone may be of benefit in the treatment of some cases of AV conduction disturbance and that the drug, through its effects to facilitate AV conduction and abbreviate AV refractoriness, can lead to a significant and perhaps dangerous increase in ventricular rate in patients with atrial flutter or fibrillation. (J Cardiovasc Electrophysiol, Vol 1. pp. 93–102. 1990)
Laser Scanner Observations of Heterogeneous Conduction Patterns in Rabbit Epicardium Induced by Cellular Uncoupling with Heptanol
Authors: HILL BRUCE C. , COURTNEY KENNETH R. , DELMAR MARIO
Published: May 2007

Heptanol Disrupts Epicardial Conduction. This study examines how severely reduced intercellular electrical coupling affects the pattern of activation of left ventricular rahhit epicardium. Five thin (< 1‐mm thick) flaps of < 60 mm2 were stained in vitro with potentiometric dye WW781. A helium‐neon laser beam was scanned over 63 spots on each flap, and the voltage‐dependent fluorescence intensity from each spot was used to construct maps of the activation resulting from pacing at a single site. Introducing heptanol (1.75 mM) produced lines of conduction hlock in four of the five preparations after times ranging from 7 to 71 minutes; at varying intervals during this time, activation patterns were obtained. Fiber orientation was later determined from histologic sections. Heptanol changed the relatively uniform conduction seen under control conditions to heterogeneous patterns having regions of slowed conduction and lines of partial and complete block oriented predominantly parallel to the fiber direction (i.e., transverse propagation was blocked). The two partial blocks, which did not extend across the entire tissue, caused the activation wave to pivot around one end of the block line. The subsequent retrograde activation of the line's distal side was consequently delayed. Two points on opposite sides of these hlocks, separated by < 1 mm, had activation times differing by as much as 89 msec rather than a normal 3–5 msec. Thus, sufficient uncoupling can alter conduction pathways on the scale of a few millimeters. The resulting dispersion in activation times at closely spaced points may predispose poorly‐coupled cardiac tissue to development of reentrant arrhythmias. (J Cardiovasc Electrophysiol. Voi. I, pp, 426–436. October 1990)
Competitive Anterograde and Retrograde Atrioventricular Junctional Activation in Atrial Fibrillation
Authors: WITTKAMPF FRED H.M. , JONGSTE MIKE J.L. DE , MEIJLER FRITS L.
Published: May 2007

Reset and Cancellation. In eight medically‐treated patients with chronic atrial fibrillation and a random ventricular rhythm, we studied the effect of single right ventricular stimuli delivered after each eighth spontaneous R wave during at least 1 hour. The coupling interval of the extrastimulus was fixed and differed marginally from the shortest spontaneous RR interval. The histograms of spontaneous RR intervals and of the “compensatory” pauses following the ventricular extrasystoles were calculated. Analyses of these histograms and simulation of the interaction between anterograde and retrograde impulses in a computer model suggests that in seven of the eight patients the compensatory pause may be caused by two distinctly different mechanism.s: (1) reset of the timing cycle of atrioventricular nodal activation by relatively early retrograde impulses: and (2) interception of anterograde impulses by relatively late ventricular extrasystoles. The finding that early retrograde impulses are not blocked by concealed atrioventricular nodal conduction makes the existence of decremental conduction and extinction of atrial impulses at different levels within the node unlikely. The results of this study support the hypothesis that the distal side of a weakly coupled junctional area inside the AV node behaves as a pacemaker for the ventricular rhythm during atrial fibrillation. (J Cardiovasc Electrophysiol, Vol. 1. pp. 448–456, October 1990)
Experience with Kapton‐Based Bipolar Electrode Arrays Used During Computerized Intraoperative Mapping
Authors: PIEPER CARL F. , LAWRIE GERALD , PARSONS DANIEL , LACY JEFFREY , ROBERTS ROBERT , PACIFICO ANTONIO
Published: May 2007

Kapton Arrays for Computerized Mapping. A new technology for intraoperative mapping of the sites of origin and propagation of supraventricular (SVT) and ventricular tachycardia (VT) was implemented and evaluated. Kapton forms a thin, flexible substrate on which copper layers can be bonded, etched, and interconnected similar to a multilayered printed circuit board. Narrow Kapton electrode assemblies with 20 contacts spaced over 113 mm were used to construct epicardial sock electrode arrays (Ep) having 238 electrodes and endocardial balloon electrode arrays (En) having 168 electrodes. These arrays were used for mapping 20 consecutive patients undergoing surgery for SVT or VT. In 10 surgeries for VT, bipolar electrograms from 1,045 Ep and 606 En electrode pairs were examined. Responses were recorded from 88.7% Ep and 94.9% En sites. Of 118 Ep sites not showing a response, 27.1 % were due to poor electrode contact near the apex, or AV groove, and 70.3% approximated unexcitable tissue. Among the 31 En sites showing no response, 35.5% were located about the mitral annulus, and 32.3% over unexcitable tissue. In 10 surgeries for SVT, bipolar electrograms from 1,114 E p electrode pairs were studied. Responses were seen at 94.3% sites. Of the 63 sites not showing a response, 63.5% resulted from poor electrode contact near the apex or AV groove. These electrode arrays, utilizing Kapton strips, have proven highly effective and reliable for computerized intraoperative recording. (J Cardiovasc Electrophysiol, Vol. 1, pp. 496–505, December 1990)
Measurement of Human Ventricular Effective Refractory Periods: Effect of Incremental Versus Decremental Extrastimulation
Authors: BEAUREGARD LOU‐ANNE M. , FRIEHLING TED D. , MARINCHAK ROGER A. , KOWEY PETER R.
Published: May 2007

Incremental Versus Decremental Extrastimulation for Refractoriness. Measurement of ventricular refractoriness is performed routinely at electrophysiological study but methods of refractory period determination have not been standardized. This study compared the difference between refractory period measurements hy incremental and decremental extrastimulns techniques. Twenty‐six patients were included and a > 5‐msec increase in incremental compared to decremental ventricular effective refractory period (V ERP) was found in all (hysteresis interval). There was no significant effect of order of extrastimulus protocol, right ventricular site, or current strength on the hysteresis interval. There was an effect of longer duration of drive to increase hysteresis interval. When incremental extrastimulation was performed first, there was an increased hysteresis interval at shorter cycle lengths of drive, whereas when decremental extrastimulation was performed first, there was an increased hysteresis interval in sinus rhythm. We conclude that decremental extrastimulation yields shorter refractory periods tban incremental extrastimulation, as a combined effect of cycle length shortening and duration of pacing. A standard method for determining ventricular refractoriness should he considered. (J Cardiovasc Electrophysiol, Vol. 1, No. 6, pp. 506–511 December 1990)
Transmembrane Potential Characteristics and Muscarinic and Beta‐Adrenergic Responsiveness in Purkinje Fibers From a Canine Model of Lethal Ventricular Arrhythmias
Authors: HAMRA MARY , VIAMONTE VICTOR MOLINA , ROSEN MICHAEL R.
Published: May 2007

Autonomic Modulation of Lethal Arrhythmias. Susceptibility to sudden death in dogs with healed myocardial infarction can be defined by the response to transient ischemia during treadmill exercise and can often be predicted by the baroreceptor slope, which is determined from least squares regression of the RR interval, or heart rate, response to increasing systolic pressure during a phenylephrine infusion. We used standard microelectrode techniques to study isolated Purkinje fiber bundles as well as subendocardial Purkinje fibers overlying the infarcted myocardium of dogs classified by treadmill testing as resistant or susceptible to sudden death. We determined the response to isoproterenol (Iso) alone and in the presence of acetylcholine (ACh). Control action potential (AP) characteristics for both groups were similar except for the following: in normal Purkinje fibers, susceptible dogs had a significantly lower AP overshoot and Vmax than resistant dogs. In addition, fibers from the in arct zones of susceptible dogs had lower maximal diastolic potentials than those from the normal Purkinje fibers of susceptible dogs. Iso significantly shortened AP duration in normal and infarct zone fibers of both groups. ACh alone had no effect on AP duration. In the infarct zone, ACh 10−7M did not antagonize Iso‐induced shortening of AP duration in susceptible or resistant dogs; but ACh 10−5M completely blocked Iso effects in resistant dogs. In normal Purkinje fibers, ACh antagonism of Iso effects was seen in susceptible and resistant animals. Iso and ACh had no significant effect on other transmembrane potential characteristics. The differences between resistant and susceptible dogs in control transmembrane characteristics and accentuated antagonism may contribute to the substrate that increases the likelihood of sudden death in this model.
Selective Class III Antiarrhythmic Properties of a Novel Agent, UK‐66,914, During Chronic Myocardial Infarction
Authors: ONUFER JOHN R. , DALRYMPLE HARRIS W. , CORR PETER B.
Published: May 2007

Antiarrhythmic Properties of UK‐ 66,914. UK‐66,914 is a potent Class III antiarrhythmic agent that has no effect on conduction velocity in normal tissue in vitro. The present study was performed to evaluate the influence of UK‐66,914 on conduction velocity in vivo in canine hearts with a previous myocardial infarction. Detailed three‐dimensional mapping of the heart in vivo was obtained using simultaneous recordings from 232 transmural sites. In dogs with a chronic anterior myocardial infarction, UK‐66,914 (50 μg/kg) did not alter conduction velocity in regions exhibiting normal conduction (gt; 50 cm/sec) or regions with slowed conduction (< 50 cm/sec) despite an 11%‐15% increase in the ventricular effective refractory period. UK‐66,914 prevented the induction of ventricular tachycardias by programmed electrical stimulation due to lengthening of the effective refractory period with no direct or indirect effects on conduction velocity in dogs with chronic infarcts of 1‐year duration. Because the endocardial border zone surrounding the infarct was critical to the development of the reentrant pathway in vivo, studies were performed in tissue from this region in vitro utilizing a high‐resolution, 224 bipolar grid recording array. The effects of UK‐66,914, d‐sotalol, and procainamide on conduction velocity were compared in this region at concentrations that elicited a comparable increase in the effective refractory period of 40 msec. UK‐66,914 and d‐sotalol did not alter conduction velocity in regions with conduction velocities > 30 cm/sec, 15‐30 cm/sec, or < 15 cm/sec, whereas procainamide significantly decreased conduction velocity at all three levels. Evaluation of the hemodynamic profile of UK‐66,914 revealed no negative ionotropic effects in conscious dogs even at doses twentyfold those required to elicit increases in the effective refractory period. Therefore, UK‐66,914 is a potent and specific Class III antiarrhythmic agent, which does not alter conduction velocity in hearts with a previous myocardial infarction and exerts no negative inotropic effects.
The Use‐Dependent Effects of Acute and Chronic Amiodarone Administration on His‐Purkinje Conduction and the Interaction of β‐Adrenergic Stimulation
Authors: EPSTEIN LAURENCE M. , SCHEINMAN MELVIN M. , CHIN MICHAEL C. , KATZUNG BERTRAM G.
Published: May 2007

Use‐Dependent Effects of Amiodarone. Amiodarone is a highly effective antiarrhythmic agent. However, its exact mechanism of action remains uncertain. Prior studies suggest that intravenous amiodarone produces different electrophysiologic effects than chronic amiodarone administration. In addition, the effects of other antiarrhythmic agents and β‐adrenergic stimulation on the electrophysiologic effects of amiodarone have not been well defined. In this study, we sought to evaluate the use‐dependent effects of intravenous (acute) versus oral (chronic) amiodarone administration on His‐Purkinje conduction in a closed‐chest canine model. We also sought to evaluate the effects of intravenous lidocaine and isoproterenol on the use‐dependent effects of chronically administered oral amiodarone. We found: (1) Acutely administered intravenous amiodarone (5 mg/kg bolus, followed by a 0.05 mg/kg/min infusion) does not produce a significant use‐dependent effect on His‐Purkinje conduction (serum amiodarone level 2.7 ± 1.1 mg/L), and acute beta blockade did not enhance use‐dependent effects of amiodarone; (2) Chronically administered oral amiodarone (1,000 mg/day ± 2 weeks) produced significant use‐dependent effects on His‐Purkinje conduction at similar serum drug concentrations (mean level 2.6 ± 1.5 mg/L; (3) Intravenous lidocaine (10 mg/kg bolus, 0.2 mg/kg/min infusion) produced significant additional use‐dependent effects to that of chronic oral amiodarone but only at rapid paced rates (cycle length 300‐210 msec); and (4) Isoproterenol (5 μg/min infusion) significantly attenuated the use‐dependent effects of chronically administered amiodarone. The mechanism of action of acutely administered intravenous amiodarone appears to be different from that of chronic oral amiodarone. In addition, the marked use‐dependent effects observed after chronic amiodarone administration were reversed after catecholamine administration suggesting that attenuation of use dependence by sympathetic stimulation may negate some of salutary effects of amiodarone.
Determinants of Antidromic Wave Front Propagation During Entrainment of Reentrant Arrhythmias
Authors: STEVENSON WILLIAM G. , WOO MARY A.
Published: May 2007

Antidromic Conduction. During entrainment or resetting of ventricular tachycardia, the distance a stimulated antidromic wave front propagates determines the degree of QRS fusion observed. Determinants of antidromic wave front propagation distance during stimulation at reentry circuit sites were studied in computer simulations of figure eight reentry circuits. When not limited by refractory tissue, antidromic propagation distance depended on the stimulus timing, the conduction velocity in the antidromic direction away from the stimulus site, and the time available for propagation before collision with a returning orthodromic wave front. The latter was determined by the conduction time through the circuit in the orthodromic direction from the stimulus site. Faster conduction from the stimulus site in the orthodromic direction relative to the antidromic direction diminished antidromic wave front propagation distance. Consequently, in circuits with heterogeneous conduction velocities, antidromic propagation distance was dependent on the location of the stimulus site. Stimulation in slow areas limited antidromic propagation distance, although increasing stimulus prematurity increased antidromic propagation distance markedly if the antidromic wave front reached faster tissue. These findings explain the ability of rapid or premature stimuli to entrain or reset tachycardia without producing detectable antidromic wave front effects (QRS fusion) on the surface electrocardiogram when the stimulation site is located centrally within slowly conducting areas in the reentry circuit. However, greater antidromic propagation occurs with stimulation at or near more rapidly conducting sites increasing the likelihood that antidromic effects will be seen on the surface electrocardiogram.
Signal Averaging of the Surface QRS Complex: Practical Applications
Authors: GOMES J. ANTHONY , WINTERS STEPHEN L. , IP JOHN
Published: May 2007

Signal‐Averaged ECG. Signal averaging of the surface QRS complex has been used in recent years to detect electrical signals of small amplitude not otherwise evident on the surface ECG. The technique enables detection of low‐amplitude signals in the terminal portion of the QRS complex and the ST segment. These low‐amplitude signals termed late potentials (LPs) have been correlated with the presence of fragmented electrical activity recorded from endocardial and epicardial sites due to inhomogeneous propagation of conduction in scarred myocardium. Recent studies have supported the value of the signal‐averaged ECG for risk stratification postmyocardial infarction, in the management of patients with syncope and patients with sustained ventricular tachycardia (VT), and survivors of cardiac arrest.
Variations in Human Atrial Flutter Cycle Length Induced by Ventricular Beats: Evidence of a Reentrant Circuit with a Partially Excitable Gap
Authors: LAMMERS WIM J.E.P. , RAVELLI FLAVIA , DISERTORI MARCELLO , ANTOLINI RENZO , FURLANELLO FRANCESCO , ALLESSIE MAURITS A.
Published: May 2007

Variations in Atrial Flutter Cycle Length. Introduction: The purpose of this investigation was to study the mechanisms responsible for small variations in atrial flutter cycle lengths. Methods and Results: In a study group of 11 patients with common atrial flutter, atrial electrograms were recorded from an intraesophageal lead together with a surface lead (V1). Upon the onset of the QRS complex, atrial flutter intervals consistently increased by an average of 1.8% (SD± 0.9; P <0.01) and subsequently decreased by 2.1% (SD ± 0.8; P <0.01) before returning to the average flutter rate. Carotid sinus massage, which temporally prevented ventricular activation, markedly reduced the variations in atrial flutter intervals. Ventricular pacing at different rates clearly demonstrated that the pattern in atrial flutter intervals was coupled to the moment of ventricular contraction. The hypothesis was formulated that these periodic variations in atrial flutter intervals following a ventricular contraction were caused by the influence of stretch of the atrial myocardium on the conduction properties of a circulating impulse in the atrium. The secondary decrease in flutter rate could be explained if a partial excitable gap is assumed between head and tail of the circus movement. This hypothesis was tested in a simulation study, which revealed that the alternation in intervals as found in patients could only be reproduced if the excitable gap in the circus movement was partially excitable. Conclusion: In conclusion, the analysis of variations in atrial flutter cycle lengths points to a mechanism of circus movement with a partially excitable gap in common atrial flutter.
Activation Time Detection Algorithms Used in Computerized Intraoperative Cardiac Mapping: A Comparison with Manually Determined Activation Times
Authors: PIEPER CARL F. , BLUE RUSSELL , PACIFICO ANTONIO
Published: May 2007

Activation Time Detection for Intraoperative Mapping.
Introduction: Local activation determined from monopolar electrograms usually is marked at the time of the minimum slope. In bipolar recordings, the peak, the maximum absolute slope, the baseline crossing of the segment containing the maximum absolute slope, and morphological criteria have been used. The purpose of this work is: (1) to compare activation times determined using these algorithms with activation times corrected by electrophysiologists; and (2) to determine which computerized algorithm requires fewest operator correction of outliers. Methods and Results: Monopolar and bipolar electrograms were collected from the epicardium of subjects undergoing surgery for ventricular tachycardia and Wolff‐Parkinson‐White syndrome, and the above bipolar and monopolar algorithms were evaluated. The electrophysiologists viewed adjacent channels and evolving isochronal maps but not the computer markings. The morphological algorithm compared most favorably with times marked up by electrophysiologists having an overall average difference of 2.2 ± 3.1 msec. For monopolar data, a five point, least square fit, second‐order slope approximation algorithm most closely agreed with the electrophysiologist corrected algorithm (3.2 ± 4.0 msec). The morphological and least square algorithms also produced the fewest outliers (3.1% and 5.7%, respectively). When outliers were removed, bipolar and monopolar discrepancies were reduced to 1.8 ± 1.9 and 2.5 ± 2.3 msec, respectively. Conclusions: Thus, among those algorithms tested, an algorithm based on morphological criteria is best suited for computer determination of bipolar activation times and compares favorably to variations between electrophysiologist corrected and computer marked activation times determined traditionally by the largest negative slope in monopolar data. Identification of outliers using contextual and improved morphological algorithms may improve computerized mapping system performance.
The Atrial Electrogram During Clinical Electrophysiologic Studies: Onset versus the Local/Intrinsic Deflection
Authors: FISHER JOHN D. , BAKER JAY , FERRICK KEVIN J. , FRAME ROSEMARY , KIM SOO G. , ROTH JAMES A. , MERCANDO ANTHONY D.
Published: May 2007

The Local Atrial Deflection.
Introduction: As a wave front passes unfiltered bipolar recording electrodes, the point of local depolarization is marked by a maximal change in voltage, i.e., the intrinsic deflection. However, during electrophysiologic studies, the depolarization (A) on the lead recording the His‐bundle potential traditionally has been measured at the first rapid reproducible deflection on a filtered electrogram. This methodology permits considerable latitude for subjective interpretation. The purpose of this study was to assess the timing of the atrial electrogram using the intrinsic deflection of relatively unfiltered electrograms (0.1‐4.0 to 1,250 Hz) or the equivalent on filtered recordings. Methods and Results: To do this we studied 70 patients without evidence of atrial or atrioventricular (AV) nodal disease, documenting the difference in timing between the A wave as traditionally measured and as measured at its peak local deflection (AL) determined from simultaneously recorded filtered and relatively unfiltered electrograms. New ranges based on the AL were established for timing of intra‐atrial and AV nodal conduction intervals. The P‐A (41 ± 11 msec) was significantly shorter than the P‐AL (55 ± 12) and the A‐H (80 ± 20) was longer than the AL‐H (66 ± 21 msec), both P <0.001. Interobserver differences in measurements were smaller when using the local (AL) rather than traditional criteria. Conclusions: Conventional measurement of the A deflection provides only a rough estimate of local depolarization of the atrium near the AV node. The criteria proposed in the present article may (1) provide a better estimate of the timing of local depolarization; (2) have application in computerized timing of intervals; and (3) decrease technical problems and subjective error.
Changes in Late Potential Measurements as a Function of Decreasing Bandwidth
Authors: BERBARI EDWARD J. , RAJAGOPALAN C.V. , LANDER PAUL , LAZZARA RALPH
Published: May 2007

Bandwidth of Late Potentials Introduction: Limited bandwidth systems such as Holter recorders are being used to record cardiac late potentials. Standard late potential systems have a low‐pass frequency of 300 Hz. This suggests that Holter tape systems may significantly distort the late potential measurements, when compared to standard late potential systems. Methods and Results: Signal‐averaged recordings were obtained with an analog bandwidth of 0.05‐300 Hz. Digital filters were then used to do high‐pass filtering and low‐pass filtering. All XYZ signal‐averaged recordings were low‐pass filtered at frequencies of 250, 150, 100, 75, 50, and 25 Hz using a second order Butterworth filter. A fourth order 40 Hz bidirectional high‐pass filter was then applied to each set of recordings. The QRS duration (QRSd) was measured in the filtered vector magnitude. Thirty‐eight syncope patients who had negative electrophysiologic studies for ventricular tachycardia, no prior infarction, normal ejection fractions (> 50%), and a QRSd <120 msec served as the negative late potential group. Thirty‐seven patients with clinical ventricular tachycardia, a positive electrophysiologic study for ventricular tachycardia, and a QRSd>120 msec served as the positive late potential group. Conclusions: A statistically significant lengthening of the QRSd (P <0.05) was observed in the patients with late potentials between the 250 Hz and 25 Hz low‐pass filter. There was a statistically significant shortening of the QRSd in the negative late potential patients between 250 Hz and 25 Hz, as well as between 250 Hz and 50 Hz, with P<0.05 in both cases. Thus, significant changes in late potentials are seen in limited bandwidth recordings that may limit the clinical usefulness of such systems.
Behavioral Triggers of Silent and Symptomatic Myocardial Ischemia
Authors: KRANTZ DAVID S. , GABBAY FRANCES H. , HEDGES SUSAN M. , KLEIN JACOB , NEBEL LINDA E. , HELMERS KARIN F. , PATTERSON STEPHEN , SAMETH JULIA L. , GOTTDIENER JOHN S. , ROZANSKI ALAN
Published: May 2007

Behavior and Myocardial Ischemia. Recent ambulatory electrocardiography studies reveal that myocardial ischemia out‐of‐hospital exhibits features that may not be evident during controlled exercise testing. Specifically, out‐of‐hospital ischemia: (1) is more frequently asymptomatic or silent; (2) occurs during a wide variety of mental, as well as physical, activities; (3) is triggered at relatively low heart rate elevations compared to exercise; (4) exhibits a circadian rhythm; and (5) exhibits variability over time. This article reviews recent field and laboratory research suggesting that behavioral factors, including mental stress, may contribute to the typical features of myocardial ischemia out‐of‐hospital.
Arrhythmogenic Role of Autonomic Innervation During Ischemia/Infarction and the Long QT Syndrome
Authors: ZIPES DOUGLAS P.
Published: May 2007

Autonomic Innervation During Ischemia/Infarction and Long QT Syndrome. Although it is generally well accepted that the autonomic nervous system can promote, precipitate, or prevent the development of cardiac arrhythmias, the mechanisms by which this transpires are incompletely understood. This review will focus on selected recent observations concerning autonomic innervation of the heart, the effects of myocardial ischemia and infarction on such innervation, and the modulation of arrhythmias in the long QT syndrome.
Shift and Termination of Functional Reentry in Isolated Ventricular Preparations with Quinidine‐Induced Inhomogeneity in Refractory Period
Authors: FAST VLADIMIR G. , PERTSOV ARCADY M.
Published: May 2007

Mechanism of Reentry's Instability. Introduction: The purpose of this investigation was to study the mechanisms responsible for instability and termination of functionally determined reentry.

Methods and Results: The activation sequence was recorded using multielectrode mapping technique in preparations isolated from rabbit right ventricle. In nine preparations, functional inhomogeneity was created on the epicardial surface. For this purpose, two parts of a preparation divided by a thin rubber barrier were superfused by different solutions: normal Tyrode's solution and Tyrode's solution containing quinidine (5–10 mg/L). As a result, there was a difference of refractory period of 45 ± 12 msec (n = 6). Premature stimulation of sites situated in the normally superfused region led to the appearance of unstable reentrant circuits at the border of inhomogeneity (32 cases) in seven of the nine preparations. In most cases (24 of 32) reentrant circuits shifted along the border of inhomogeneity. Reentrant circuits with clockwise and counterclockwise rotations had opposite directions of shift. Because of the shift, reentrant circuits moved to the border of the preparation where they were extinguished.

Conclusion: Our results suggest that inhomogeneity in refractoriness that gives rise to initiation of reentrant circuits also causes their termination. (J Cardiovasc Electrophysiol, Vol. 3, pp. 255–265, June 1992)
Idiopathic Long QT Syndrome Exacerbated by Beta‐Adrenergic Blockade and Responsive to Left Cardiac Sympathetic Denervation: Implications Regarding Electrophysiologic Substrate and Adrenergic Modulation
Authors: MALFATTO GABRIELLA , ROSEN MICHAEL R. , FORESTI AUGUSTO , SCHWARTZ PETER J.
Published: May 2007

Electrophysiologic Substrate of Long QT Syndrome. Introduction: The mechanisms of T wave abnormalities and arrhythmias in patients affected by the long QT syndrome (LQTS) are unclear, as are the reasons why a high‐risk subgroup (20%) continues to have syncope during therapy with beta blockers but is protected after left cardiac sympathetic denervation (LCSD). Afterdepolarizations, both early (EAD) or delayed (DAD), have been implicated as likely electrophysiologic substrates for the ECG abnormalities and arrhythmias in LQTS. To test this hypothesis, we analyzed nine Hotter recordings of a LQTS patient typical of the high‐risk subgroup.

Methods and Results: We applied to the ECG rules derived from previous in vitro and in vivo studies, which relate the coupling intervals of the dysrhythmic beats to the preceding cycle lengths, to discriminate among arrhythmia mechanisms. In the absence of therapy, the patient's ECG showed peaked T waves, with a notched second component accentuated by sinus pauses. The amplitude of the notches increased directly with the preceding RR interval (r = 0.58, P < 0.05), as it is observed with EAD. Therapy with the beta blocker propranolol did not modify the notches, which maintained their amplitude and their relationship with the preceding RR (r = 0.62, P < 0.05). Moreover, during beta‐blocker therapy, ventricular premature beats, couplets, and runs of ventricular tachycardia (VT) occurred. The coupling intervals of ventricular premature beats and couplets were not influenced by the preceding RR intervals. By contrast, the coupling interval of the first beat of VT decreased as the preceding RR shortened, as it occurs with DAD‐induced triggered activity. After LCSD, T wave notch amplitude was reduced (P < 0.05) and was no longer influenced by the preceding RR (r = 0.31, P = 0.22). The same was true when the calcium entry blocker verapamil was administered.

Conclusion: In this patient, T wave abnormalities and some ventricular arrhythmias had the behavior observed in vitro for EAD and the consequent triggered activity. However, the cycle length dependence of VT manifested the behavior observed in vitro for DAD and the related triggered activity. The fact that these phenomena were accentuated by beta blockade and disappeared after LCSD suggests that the alpha‐adrenergic receptor‐effector system may be a modulator of T wave abnormalities and arrhythmias in some patients unresponsive to beta blockade and protected by LCSD. (J Cardiovasc Electrophysiol, Vol. 3, pp. 295–305, August 1992)
Effects of Flunarizine on Impulse Initiation in Canine Purkinje Fibers
Authors: PARK JEANNY K. , DANILO PETER , ROSEN MICHAEL R.
Published: May 2007

Effects of Flunarizine on Impulse Initiation. Introduction: The calcium channel blocker, flunarizine, selectively blocks accumulation of intracellular calcium during conditions of calcium overload. It has been reported to selectively terminate delayed after depolarization‐induced arrhythmias in intact dogs.

Methods and Results: Using standard microelectrode techniques, we studied the effects of flunarizine on the transmembrane action potential and various arrhythmogenic mechanisms in canine Purkinje fibers. Flunarizine significantly decreased the fast response action potential duration at 50% repolarization in a concentration‐dependent manner (10‐8 to 10‐5M), but had no effect on maximum diastolic potential, overshoot, maximum upstroke velocity (Vmax), or APD at 90% repolarization. For Ca2+‐induced slow response action potentials, flunarizine decreased the overshoot, and prolonged action potential duration at both 50% and 90% repolarization. It had no effect on automaticity of Purkinje fibers exposed to solutions containing either low [K+] or barium chloride. Flunarizine, 10‐5M, inhibited the development of both ouabain‐induced and calcium‐ and catecholamine‐induced delayed after depolarizations. It did not inhibit the development of cesium‐induced early afterdepolarizations.

Conclusions: Thus, in vitro, flunarizine selectively suppresses delayed after depolarizations and has no effects on early afterdepolarizations or normal or abnormal automaticity. Hence, its utility in intact animal models of triggered arrythmias is borne out mechanistically in these isolated tissue studies. (J Cardiovasc Electrophysiol, Vol. 3, pp. 306–314, August 1992)
Alcohol Ablation for Tachycardia Therapy
Authors: OKISHIGE KAORU , FRIEDMAN PETER L.
Published: May 2007

Alcohol Ablation for Tachycardia Therapy. Selective administration of ethanol into branches of the coronary arterial circulation has been proposed as a means of ablating cardiac fibers that give rise to cardiac arrhythmias, no matter where in the heart they might be located. In patients with uncontrollable ventricular rates in the setting of atrial fibrillation or atrial flutter, ethanol has been infused into the atrioventricular (AV) nodal artery in order to abolish or modify AV nodal conduction. Such a procedure is technically feasible in approximately 80% of patients and is successful in 70%–80% of individuals who are treated. Many of these patients require permanent pacemaker implantation because of chronic complete AV block. Intracoronary ethanol ablation has also been used to treat patients with AV nodal reentrant supraventricular tachycardia and ectopic atrial tachycardia, but there is scant clinical experience with the technique in these arrhythmias. Among patients with incessant or recurrent ventricular tachycardia (VT), intracoronary ethanol ablation has abolished clinical recurrences of arrhythmia in 78% of treated individuals. However, inability to identify a VT‐related arterial branch and other technical considerations may limit application of ethanol ablation to fewer than 50% of potential candidates with VT. Ethanol ablation is generally well tolerated, but significant complications have occurred, including ethanol‐induced occlusion of nontarget coronary arteries leading to unintended myocardial infarction. Procedure‐related death has also occurred. Ethanol ablation shows promise as a method for abolishing intractable tachycardias but further study is required to improve the safety of the technique and to define more precisely which patients are the best candidates in whom to consider this approach. (J Cardiovasc Electrophysiol, Vol. 3, pp. 354–364, August 1992)
Role of Potassium Currents on Cell Excitability in Cardiac Ventricular Myocytes
Authors: DELMAR MARIO
Published: May 2007

Potassium Currents and Cell Excitability. Ventricular cell excitability has been mostly associated with the ability of sodium currents to generate an action potential upstroke. However, even in the presence of normal sodium currents, a cell will not generate an active response if it is unable to depolarize from the resting potential to the activation threshold. This article summarizes recent data demonstrating that potassium currents can act as important modulators of cell excitability. In fact, potassium currents can play a major role in determining the dynamics of Wenckebach periodicity, hysteresis of excitability, and active facilitation in ventricular myocytes. The article discusses the specific roles that the inward rectifier, IKb the delayed rectifier, IK, and the ATP‐sensitive, IK‐ATP currents play on the dynamic modulation of cell excitation. (J Cardiovasc Electrophysiol, Vol. 3, pp. 474–486. October 1992)
Cellular and Clinical Electrophysiology of Verapamil‐Sensitive Ventricular Tachycardias
Authors: LAUER MICHAEL R. , BING LIEM L. , YOUNG CHARLIE , SUNG RUEY J.
Published: May 2007

Verapamil‐Sensitive Ventricular Tachycardias. Ventricular tachycardia (VT) due to reentry is often associated with organic structural heart disease, such as coronary artery disease with previous myocardiai infarction, and primary or secondary cardiomyopathy. Treatment of this form of VT generally requires the use of potent antiarrhythmic drugs such as procainamide, quinidine, and amiodarone, or nonpharmacologic interventions such as endocardial resection and implantation of cardioverter defibrillators. Some forms of VT, typically occurring in younger patients and not associated with structural heart disease, may be due to a mechanism other than reentry and may be terminated or prevented by Ca2+ channel or beta blockers. Because these tachycardias are often so effectively treated with these rather benign agents, all patients with sustained VT undergoing an electrophysiologic study should be carefully evaluated to rule out the possibility of having these forms of VT. These tachycardias may be induced by treadmill exercise testing, programmed electrical stimulation, and/or catecbolamine infusion. While it appears that the mechanisms of these tachycardias may be caused by triggered activity related to afterdepolarizations or enhanced automaticity, there is evidence that some may in fact be due to reentry involving Ca2+‐dependent slow conduction. The cellular mechanisms of triggered activity and enbanced automaticity, and their relation to clinical ventricular arrhythmias, are discussed. (J Cardiovasc Electrophysiol, Vol. 3. pp. 500–514 October 1992)
Magnetic Field Interference in High‐Resolution Electrocardiography
Authors: AKER ERIC , SAINI VIKAS , MANOLIS ANTONIS S. , ESTES N.A. MARK
Published: May 2007

Magnetic Field Interference. Introduction: High‐resolution electrocardiography, with or without signal averaging, requires extremely low levels of extraneous noise pickup. A significant amount of such interference is transmitted to the patient electrode wires as a magnetic (as opposed to electric) field, which is unresponsive to many commonly used shielding methods.

Methods and Results: To investigate the source and quantify the strengths of magnetic fields, we used a battery‐powered device of our own design and performed magnetic field measurements in various locations in two hospitals. We found that significant sources of magnetic interference were cathode ray tube defiection coils, electric motors, and power transformers on wall‐mounted ophthalmoscopes or on the electrocardiographic equipment itself. The lowest noise level could be produced by running the patient electrode wires twisted closely together and by distancing the magnetic field sources, including electrocardiographic equipment.

Conclusion: We conclude that magnetic fields at typical locations in modern hospitals are usually of such strength as to cause significant interference in high‐resolution electrocardiography. To reduce such an interference, the patient electrode wires should be twisted together and all suspected magnetic field sources, including the signal‐averaging equipment itself, should be placed as remotely from the patient as possible. (J Cardiovasc Electrophysiol. Vol. 3. pp. 34–39, February 1992)
Activation of ATP‐Sensitive Potassium Channels Underlies Contractile Failure in Single Human Cardiac Myocytes During Complete Metabolic Inhibition
Authors: COHEN NERI M. , LEDERER WJ , NICHOLS COLIN G.
Published: May 2007

ATP‐Sensitive Potassium Channels in Human Heart. Introduction: The purpose of this study was to examine the electrophysiologic derangements that underlie contractile failure in single human heart muscle cells exposed to metabolic inhibition.

Methods and Results: Single myocytes were isolated from right atrial appendage specimens obtained intraoperatively from patients undergoing routine cardiac surgery. On exposure to lO‐mM 2‐deoxyglucose (to inhibit glycolysis) and 2‐mM cyanide (to inhibit oxidative phosphorylation), twitch shortening decreased to undetectable levels over 5–6 minutes. The action potential duration declined in parallel with the contractile failure. Using voltage clamp depolarizations of a fixed duration the twitch was maintained in metabolic blockade until the development of maintained (rigor) contracture. At this time a large increase in K+ conductance, which can be attributed to the activation of ATP‐sensitive K + channels (K ATP channels), was measured. In isolated inside‐out membrane patches, the ATP dependence of KaTP channel activity was described by a sigmoid curve with Ki,ATP (ATP concentration required for half‐maximal inhibition of K ATPchannel activity) = 8 μM and Hill coefficient (nH) = 1.2. The single channel current‐voltage relationship reversed close to the K + equilibrium potential and the conductance was approximately linear (g = 29 pS) over the voltage range included in the action potential (‐60 m V to +20 mV).

Conclusion: In human atrial cardiac myocytes subjected to complete metabolic inhibition, contractile failure is caused by action potential shortening resulting from an increase in K + conductance presumably through the activation of KATP channels. (J Cardiovasc Electrophysiol, Vol. 3, pp. 56–63, February 1992)