bluuebunny/crossref_metadata_2025_split huggingface dataset:
Independent Autonomic Modulation of the Human Sinus and AV Nodes: Evidence From Beat‐to‐Beat Measurements of PR and PP Intervals During Sleep
Authors: KOWALLIK PETER , MEESMANN MALTE 
Published: May 2007

Autonomic Modulation of Sinus and AV Nodes. Introduction: Evidence from animal experiments indicates that the autonomic nervous system may influence the sinus (SA) and atrioventricular (AV) nodes differently. We investigated, therefore, whether there are spontaneous functional differences in the innervation of the SA and AV nodes in man. Methods and Results: This study was performed in 10 healthy males (ages 21 to 26 years) during strict bed rest from 10 pm to 6 am. Three ECG leads were digitized on‐line. PR and PP intervals were determined on a heat‐to‐beat basis off‐line using a correlation algorithm with an accuracy of ± 2 msec and were verified visually. During; major body movements, there were sudden decreases in PP intervals of 36 to 827 msec (mean 335) for periods of 6 to 265 seconds (mean 24), During these phases of heart rate (HR) acceleration, PR intervals showed either concomitant shortening (9 to 30 msec), no change, or lengthening (6 to 25 msec). Furthermore, tonic changes in the PR interval occurred over 15‐minute periods during which the range of PP intervals was constant. Additionally, recovery‐adjusted PR interval (PR ‐ b2/RP) and cycle length were negatively correlated for some periods, which confirmed independent autonomic effects on SA node and A V node. Conclusion: Beat‐to‐beat measurement of PR intervals allows for evaluation of autonomic effects on the human AV node. The different patterns in PR intervals during sudden spontaneous increases in HR and the tonic changes in PR interval indicate that the autonomic inputs to the SA and AV nodes are, in principle, independent of each other.
Responses of the Transmembrane Potential of Myocardial Cells during a Shocks
Authors: ZHOU XIAOHONG , ROLLINS DENNIS L. , SMITH WILLIAM M. , IDEKER RAYMOND E. 
Published: May 2007

Responses of Transmembrane Potential During a Shock. Introduction: The purpose of this investigation was to study the transmembrane potential changes (δVm) during extracellular electrical field stimulation. Methods and Results: Vm was recorded in seven guinea pig papillary muscles in a tissue hath by a double‐barrel microelectrode with one barrel in and the other just outside a cell while shocks were given across the bath. The short distance (15 to 30 μm) between the two microelectrode tips and alignment of the tips parallel to the shock electrodes eliminated the shock artifact. Following ten SI stimuli, an S2 shock field created by a 10‐msec square wave was delivered during the action potential plateau or during diastole through shock electrodes 1 cm on either side of the tissue. Four shock strengths creating field strengths of 1.7 ± 0.1, 2.9 ± 0.2, 6.1 ± 0.6. and 8.8 ± 0.9 V/cm were given for the same impalement. Both shock polarities were given at each shock strength. For shocks delivered during the action potential plateau, the magnitudes of the peak δVm caused by the above four potential gradients were 21.1 ± 8.2, 33.6 ± 13.6, 49.9 ± 24.2, and 52.3 ± 28.0 mV (P < 0.05 among the four groups) for the shocks causing depolarization and 37.9 ± 14.2,56.6 ± 16.4,83.1 ± 19.4. and 92.9 ± 29.1 mV (P < 0.05 among the four groups) for the shocks causing hyperpolarization. Though δVm increased as potential gradients increased, the relationship was not linear. The magnitude of hyperpolarization was 1.9 ± 0.5 times that of depolarization when the shock polarity was reversed (P < 0.05). As potential gradients increased from 1.7 ± 0.1 to 8.8 ± 0.9 V/cm, the time constant of the membrane response decreased significantly from 3.5 ± 1.8 to 1.6 ± 0.7 msec for depolarizing shocks and from 6.0 ± 3.1 to 3.4 ± 1.9 msec for hyperpolarizing shocks (P < 0.01 vs depolarizing shocks). For shocks delivered during diastole, hyperpolarizing shocks induced triphasic changes in Vm during the shock, i.e., initial hyperpolarization, then depolarization, followed again by hyperpolarization. Conclusion: During the action potential plateau, the membrane response cannot be represented by a classic passive RC membrane model. During diastole, activation upstrokes occur even during hyperpolarization caused by shocks creating potential gradients between aproximately 2 and 9 V/cm.
Temperature Measurement as a determinant of Tissue Heating During Radiofrequency Catheter ablation: An Examination of Electrode Thermistor Positioning for Measurement Accuracy
Authors: McRURY IAN D. , WHAYNE JAMES G. , HAINES DAVID E. 
Published: May 2007

Thermometry and Radiofrequency Catheter Ablation. Introduction: Temperature monitoring has been proposed as a control for lesion occurrence and dimension during radiofrequency transcatheter ablation. Effective temperature measurement depends on thermistor positioning relative to the heated cardiac tissue and the convective cooling effects of the circulation. But the accuracy of a single tip thermistor as a measure of peak electrode‐tissue interface temperature is unknown. Methods and Results: A standard 8‐French, 4‐mm electrode catheter with 5 thermistors (1 tip thermistor, 4 radial thermistors) was used to deliver radiofrequency energy in vitro to 3 porcine right ventricles and in vivo to 7 mongrel dogs. In vitro, the catheter orientation was varied. In vivo the catheter was positioned under fluoroscopy at a variety of atrial, tricuspid annular, and ventricular sites, with no attempt to adjust catheter orientation. In both cases varied discrete power levels were used so that a wide temperature range was attained. Lesions created in vivo with a standard, single thermistor tipped electrode were compared to those of a catheter with a thermistor extending 1 mm from the tip. Power was varied and tip thermistor temperatures recorded. All lesions were examined pathologically. Comparisons of radial thermistor temperature to tip thermistor temperature for 3 catheter orientations in vitro resulted in tip thermistor underestimation of peak electrode‐tissue interface temperature by a median of 0.5°C in 35% of the perpendicular orientations, 1.9°C in 82% of the 45 orientations, and 5°C in 83% of the parallel orientations. During in vivo trials, the tip thermistor underestimated the peak electrode‐tissue interface temperature during 2 of 51 lesions by 1.2°C and 7.6°C. There was a sudden rise in electrical impedance in 17 of 51 radiofrequency energy deliveries. Only one case was observed where the peak electrode‐tissue interface temperature was below 95°C. The normal to extended tip thermistor configurations analysis showed similar relationships between lesion size and temperature. Conclusions: Accuracy of a single tip thermistor was found to be dependent upon catheterlissue orientation. With routine catheter positioning in vivo, the tip thermistor was a good indicator of peak electrode‐tissue interface temperature. Thus with power regulation to avoid temperatures greater than 90°C, a single flush‐mounted tip thermistor is probably adequate for temperature monitoring of lesion formation and avoidance of impedance rises.
Internal Defibrillation with Smaller Capacitors: A Prospective Randomized Cross‐Over Comparison of Defibrillation Efficacy Obtained with 90‐μF and 125‐μF Capacitors in Humans
Authors: BLOCK MICHAEL , HAMMEL DIETER , BÖCKER DIRK , BORGGREFE MARTIN , SEIFERT THOMAS , FASTENRATH CHRISTIAN , SCHELD HANS H. , BREITHARDT GÜNTER 
Published: May 2007

Defibrillation with Small Capacitance. Introduction: The size of current implantable cardioverter defibrillators (ICD) is still large in comparison to pacemakers and thus not convenient for pectoral implantation. One way to reduce ICD size is to defibrillate with smaller capacitors. A trade‐off exists, however, since smaller capacitors may generate a lower maximum energy output. Methods and Results: In a prospective randomized cross‐over study, the step‐down defibrillation threshold (DFT) of an experimental 90‐μF biphasic waveform was compared to a standard 125‐μF biphasic waveform. The 90‐μF capacitor delivered the same energy faster and with a higher peak voltage but provided only a maximum energy output of 20 instead of 34 J. DFTs were determined intraoperatively in 30 patients randomized to receive either an endocardial (n = 15) or an endocardial‐subcutaneous array (n = 15) defibrillation lead system. Independent of the lead system used, energy requirements did not differ at DFT for the experimental and the standard waveforms (10.3 ± 4.1 and 9.5 ± 4.9 J, respectively), but peak voltages were higher for the experimental waveform than for the standard waveform (411 ± 80 and 325 ± 81 V, respectively). For the experimental waveform the DFT was 10 J or less using an endocardial lead‐alone system in 10 (67%) of 15 patients and in 12 (80%) of 15 patients using an endocardial‐subcutaneous array lead system. Conclusions: A shorter duration waveform delivered by smaller capacitors does not increase defibrillation energy requirements and might reduce device size. However, the smaller capacitance reduces the maximum energy output. If a 10‐J safety margin between DFT and maximum energy output of the ICD is required, only a subgroup of patients will benefit from 90‐μF ICDs with DFTs feasible using current defibrillation lead systems.
Electrophysiologic Determinants of Ventricuiar Rate in Human Atrial Fibriliation
Authors: ASANO YUKIO , SAITO JUNICHI , YAMAMOTO TOSHIO , UCHIDA MASATSUGU , YAMADA YUICHI , MATSUMOTO KAZUO , MATSUO HIROSHI 
Published: May 2007

Ventricular Rate During AF. Introduction: The mechanisms of the ventricular response during atrial fibrillation (AF) remain uncertain. The parameters obtained during an electrophysiologic study, including atrial rates during AF, were analyzed to clarify further the determinants of the ventricular rate during AF. Methods and Results: Thirty patients without manifest preexcitation in whom AF was induced during electrophysiologic study were divided into two groups, Group I consisted of 20 patients (ages 55 ± 10 years) without a dual AV nodal pathway. Group 2 consisted of 10 patients (ages 53 ± 13 years) having a dual AV nodal pathway. The correlation coefficient between the mean RR interval during AF (mRR) and the mean intra‐atrial potential interval during AF (mff) was positive (0.05 [P < 0.05] in group 1 and 0.37 [P = NS] in group 2). The correlation coefficient of the mRR against the functional refractory periods of the AV node (AVFRP) was 0.73 (P < 0.001) in group 1. The correlation coefficients between mRR and the fast AV nodal pathway functional refractory periods and the slow AV nodal pathway effective refractory periods (SPERP) were 0.58 (P = NS) and 0.7 (P < 0.05) in group 2, respectively. The correlation coefficients between mRR against (mff × AVFRP)1/2 in group 1 and (mff × SPERP)1/2 in group 2 were 0.8 (P < 0.001) and 0.72 (P < 0.05), respectively. Conclusions: This clinical study did not indicate an inverse relation between the atrial and ventricular rates that had been reported by the previous experimental study. The ventricular rate during AF appeared to be quantitatively related to the atrial rate via AV node function. The importance of the slow pathway in determining the ventricular rate during AF was observed.
Circadian Variation of Heart Rate Variability in Postinfarction Patients With and Without Life‐Threatening Ventricular Tachyarrhythmias
Authors: KLINGENHEBEN THOMAS , RAPP ULI , HOHNLOSER STEFAN H. 
Published: May 2007

Circadian Variation of HRV. Introduction: Determination of heart rate variability (HRV) is widely used for noninvasive assessment of cardiac autonomic tone. A decreased HRV is associated with an increased mortality in patients surviving an acute myocardial infarction. There are, however, only sparse data about the circadian variation of different components of HRV that may be linked to the well‐known circadian fluctuations in the occurrence of sudden death. In addition, the potential prognostic impact of circadian variations of HRV has not been examined. Methods and Results: The present study compared the circadian variation of HRV from 14 postinfarction patients who had survived at least one episode of out‐of‐hospital cardiac arrest (cardiac arrest group) with that of 14 age‐ and sex‐matched patients without a history of malignant arrhythmias after their index infarct (control group). Several time‐ and frequency‐domain measures of HRV were assessed from 24‐hour Holter recordings. Circadian variations of high‐ (HF), low‐ (LF), and total‐frequency (TF) components were determined by calculating for each parameter the hourly difference from the day's mean. The average of these differences was calculated for every hour as well as for predefined day and night periods. There was no significant difference between the two groups with regard to HRV indices that predominantly reflect vagal tone, such as SDNN (78 ± 25 vs 96 ± 24 msec), pNN50 (2.7%± 4.6% vs 4.9%± 4.2%), or HF (6.3 ± 3.0 vs 7.8 ± 3.2 msec; cardiac arrest vs control group). There was also no significant difference in the circadian variation of LF or TF between the two groups during daytime and nighttime. However, a significant difference in circadian variation of HF was found during daytime (0.02 ± 0.5 vs ‐0.6 ± 0.5 msec; P = 0.006) and nighttime (0.19 ± 0.64 vs 1.5 ± 0.75 msec; P = 0.0002). In cardiac arrest survivors, there was no difference in the mean deviation of HF between the day‐and the nighttime periods. Conclusions: These results show an almost complete abolition in circadian variation of parasympathetic tone in postinfarction patients surviving an episode of out‐of‐hospital cardiac arrest, whereas circadian variation of sympathetic tone is comparable to that of postinfarction patients without arrhythmic episodes. These findings indicate that determination of diurnal variation of HRV may add to the prognostic value of HRV with respect to identifying patients at high risk of sudden death.
The Effect of Cardiac Compression on Defibrillation Efficacy and the Upper Limit of Vulnerability
Authors: IDRISS SALIM F. , ANSTADT MARK P. , ANSTADT GEORGE L. , IDEKER RAYMOND E. 
Published: May 2007

Compression Affects Defibrillation and ULV. Introduction: We determined the effects of decreasing the ventricular blood volume and altering cardiac geometry on defibrillation, the upper limit of vulnerability (ULV), and the relationship between them. Methods and Results: In six pigs, fibrillation/defibrillalion trials were performed with a left ventricular apex patch to a superior vena cava catheter electrode configuration and a biphasic waveform. Thirty trials each were performed on a compressed versus noncompressed (normal) heart. Compression was achieved using direct mechanical ventricular actuation. Dose‐response curves were constructed, and the 50% probability points (KD50) were compared for leading edge voltage (LEV), leading edge current (LEI), and total energy (TE). In another 12 pigs, triplicate defibrillation thresholds (DFTs) and ULVs were determined for each heart state. The T wave was scanned with shocks in 10‐msec steps for determining the ULV. Compression resulted in decreased ED50s for LEV (δ= 138 ± 77 V, P < 0.05, mean ± SD), LEI (A = 1.57 ± 0.7 A, P < 0.05), and TE (δ= 4.9 ± 3.6 J, P < 0.05) compared to normal. In the second study, compression significantly reduced DFT (P < 0.02) and ULV (P < 0.02) for LEV, LEI, and TE compared to normal. The ULV tended to be lower than the DFT for the normal heart state (δ= 23 ± 46 V LEV; P = NS). However, the ULV was significantly greater than the DFT for the compressed heart state (A = 19 ± 25 V LEV; P < 0.03). Conclusions: Shock delivery during cardiac compression improves defibrillation efficacy. Additionally, cardiac compression decreases both DFT and ULV, which supports the ULV hypothesis of defibrillation. Finally, maintaining the heart's geometric and volumetric state during ULV testing in paced rhythm and DFT testing in ventricular fibrillation moves the ULV higher than the DFT—the position predicted by the ULV hypothesis for defibrillation.
AV Nodal‐His‐Purkinje Reentry: A Novel Form of Tachycardia
Authors: MARKOWITZ STEVEN M. , STEIN KENNETH M. , ENGELSTEIN ERICA D. , LERMAN BRUCE B. 
Published: May 2007

AV Nodal‐His‐Purkinje Reentry. Introduction: Bundle branch reentry (BBR) typically occurs in patients with dilated cardiomyopathy and infra‐Hisian conduction system disease. The macroreentrant circuit of BBR is confined to the His‐Purkinje system (HPS) and ventricular myocardium. As such, the atrioventricular (AV) node plays no role in the tachycardia circuit. Methods and Results: In the present study, we identified a novel form of wide complex tachycardia in a patient with coronary disease and severe aortic regurgitation. The tachycardia morphology was right bundle branch block with a left superior axis. Ventriculoatrial block was present during tachycardia. An unusual feature of this rhythm was two sequential His‐bundle deflections (H and H′) for each ventricular beat of tachycardia. The H′V interval was identical to the HV interval during supraventricular rhythm. Changes in the ventricular cycle length (VV) preceded changes in the HH interval, consistent with retrograde activation of the first His‐bundle deflection. Changes in the H ‘H’interval preceded changes in the VV interval, consistent with anterograde activation of the second His‐bundle deflection. Tachycardia could be terminated with ventricular extrastimuli that did not capture the proximal HPS as well as with ventricular extrastimuli that advanced the His deflection, consistent with block in the HPS and in the AV node, respectively. Reproducible termination of the tachycardia following the first His deflection was demonstrated with adenosine, consistent with an upper pivot in the AV node. Conclusions: We have identified a new form of reentrant tachycardia in which the AV node, HPS, and ventricular myocardium each obligatorily participates in the tachycardia circuit, with the left posterior fascicle and right bundle functioning as the anterograde and retrograde limbs, respectively. Unlike BBR, however, the His bundle is activated twice as the wavefront pivots in the AV node. This model requires longitudinal dissociation at the levels of the AV node and His bundle.
In Vivo and In Vitro Electrophysiologic Effects of Terodiline on Dog Myocardium
Authors: PRESSLER MILTON L. , WARNER MARGARET R. , RUBART MICHAEL , RARDON DAVID P. , ZIPES DOUGLAS P. 
Published: May 2007

Electrophysiologic Effects of Terodiline. Introduction: Terodiline hydrochloride, widely prescribed for urinary incontinence, has been reported to cause bradycardia and torsades de pointes. Methods and Results: In this study, we characterized the electrophysiologic effects of terodiline in dog cardiac tissues in vivo and in isolated canine cardiac Purkinje fibers. Terodiline (1 to 10 μM) resulted in dose‐dependent reduction of action potential amplitude and maximal upstroke velocity (Vmax). The threshold for these effects was ∼ 2 μM (0.6 mg/L), and the changes were cycle‐length dependent. Terodiline (≥ 2 μM) also depressed the action potential plateau but did not significantly alter action potential duration at concentrations ≤ 10 μM. In vivo studies demonstrated that high doses of terodiline (3 mg/kg) lengthened AH and HV intervals, slowed spontaneous sinus rate, prolonged ventricular refractoriness, and inhibited vagally induced slowing of the sinus node. Sympathetic effects on spontaneous sinus rate were unchanged. In both isolated canine Purkinje fibers and anesthetized dogs, terodiline did not evoke afterdepolarizations, repetitive firing, or ventricular tachyarrhythmias under normal or hypokalemic conditions. Conclusion: Our findings suggest that terodiline (≤ 1 to 2 μM) leads to blockade of sodium and calcium channels as well as muscarinic receptors in canine cardiac tissues.
Electrophysiologic Characteristics of M Cells in the Canine Left Ventricular Free Wall
Authors: SICOURI SERGE , ANTZELEVITCH CHARLES 
Published: May 2007

Characteristics of M Cells. Introduction: Recent studies have described the existence of M cells in the deep structures of the canine and human ventricle. The present study was designed to further characterize the M cell with respect to its distribution across the canine left ventricular free wall and the dependence of its action potential on [K+]0. Methods and Results: We used standard microelectrode techniques to record transmembrane activity from deep subepicardial or transmural strips isolated from the canine left ventricular free wall near the base as well as subendocardial Purkinje fibers. M cell behavior (steep APD‐rate relation) was observed at depths of 1 to 7 mm from the epicardial surface (deep subepicardium to mid‐myocardium). M cells were found to be distributed uniformly in the deep subepicardium and did not appear in discrete bundles. We observed transitional behavior throughout the wall. The maximum rate of rise of the action potential upstroke, Vmax, increased sharply between epicardium and deep subepicardium (176 ± 13 to 332 ± 61 V/sec), remained high throughout the mid‐myocardium and deep subendocardium, and returned to lower values only in the superficial layers of the endocardium (205 ± 21 V/sec). The relationship between Vmax and takeoff potential in the M cell was fit by a Boltzmann equation with a V V0.5 of ‐68.6 ± 1.5 mV and k of 3.4 ± 0.5. The relationship between resting membrane potential (RMP) and [K+]0 in the M cell was exponential from 8 to 20 mmol/L (58 mV change in RMP per 10‐fold change in [K+]0), deviating from K+ electrode behavior at [K+]0, < 8 mmol/L. RMP in M cells continued to hyperpolarize at [K+]0 < 2.5 mmol/L, reaching potentials of approximately ‐110 mV at I+]0, of 1 mmol/L. In contrast, subendocardial Purkinje fibers depolarized at these low levels of [K+]0. Unlike endocardium and epicardium, M cells developed early afterdepolarizations at low [K+]0 and slow rates. Conclusions: Our data indicate that the M cells are widely distributed in the intramural layers of the canine left ventricular free wall. M cells and transitional cells occupy 30% to 40% of the left ventricular wall and an estimated 20% to 40% of the mass of the ventricles of the normal canine heart. They display characteristics common to both myocardial and specialized conducting cells. Like Purkinje fibers, M cells exhibit a relatively large Vmax and steep APD‐rute relations that are modulated by [K+]0. Unlike Purkinje fibers, M cells do not appear in bundles, they do not depolarize at [K+]0 < 2.5 mmol/L, nor do they exhibit phase 4 depolarization.