Tachycardia Around a Fixed Obstacle in Anisotropic Myocardium
|
|
- Denis Holmes
- 5 years ago
- Views:
Transcription
1 1307 Differential Effects of Heptanol, Potassium, and Tetrodotoxin on Reentrant Ventricular Tachycardia Around a Fixed Obstacle in Anisotropic Myocardium Josep Brugada, MD; Lluis Mont, MD; Lucas Boersma, MD; Charles Kirchhof, MD; and Maurits A. Allessie, MD Background. The aim of this study was to test the hypothesis that electrical uncoupling and depression of the fast sodium channels have differential effects on propagation of the electrical impulse relative to the fiber orientation. Methods and Results. In a model of reentrant ventricular tachycardia (VT) (mean cycle length, 144±13 msec) around a ring of anisotropic myocardium in 10 Langendorff-perfused rabbit hearts, the effects of extracellular K+ concentration ([K'],) and heptanol were studied. [K']. and heptanol each had a dose-dependent effect on VT cycle length. However, high [K+]. slowed the VT mainly by depressing longitudinal conduction, whereas heptanol preferentially depressed transverse conduction. The ratio between longitudinal and transverse conduction velocities progressively decreased with high [K']. and progressively increased with heptanol. Heptanol terminated VT at a mean concentration of 3.5±0.5 mm. The cycle length before termination was msec (p<0.001). In eight of 10 experiments, termination occurred by failure of conduction during transverse propagation. VT terminated at a mean [K']. of 11.6± 1.8 mm. The cycle length before termination was msec (p<0.01). In seven of 10 cases, termination occurred by failure of conduction during longitudinal propagation. In the remaining five episodes (two with heptanol and three with high [K'].), termination occurred by collision of the reentrant beat with an antidromic impulse being reflected within the ring. In a separate series of six hearts, tetrodotoxin was administered during VT. Like high [K']., tetrodotoxin prolonged the cycle length of the VT by preferentially slowing longitudinal conduction, and VT was terminated by longitudinal block. Conclusions. During reentrant VT, electrical uncoupling of cells by heptanol or modification of active membrane properties by high [K'],, or tetrodotoxin has a differential depressing effect on propagation of the impulse relative to the fiber orientation. (Circulation 1991;84: ) Deirectional differences in conduction velocity of impulse propagation relative to fiber orientation is a well known characteristic of ventricular myocardium based on a different effective axial resistance parallel and perpendicular to the fiber orientation.1-4 Spach et a15 demonstrated that From the Department of Physiology, University of Limburg, Maastricht, The Netherlands. Supported by a fellowship (to J.B.) from the Royal Netherlands Academy of Arts and Sciences. This research received the first place in the Young Investigators Award competition of the American College of Cardiology, Atlanta, Ga., Address for reprints: Josep Brugada, MD, Department of Physiology, Biomedical Center, P.O. Box 616, University of Limburg, 6200 MD Maastricht, The Netherlands. Received July 31, 1990; revision accepted April 23, the passive anisotropic properties of cardiac muscle play an important role in the excitability and safety factor of conduction. They also showed that increasing the junctional resistance with ouabain preferentially depressed impulse conduction transverse to the fiber orientation.6 Balke et a17 and Delmar et a18 demonstrated that the selective increase in junctional resistance by administration of heptanol9,10 caused a See p 1447 preferential slowing of conduction and conduction block of transverse propagating wave fronts without affecting the amplitude or maximum rate of depolarization of the action potential. There is increasing evidence for the reentrant nature of ventricular tachycardias (VTs) in the
2 1308 Circulation Vol 84, No 3 September 1991 TABLE 1. Effects of Increasing Doses of Heptanol on Ventricular Tachycardia Heptanol (mm) Rabbits (n) VTCL ±35* t 357±84t 488±118t (+23%) (+60%) (+148%) (+239%) 6L 69±10 63±12* t 46+12t 38±4t (-9%) (-24%) (-33%) (-45%) 0Z ±5t 12±5t 9±4t 7±2t (-19%) (-43%) (-57% ) (-67%) OL/Or ± ±1* 5.0±lt t VTCL, ventricular tachycardia cycle length (msec); 0L longitudinal conduction velocity (cm/sec); OT, transverse conduction velocity (cm/sec). *p<0.01, tp< chronic phase of myocardial infarction.1112 During intraventricular reentry, one might expect the impulse to propagate parallel to the fiber direction in some segments of the circuit and perpendicular in others. In the present study, we tested the hypothesis that during sustained reentrant VT, uncoupling agents such as heptanol would terminate VT by selective blockade of transverse conduction, whereas depression of the upstroke of the action potential by high extracellular K' concentration ([K'].) or tetrodotoxin (TTX) terminates VT by preferential depression of longitudinal propagation.5,13 Methods Sixteen Flemish rabbits of either sex weighing kg were used for this study. The experimental model consisted of a ring of healthy epicardium in the left ventricle of Langendorff-perfused rabbit hearts created by a cryoprocedure.1415 A detailed description of the experimental model, recording and stimulation techniques, conduction velocity measurements, and histological examination is given in the companion report.16 Experimental Protocols In 10 experiments, the protocol consisted of two parts executed in the order explained below in five and in the reverse order in the other five. First, the effects of increasing heptanol concentration on reentrant VT were studied. Thirty minutes after induction of sustained reentrant VT by programmed electrical stimulation, heptanol was added to the perfusion fluid in a concentration of 1.0 mm. Every 30 minutes, the concentration of heptanol was increased in steps of 1.0 mm until tachycardia terminated. Continuous on-line recording of activation maps allowed careful monitoring of the time course and dose-dependent effects of heptanol on VT cycle length and longitudinal conduction velocity (0G) measured at the left free wall and transverse conduction velocity (0T) measured at the corridor between the left anterior descending coronary artery (LAD) and the obstacle. The site of VT termination was correlated with the histologically determined fiber orientation. During washout of heptanol, VT was induced again by programmed electrical stimulation; after the cycle length of the VT had returned to its control value, the same protocol was repeated by increasing the [K'], Starting from a control value of 4 mm, the [K+]0 in the perfusion fluid was increased in steps of 2 mm at 5-minute intervals until VT terminated. The effects of increasing [K'], on VT cycle length, 6L and XT, and the site of VT termination were compared with the results obtained during previous heptanol administration. In a separate series of six hearts, TTX was added to the perfusate in increasing doses of 1, 2, 5, 10, 20, and 30,uM until VT terminated. Each dose was given during a period of 5 minutes. Data Analysis Each preparation served as its own control. Results are expressed as mean±+sd. Comparisons between control and administration of heptanol, high [K+], or TTX were performed with Student's t test for paired data. Comparison between the effects of heptanol and the effects of [K+]0 was performed with an analysis of variance. A value of p<0.05 was considered to be statistically significant. Results Characteristics of Ventricular Tachycardia During the control period, epicardial mapping showed that in all cases VT was a result of reentry of the impulse around the obstacle. The cycle length of VT ranged from 130 to 176 msec in different experiments (mean length, msec). During the control period of 30 minutes, the cycle length was constant (+3 msec), and spontaneous termination was never observed. During VT, conduction velocity was different in different segments of the ring depending on the angle between the direction of propagation and epicardial fiber orientation. During longitudinal propagation (angle between fiber orientation and direction of propagation, 2±3 ), 0L was 70±9 cm/sec (range, cm/sec). During transverse conduction (angle between fiber orientation and direction of propagation, 89+±40), O
3 Brugada et al Reentry and Safety for Conduction 1309 CONTROL HEPTANOL 1 mm ZT l]l31i HEPTANOL 2mM HEPTANOL 3mM FIGURE 1. Activation maps of counterclockwise tachycardia during control period and administration of 1, 2, and 3 mm heptanol. Numbers indicate local activation times in msec. Isochrones are drawn at 10-msec intervals. Large numbers in center of each panel indicate cycle length of tachycardia in msec. Heptanol caused a dose-dependent increase in cycle length of tachycardia because ofpreferential slowing of transverse conduction. LAD, left anterior descending coronary artery. was 21±4 cm/sec (range, cm/sec). The anisotropic ratio (0JO/r) was (range, ). Effects of Heptanol and High [K'], on Ventricular Tachycardia Heptanol had a dose-dependent effect on VT cycle length. The time course of the effect of heptanol showed that steady-state values were reached after approximately 20 minutes. Heptanol (1.0 mm) increased the cycle length by 23% (p<0.002), 2.0 mm increased it by 60% (p<0.001), 3.0 mm increased it by 148% (p<0.001), and 4 mm increased it by 239% (p<0.001, n=6). Heptanol also had a dose-dependent effect on conduction velocity; however, 6G was
4 1310 Circulation Vol 84, No 3 September 1991 CONTROL 3 mm Heptanol 5? ~ ~~ ~ ms 358 ms A 2 c 62. C FIGURE 2. Maps, schematics, and electrograms of impulse propagation through narrow corridor between left anterior descending coronary artery and obstacle during a single tachycardia before and after administration of 3 mm heptanol. Upper panels: Activation times are given in msec, and isochrones are drawn at 10-msec intervals. Distance between electrodes is 2.25 mm. Middle panels: Pathway of impulse propagation is schematically indicated. Encircled letters and numbers refer to sites of recording of electrograms given in lower panels. During control, cycle length of ventricular tachycardia was 132 msec. After heptanol administration, cycle length was prolonged to 358 msec, mainly as a result of extreme slowing of conduction in this area. (See text for further description.)
5 Brugada et al Reentry and Safety for Conduction 1311 TABLE 2. Effects of Increasing Extracellular K' Concentration on Ventricular Tachycardia [K+]. (mm) Rabbits (n) VTCL 142± * 194±54t 259±96t 381±89t 774±378t (+12%) (+37%) (+82%) (+168%) (+445%) OL 71±8 63±7t 53±84 36±84 21±5t 11±3t (-11%) (-25%) (-49%) (-70%) (-85%) OT 21±3 19±3t 18±4: 15±44 10±24 8±3t (-10%) (-14%) (-29%) (-52%) (-62%) k/ot 3.4± ± ± ± ±0.3t 1.5±0.3t [K+]0, extracellular potassium concentration; VTCL, ventricular tachycardia cycle length (msec); 6L, longitudinal conduction velocity (cm/sec); 6r, transverse conduction velocity (cm/sec). *p<0.05, tp<0.01, tp< more sensitive to heptanol administration than 6L. As a result, the anisotropic ratio progressively increased from during control to 5.3±0.9 (p<0.01) for 4 mm heptanol (see Table 1). In Figure 1, the activation maps during a sustained counterclockwise VT are shown during control and administration of 1, 2, and 3 mm heptanol. During control, the VT had a stable cycle length of 147 msec. At the corridor between the LAD and the obstacle where the impulse propagated perpendicular to the fiber orientation, crowding of isochrones indicates that conduction velocity was much slower (6,, 21 cm/sec) than in the left free wall where the impulse propagated parallel to the fiber orientation (6L, 69 cm/sec). At increasing doses of heptanol, the VT slowed progressively to a cycle length of 345 msec. This increase in cycle length was caused mainly by a preferential slowing of transverse conduction at the corridor between the LAD and the central obstacle, whereas longitudinal conduction was less affected. For 3 mm heptanol, areas of very slow conduction and conduction block (local delays as long as 60 msec between two electrodes) appeared in the segment of transverse conduction. Effective 6, was now reduced to 8 cm/sec, whereas 6L was 54 cm/sec. In all experiments, average O6 and 6L values during administration of 3 mm heptanol were 9±4 and 46±12 cm/sec. In Figure 2, another example of the effects of heptanol on transverse conduction is shown. In this figure, only the transverse conduction at the corridor between the LAD and the obstacle is shown together with some electrograms recorded from that region. During control, the counterclockwise VT had a cycle length of 132 msec. In the segment of transverse conduction, the circulating impulse was propagating slowly but smoothly. The pairs of unipolar electrograms (A-A', B-B',...) recorded at either side of the narrow pathway were almost simultaneously activated, demonstrating that the impulse was transmitted through this area as a uniform, nonfragmented wave front. After the administration of 3 mm heptanol, the cycle length of the VT was considerably prolonged to 358 msec. The activation map from the area of transverse conduction showed that this prolongation of VT cycle length was caused mainly by a dramatic increase in conduction time in this segment of the circuit. During control, this segment of the ring was activated in 49 msec, whereas during heptanol administration (3 mm), the total conduction time prolonged to 259 msec. As shown schematically in Figure 2 (middle panel), the impulse now propagated in a zig-zag pattern, meandering around multiple lines of transverse block (thick lines), making the actual length of the pathway about fourfold longer than that during control. Stepwise increase of [K'], in the same hearts caused a progressive prolongation of the VT cycle length. At each concentration, steady-state values were obtained after approximately 3 minutes. The VT cycle length increased by 12% for 6 mm [K'], (p<0.04), by 37% for 8 mm (p<0.006), by 82% for 10 mm (p<0.003), by 168% for 12 mm (p<0.004, n=5), and by 445% for 14 mm (p<0.04, n=4). Comparison of the effects of [K']. on longitudinal and transverse conductions showed that increasing [K']. depressed longitudinal conduction more than it depressed transverse conduction. As a result, the anisotropic ratio progressively decreased at increasing [K']. concentrations-from during control to 1.5±0.3 for 14 mm [K+], (p<0.001) (see Table 2). In Figure 3, the activation maps of a clockwise VT during 4, 6, 10, and 12 mm [K+], are shown. During control, the VT had a stable cycle length of 134 msec, 6, was 19 cm/sec, and OL was 66 cm/sec (ratio, 3.5). At increasing [K+]0, the VT cycle length progressively prolonged to 467 msec at 12 mm [K+].. During administration of 12 mm [K+]., 6L was 19 cm/sec and 6, was 9 cm/sec (ratio, 2.1). Comparison of the effects of heptanol and high [K+], on the anisotropic ratio is shown in Figure 4. During increasing doses of heptanol, the anisotropic ratio progressively increased from 3.4 to 5.3. In contrast, during high [K+],, the anisotropic ratio progressively decreased from 3.4 to 1.5. Termination of Venticular Tachycardia by Heptanol and High [K+]0 Heptanol administration and high [K+]. terminated all episodes of VT. The mean concentration of
6 1312 Circulation Vol 84, No 3 September 1991 K+ 4 mm \ \ C ms 78 7S A a Ii in> S e 8 apex K+6 mm \ i2 19\2326w & \ t185 4;iF= ms U a ( t 15 C? s.\m q \39<\ 37A jjj t L mns 11 s t " 51S /3 K+ 10 mm K+ 12mM FIGURE 3. Activation maps of a single clockwise circulating tachycardia during increasing concentrations of extracellular K' (4, 6, 10, and 12 mm). Cycle length of tachycardia (large numbers in msec in center of map) increased with increasing concentrations of K+. Numbers indicate local activation times in msec. Isochrones are drawn at 10-msec intervals. LAD, left anterior descending coronary artery. heptanol at which VT terminated was 3.6±0.5 mm. Before termination, the VT cycle length was 446±+120 msec (p<0.001 versus control). Mean [K'], at which VT terminated was 11.6±+1.8 mm. The VT cycle length before termination was 493+±341 msec (p<0.01 versus control). During heptanol administration in eight of 10 experiments, termination occurred by failure of the wave front to propagate through the corridor between the LAD and the obstacle. During high [KJ]o in seven of 10 experiments, termination occurred by longitudinal conduction block. In Figure 5, the termination of a clockwise
7 6 5 >4 I3 2 1 o Heptanol,mM Heptanol K+ mm K' FIGURE 4. Plots of anisotropic ratios of longitudinal conduction velocity (LCV) and transverse conduction velocity (TCV) during tachycardia to increasing doses ofheptanol and extracellular K' concentrations. *p<0.01 compared with control. VT during heptanol administration (upper panels) and during high [K'], (lower panels) is shown with the histological determination of fiber orientation at the site of termination. The tachycardias, which were initiated in the same heart, were identical during control (cycle length, 165 msec). During heptanol administration, shortly before termination (left upper panel), the VT had a cycle length of 390 msec because of severe depression of transverse conduction. Several areas of large local conduction delays and crowding of isochrones were found in this area. Termination of VT (middle upper panel) occurred as a result of failure of the impulse to propagate across one of these areas. As shown by the histological section in the right upper panel, conduction was perpendicular to the epicardial fiber orientation in the area of block. During high [K'],, the last reentrant beat (left lower panel) had a cycle length of 386 msec. Although transverse conduction in the corridor between the LAD and the obstacle now remained uniform, local delays in conduction and crowding of isochrones appeared in the free wall of the left ventricle during longitudinal conduction of the circulating wave front. Termination of VT by high [K+]0 (middle lower panel) occurred by failure of the impulse to propagate across these areas of conduction delay. Histological determination of the fiber orientation showed that conduction block occurred while the impulse was propagating parallel to the fiber orientation (right lower panel). In a minority of experiments (two of 10 during heptanol and three of 10 during high [K'],), termination of VT was not caused by primary conduction block in a certain segment of the circuitous pathway but rather by collision with another wave front, which was reflected in the ring. In Figure 6, an example of termination of VT by collision with a returning wave during heptanol administration is given. Fifteen unipolar electrograms spaced at equal intervals around Brugada et al Reentry and Safety for Conduction 1313 the obstacle are shown. During sustained VT, the circulating impulse propagated from electrode 1 to electrode 15 with fast conduction between electrodes 1 and 8 and slow conduction between electrodes 10 and 14, which were located at the corridor between the LAD and the obstacle. During the last beat of the VT, the sequence of activation was suddenly reversed in part of the ring (electrodes 1-9) and propagated as a returning impulse against the direction of the original circulating impulse. The two wave fronts propagating in opposite directions around the ring collided at electrode 1, resulting in sudden termination of the VT. During heptanol administration, the point of reflection in both cases was located in the area of severely depressed transverse conduction, whereas during high [K+]0, in all three cases the returning wave originated from the area of depressed longitudinal conduction. The isochrone maps from the area of reflection showed that the returning wave was not caused by "true" reflection.17 A returning wave originated when the circulating impulse encountered arcs of conduction block not extending along the entire width of the ring. As a result, the impulse could continue its normal orthodromic course while simultaneously starting an antidromic wave by microreentry through the incomplete arc of unidirectional block. Effects of Tetrodotoxin on Ventricular Tachycardia In a different series of six hearts, the effects of YTX on reentrant VT were studied. TTX was administered at increasing doses (1, 2, 5, 10, 20, and 30,uM) at 5-minute intervals until VT terminated. The mean concentration of TTX at which VT terminated was 25+5,uM. The VT cycle length increased from msec during control to 793 ± 122 msec before termination (p<0.001). 0L and 0T values during control were 67±7 and 23+2 cm/sec (anisotropic ratio, ) compared with 17+6 and 8±2 cm/sec (ratio, 2.1±0.3), respectively, during TTX just before termination of VT. In four of six hearts, VT terminated by longitudinal conduction block. In the remaining two hearts, VT terminated by collision of the circulating impulse with an antidromically returning wave front. An example of the effects of TTX on VT is given in Figure 7. During control, the counterclockwise VT had a cycle length of 171 msec. Administration of 5 and 10,uM TTX prolonged the cycle lengths to 333 and 610 msec, respectively. A further increase in the dose of TTX to 20,uM prolonged the cycle length to 752 msec, and VT was terminated by longitudinal conduction block at a segment of the ring where conduction velocity was 62 cm/sec during control. Discussion Our experimental model consisted of a ring of normal perfused epicardium with uniform anisotropic properties. Because of the natural epicardial fiber orientation, during reentrant VT the circulating wave front travels parallel to the fiber orientation in some segnents and perpendicular to the fiber axis in other
8 1314 Circulation Vol 84, No 3 September 1991 Heptanol 4 mm 500,u1m K+ 12 mm - apex FIGURE 5. Activation maps during termination of tachycardia by heptanol (upper panels) and high extracellular K' (lower panels). Numbers indicate local activation times in msec. Isochrones are drawn at 10-msec intervals. Thick line and double bars indicate sites of termination of tachycardias. As can be seen from histological examinations (right panels), conduction block of circulating impulse during heptanol administration occurred while wave front propagated transverse to fiber orientation and during high K' while wave front propagated parallel to fiber orientation. LAD, left anterior descending coronary artery. segments of the ring. During control, conduction velocity was about threefold faster during longitudinal than during transverse propagation. The importance of tissue anisotropy for reentrant circuits has been emphasized by several authors.15'18-20 It has been suggested that areas of very slow conduction with multiple-component low-amplitude electrograms during reentrant tachycardia represent intrinsic asymmetry of cardiac activation because of fiber orientation.18 Enhanced tissue anisotropy could be a cause of VT because activation transverse to myocardial fibers would be sufficiently slow to permit reentry.20 If anisotropy plays an important role in initiation and perpetuation of reentrant tachycardias, the question arises of whether a new class of antiarrhythmic agents acting primarily on the passive electrical properties of myocardial fibers could be of value in prevention and treatment of reentrant tachyarrhythmias.21 Our study was designed to compare the effects of an uncoupling agent (heptanol) on reentrant VT with the effects of other substances that depress conduction velocity by inactivation or blockade of the fast sodium channels (high [K+],) and TTX). Role of Anisotropy In the early phase of ischemia, impulse conduction is slowed by a depression of the active membrane properties plus an increase in extracellular and axial resistance.22 In the chronic phase of myocardial infarction, Ursell et a123 demonstrated that although
9 Brugada et al Reentry and Safety for Conduction msec FIGURE 6. Fifteen unipolar electrograms spaced at equal intervals around obstacle are displayed during termination of tachycardia. During stable tachycardia, activation sequence was ordered from electrograms 1 to 15 with a cycle length of395 msec. Sudden change in sequence of activation produced two different wave fronts circulating in opposite directions that collided at electrogram 1, suddenly terminating tachycardia. Arrows indicate direction of activation. the action potentials had become normal again, conduction of the electrical impulse was still impaired because of the development of fibrotic septa disrupting the electrical coupling between cells in a transverse direction. Several investigators used uncoupling agents to study the role of intercellular resistance on anisotropic conduction.7'0'24 These studies showed that uncoupling had a preferential effect on conduction perpendicular to the fiber axis and in regions with a high coupling resistance in and around a myocardial infarction.1024 It has been suggested that by producing complete conduction block in these areas, the abnormalities in propagation in infarcted myocardium might be eliminated.24 In the present series of experiments, the administration of heptanol during reentrant VT affected transverse conduction to a greater extent than longitudinal conduction. This was the opposite of the effects of high [K], or TTX, which mainly affected longitudinal conduction. As a result, the anisotropic ratio in conduction velocity was increased by heptanol and decreased by high [K], or TTX. Termination of reentrant VT by heptanol occurred because of failure of transverse conduction. In contrast, termination of VT by high [K'], or 1TX was caused by failure of longitudinal conduction. However, large doses of these substances were needed to terminate VT; before termination, the VT cycle length was threefold to fourfold that of the control VT interval. This suggests that in our model, the safety factor for conduction was high both parallel and perpendicular to the fiber orientation. Thus, because of the high degree of safety factor uniformity in a circuit of normal anisotropic myocardium, a general depression of either passive or active membrane properties did not terminate VT at a suitable therapeutic range. On the other hand, in diseased myocardium, one might expect circuitous pathways that exhibit large safety factor differences. In such a substrate of reentrant VT, a moderate increase in intercellular resistance or decrease in generated excitatory current might specifically block conduction in a segment of the circuit with a relatively low safety factor. If in this segment the fibers are oriented perpendicular to the direction of the circulating impulse, an uncoupling agent might be most effective; in cases in which the impulse propagates longitudinal to the fiber axis, a sodium channel blocker might be more successful in terminating the tachycardia. Termination of Tachycardia by a Retuming Impulse in the Ring In seven of 26 VTs (two with heptanol, three with high [K'],, and two with TTX), termination of VT occurred by collision of the circulating wave front with a spontaneous antidromic returning impulse. A common feature of these returning impulses was that they originated from areas in the ring where conduction was very slow and marked local conduction delays were present. In these areas, the wavelength of the impulse was markedly shortened, allowing microreentry within the width of the ring. During heptanol administration, the returning waves always originated from the area of depressed transverse conduction, whereas during high [K+]0 and TTX administration, the site of a spontaneously returning
10 1316 Circulation Vol 84, No 3 September 1991 CONTROL TTX 5yM 0 aj is \ Apex TTX 10 pm TTX 20,M FIGURE 7. Activation maps during increasing doses of tetrodotoxin (TTX). During control, impulse propagated counterclockwise with a cycle length of 171 msec. For 5 and 10 AM T7X, cycle lengths prolonged to 333 and 610 msec, respectively. For 20,M TTX, tachycardia terminated by failure of conduction at left free wall. Cycle length before termination was 752 msec. Numbers indicate local activation time in msec. Isochrones are drawn at 10-msec intervals. Double bars indicate conduction block. LAD, left anterior descending coronary artery.
11 antidromic wave was located in a segment of depressed longitudinal conduction. In some cases, such as the one presented in Figure 2, electrical uncoupling changed uniform transverse conduction into a zig-zag pattern around multiple arcs of transverse block. This zig-zag pattern often preceded microreentry, resulting in a returning antidromic wave that terminated VT. Interestingly, in human atrial bundles, Spach et a125 observed a similar phenomenon during longitudinal propagation when sodium conductance was impaired. They showed that the induction of premature action potentials changed uniform longitudinal conduction into a dissociated zig-zag type of conduction around arcs of longitudinal block. The phenomenon of zigzag conduction appears to be of importance for the characteristics of reentrant VT by creating an area of very slow apparent conduction velocity. In the example shown in Figure 2, 0T during control was 19 cm/sec. After heptanol administration, the apparent conduction velocity decreased to 4 cm/sec. However, because of the zig-zag pattern of conduction during heptanol, the actual path length was fourfold longer than that during control. If this prolongation in path length is taken into account, a true conduction velocity of 18 cm/sec becomes evident. Thus, an area of microscopic zig-zag conduction might provide an area of extremely slow conduction in part of the circuit, whereas the actual conduction velocity is still within the physiological range. Study Limitations The use of pharmacological blocking agents to study basic electrophysiological properties is limited by other possible nonspecific drug effects. Our assumptions that heptanol affects only passive membrane properties and that high [Kt]0 selectively depresses active membrane properties are probably not entirely true. The question has been raised as to what extent the effects of heptanol on conduction are results of changes in the sodium conductance (gna).26 In dog cardiac Purkinje fibers and squid giant axons, it has been shown that apart from its main effect on internal resistance (R1), heptanol also reduces gna.2728 However, Jalife et a129 concluded that the depression of conduction by heptanol could not be explained by such a reduction in gna. They showed Brugada et al Reentry and Safety for Conduction 1317 that during complete blockade of conduction by heptanol in sheep Purkinje fibers, the cells were still able to generate normal action potentials, suggesting that the effect of heptanol on conduction was caused mainly by an increase in Ri. Our observation that longitudinal conduction was only moderately depressed during seriously depressed transverse conduction by heptanol supports this conclusion. The effects of increased [K']. on impulse propagation are thought to be caused primarily by a decrease in the membrane resting potential, resulting in decreases in threshold potential and gna and prolongation of the time constant of the foot of the action potential and the reactivation kinetics of the sodium channel system.30 However, at high [K'], values, an increase in K' conductance and a concomitant decrease in membrane resistance have also been reported.31 No effect on axial (myoplasmic and gap junction resistance) or extracellular resistance has been found.31,32 Gettes et a133 demonstrated that the slowing of conduction produced by extracellular K' concentrations of more than 9 mm were caused mainly by a depression of the fast sodium channels. Because of the possible effects of K' on membrane resistance, we studied the effects of a selective sodium channel blocker (TTX) in an additional series of six hearts. The effects of TTX on VT were comparable to those resulting from an increase in [K'],. As during high [Kt]0 administration, longitudinal propagation was preferentially depressed and VT was terminated by longitudinal conduction block. This suggests that the effects of high [K'], on VT were caused mainly by a decrease in the active membrane properties. References 1. Sano T, Takamaya N, Shimamoto T: Directional difference of conduction velocity in cardiac ventricular syncytium studied by microelectrodes. Circ Res 1959;7: Clerc L: Directional differences of impulse spread in trabecular muscle from mammalian heart. JPhysiol (Lond) 1976;255: Spach MS, Miller WIT, Geselowitz D, Barr RC, Kootsey JM, Johnson EA: The discontinuous nature of propagation in normal canine muscle: Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981;48: Spach MS, Miller WT III, Miller-Jones E, Warren RB, Barr RC: Extracellular potentials related to intracellular action potentials during impulse conduction in anisotropic canine cardiac muscle. Circ Res 1979;45: Spach MS, Kootsey JM: The nature of electrical propagation in cardiac muscle. Am J Physiol 1983;244:H3-H22 6. Spach MS, Kootsey JM, Sloan JD: Active modulation of electrical coupling between cardiac cells of the dog: A mechanism for transient and steady state variation in conduction velocity. Circ Res 1982;51: Balke CW, Lesh MD, Spear JF, Kadish A, Levine J, Moore EN: Effects of cellular uncoupling on conduction in anisotropic canine ventricular myocardium. Circ Res 1988;63: Delmar M, Michaels DC, Johnson T, Jalife J: Effects of increasing intercellular resistance on transverse and longitudinal propagation in sheep epicardial muscle. Circ Res 1987; 60: Johnston MF, Simon SA, Ramon F: Interaction of anesthetics with electrical synapses. Nature 1980;286: Deleze J, Herve JC: Effect of several uncouplers of cell-to-cell communication on gap junction morphology in mammalian heart. J Membr Biol 1983;74: Josephson ME, Horowitz LN, Farshidi A, Spear JF, Kastor JA: Recurrent sustained ventricular tachycardia: I. Mechanisms. Circulation 1978;57: De Bakker JMT, Van Capelle FJL, Janse MJ, Wilde AAM, Coronel R, Becker AE, Dingemens KP, Van Hemel NM, Hauer RNW: Reentry as a cause of ventricular tachycardia in patients with chronic ischemic heart disease: Electrophysiologic and anatomic correlation. Circulation 1988;77: Tsuboi N, Kodama I, Toyama J, Yamada K: Anisotropic conduction properties of canine ventricular muscles: Influence of high extracellular K' concentration and stimulation frequency. Jpn Circ J 1985;49: Brugada J, Boersma L, Kirchhof CJHJ, Brugada P, Havenith M, Wellens HJJ, Allessie MA: Double wave reentry as a
12 1318 Circulation Vol 84, No 3 September 1991 mechanism of acceleration of ventricular tachycardia. Circulation 1990;81: Allessie MA, Schalij MJ, Kirchhof CJHJ, Boersma L, Huyberts M, Hollen J: Experimental electrophysiology and arrhythmogenicity: Anisotropy and ventricular tachycardia. Eur Heart J 1989;10:E8-E Brugada J, Boersma L, Kirchhof C, Heynen V, Allessie M: Reentrant excitation around a fixed obstacle in uniform anisotropic ventricular myocardium. Circulation 1991;84: Antzelevitch C, Jalife J, Moe GK: Characteristics of reflection as a mechanism of reentrant arrhythmias and its relationship to parasystole. Circulation 1980;61: Cardinal R, Vermeulen M, Shenasa M, Roberge F, Page P, Helie F, Savard P: Anisotropic conduction and functional dissociation of ischemic tissue during reentrant ventricular tachycardia in canine myocardial infarction. Circulation 1988; 77: Richards DA, Blake GJ, Spear JF, Moore EN: Electrophysiologic substrate for ventricular tachycardia: Correlation of properties in vivo and in vitro. Circulation 1984;69: Dillon SM, Allessie MA, Ursell PC, Wit AL: Influences of anisotropic tissue structure on reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res 1988;63: Wit AL: Anisotropic reentry: A model of arrhythmias that may necessitate a new approach to antiarrhythmic drug development, in Rosen MR, Palti Y (eds): LethalArrhythmias Resulting From Myocardial Ischemia and Infarction. Boston, Kluwer Academic Publishers, 1989, pp Kleber AG, Riegger CB, Janse MJ: Electrical uncoupling and increase of extracellular resistance after induction of ischemia in isolated, arterially perfused rabbit papillary muscle. Circ Res 1987;61: Ursell PC, Gardner PI, Albela A, Fenoglio JJ Jr, Wit AL: Structural and electrophysiological changes in the epicardial border zone of canine myocardial infarcts during infarct healing. Circ Res 1985;56: Spear JF, Balke CW, Lesh MD, Kadish AH, Levine JL, Moore EN: Effect of cellular uncoupling by heptanol on conduction in infarcted myocardium. Circ Res 1990;66: Spach MS, Dolber PC, Heidlage JF: Influence of the passive anisotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle. Circ Res 1988;62: Mackielski JC, Nelson WL: Effects of cellular uncoupling by heptanol on conduction in infarcted myocardium (letter to the editor). Circ Res 1990;67: Nelson WL, Makielski JC: Block of cardiac sodium current by heptanol and octanol (abstract). Biophys J 1990;57:299a 28. Oxford GS, Swenson RP: n-alkanols potentiate sodium channel inactivation in squid giant axons. Biophys J 1979;26: Jalife J, Sicouri S, Delmar M, Michaels DC: Electrical uncoupling and impulse propagation in isolated sheep Purkinje fibers. Am J Physiol 1989;257:H179-H Gettes LS: Effects of ionic changes in impulse propagation, in Rosen MR, Janse MJ, Wit AL (eds): Cardiac Electrophysiology. Mount Kisco, NY, Futura Publishing Co, 1990, pp Dominguez G, Fozzard HA: Influence of extracellular K' concentration on cable properties and excitability of sheep cardiac Purkinje fibers. Circ Res 1970;26: Buchanan JW Jr, Oshita S, Fujino T: A method for measurement of internal longitudinal resistance in papillary muscle. Am J Physiol 1986;251:H210-H Gettes LS, Buchanan JW Jr, Saito T, Kagiyama Y, Oshita S, Fujino T: Studies concerned with slow conduction, in Zipes DP, Jalife J (eds): Cardiac Electrophysiology and Arrhvthmias. Orlando, Fla, Grune & Stratton, 1985, pp KEY WORDS. anisotropy * heptanol * tetrodotoxin. ventricular tachycardia * potassium
Influences of Anisotropic Tissue Structure on Reentrant Circuits in the Epicardial Border Zone of Subacute Canine Infarcts
182 Influences of Anisotropic Tissue Structure on Reentrant Circuits in the Epicardial Border Zone of Subacute Canine Infarcts Stephen M. Dillon, Maurits A. Allessie, Philip C. Ursell, and Andrew L. Wit
More informationAnisotropic Conduction in the Triangle of Koch of Mammalian Hearts: Electrophysiologic and Anatomic Correlations
JACC Vol. 31, No. 3 March 1, 1998:629 36 629 Anisotropic Conduction in the Triangle of Koch of Mammalian Hearts: Electrophysiologic and Anatomic Correlations MÉLÈZE HOCINI, MD, PETER LOH, MD,* SIEW Y.
More informationPolymorphic ventricular tachycardia (VT) has been reported
Polymorphic Reentrant Ventricular Tachycardia in the Isolated Rabbit Heart Studied by High-Density Mapping Lucas Boersma, MD, PhD; Zoltan Zetelaki, MSc; Josep Brugada, MD, PhD; Maurits Allessie, MD, PhD
More informationChapter 16: Arrhythmias and Conduction Disturbances
Complete the following. Chapter 16: Arrhythmias and Conduction Disturbances 1. Cardiac arrhythmias result from abnormal impulse, abnormal impulse, or both mechanisms together. 2. is the ability of certain
More informationAnisotropic Conduction in Monolayers of Neonatal Rat Heart Cells Cultured
Rapid Communications 59 Anisotropic Conduction in Monolayers of Neonatal Rat Heart Cells Cultured on Collagen Substrate Vladimir G. Fast, Andre G. Kleber Abstract Anisotropic impulse conduction was studied
More informationV. TACHYCARDIAS Rapid rhythm abnormalities
V. TACHYCARDIAS Rapid rhythm abnormalities Tachyarrhythmias currently account for up to 350,000 deaths annually in the US. In addition to these clearly dangerous rhythm disturbances, other forms of more
More informationCASE 10. What would the ST segment of this ECG look like? On which leads would you see this ST segment change? What does the T wave represent?
CASE 10 A 57-year-old man presents to the emergency center with complaints of chest pain with radiation to the left arm and jaw. He reports feeling anxious, diaphoretic, and short of breath. His past history
More informationThe Wavelength of the Cardiac Impulse and Reentrant Arrhythmias in Isolated Rabbit Atrium
96 The Wavelength of the Cardiac Impulse and Reentrant Arrhythmias in Isolated Rabbit Atrium The Role of Heart Rate, Autonomic Transmitters, Temperature, and Potassium Joep L.R.M. Smeets, Maurits A. Allessie,
More informationPhase 2 Early Afterdepolarization as a Trigger of Polymorphic Ventricular Tachycardia in Acquired Long-QT Syndrome
Phase 2 Early Afterdepolarization as a Trigger of Polymorphic Ventricular Tachycardia in Acquired Long-QT Syndrome Direct Evidence From Intracellular Recordings in the Intact Left Ventricular Wall Gan-Xin
More informationVentricular Reentry Around a Fixed Barrier
267 Ventricular Reentry Around a Fixed Barrier Resetting With Advancement in an In Vitro Model Robert C. Bernstein, MD, and Lawrence H. Frame, MD We studied an in vitro model of reentrant tachycardia in
More informationReentry in a Pulmonary Vein as a Possible Mechanism of Focal Atrial Fibrillation
824 Reentry in a Pulmonary Vein as a Possible Mechanism of Focal Atrial Fibrillation BERNARD BELHASSEN, M.D., AHARON GLICK, M.D., and SAMI VISKIN, M.D. From the Department of Cardiology, Tel-Aviv Sourasky
More informationLos Angeles, California.
JACC Vol. 32, No. 1 July 1998:187 96 187 Characteristics of Wave Fronts During Ventricular Fibrillation in Human Hearts With Dilated Cardiomyopathy: Role of Increased Fibrosis in the Generation of Reentry
More informationA MODEL OF GAP JUNCTION CONDUCTANCE AND VENTRICULAR TACHYARRHYTHMIA
A MODEL OF GAP JUNCTION CONDUCTANCE AND VENTRICULAR TACHYARRHYTHMIA X. D. Wu, Y. L. Shen, J. L. Bao, C. M. Cao, W. H. Xu, Q. Xia Department of Physiology, Zhejiang University School of Medicine, Hangzhou,
More informationPredicting Ventricular Tachycardia Cycle Length After Procainamide by Assessing Cycle Length-Dependent Changes in Paced QRS Duration
39 Predicting Ventricular Tachycardia Cycle Length After Procainamide by Assessing Cycle Length-Dependent Changes in Paced QRS Duration Francis E. Marchlinski, MD, Alfred E. Buxton, MD, Mark E. Josephson,
More informationAbstract Objective To examine how epicardial activation and repolarisation patterns change in the course of ischaemia, and
474 Institut für Pharmakologie, Universität Köln, Köln, Germany M Gottwald S Dhein Forschungszentrum Karlsruhe, Institut für Toxikologie Abt Biophysik, Karlsruhe, Germany E Gottwald Correspondence to:
More informationMicrostructural Basis of Conduction II Introduction to Experimental Studies
Bioeng 6460 Electrophysiology and Bioelectricity Microstructural Basis of Conduction II Introduction to Experimental Studies Frank B. Sachse fs@cvrti.utah.edu Overview Microstructural Basis of Conduction
More informationWhere are the normal pacemaker and the backup pacemakers of the heart located?
CASE 9 A 68-year-old woman presents to the emergency center with shortness of breath, light-headedness, and chest pain described as being like an elephant sitting on her chest. She is diagnosed with a
More informationThis study was supported by the National Institutes of Health, Grant HE Received for publication December 6,
Mechanisms of Ventricular Fibrillation Yoshio WATANABE, M.D. and Leonard S. DREIFUS, M.D. T was pointed out more than two decades ago, by Wegria and Wiggers, that any satisfactory theory of fibrillation
More informationSluggish Upstroke of Signal-Averaged QRS Complex. An Arrhythmogenic Sign in Patients with Anteroseptal Myocardial Infarction
Original Article Sluggish Upstroke of Signal-Averaged QRS Complex. An Arrhythmogenic Sign in Patients with Anteroseptal Myocardial Infarction Masafumi Kanemura MD, Takao Katoh MD, Takashi Tanaka MD, Shin-ichiro
More informationWolff-Parkinson-White Syndrome with Gradual Transition from Type A to Type B. Yoshikazu SUZUKI, M.D., Hajime TERADA, M.D., and Noboru YAMAZAKI, M.D.
Wolff-Parkinson-White Syndrome with Gradual Transition from Type A to Type B Yoshikazu SUZUKI, M.D., Hajime TERADA, M.D., and Noboru YAMAZAKI, M.D. SUMMARY This report documents a case which showed type
More informationCase Report Coexistence of Atrioventricular Nodal Reentrant Tachycardia and Idiopathic Left Ventricular Outflow-Tract Tachycardia
www.ipej.org 149 Case Report Coexistence of Atrioventricular Nodal Reentrant Tachycardia and Idiopathic Left Ventricular Outflow-Tract Tachycardia Majid Haghjoo, M.D, Arash Arya, M.D, Mohammadreza Dehghani,
More informationHigh-Densiy Mapping of Electrically Induced Atrial Fibrillation in Humans
1665 High-Densiy Mapping of Electrically Induced Atrial Fibrillation in Humans Karen T.S. Konings, MD; Charles J.H.J. Kirchhof, MD, PhD; Joep R.L.M. Smeets, MD, PhD; Hein J.J. Wellens, MD, PhD; Olaf C.
More informationEffects of Hypoxia, Hyperkalemia, and Metabolic Acidosis on Canine Subendocardial Action Potential Conduction
Effects of ypoxia, yperkalemia, and Metabolic Acidosis on Canine Subendocardial Action Potential Conduction 93 R.D. Veenstra, R.W. Joyner, R.T. Wiedmann, Ming-Lon Young, and Rose C. Tan duction from the
More informationPART I. Disorders of the Heart Rhythm: Basic Principles
PART I Disorders of the Heart Rhythm: Basic Principles FET01.indd 1 1/11/06 9:53:05 AM FET01.indd 2 1/11/06 9:53:06 AM CHAPTER 1 The Cardiac Electrical System The heart spontaneously generates electrical
More informationAtrioventricular (AV) Nodal Reentry Associated with 2:1 Infra-His Conduction Block during Tachycardia in a Patient with AV Nodal Triple Pathways
Atrioventricular (AV) Nodal Reentry Associated with 2:1 Infra-His Conduction Block during Tachycardia in a Patient with AV Nodal Triple Pathways Haruhiko ABE, M.D., Takashi OHKITA, M.D., Masasuke FUJITA,
More informationIntroduction. Circulation
Introduction Circulation 1- Systemic (general) circulation 2- Pulmonary circulation carries oxygenated blood to all parts of the body carries deoxygenated blood to the lungs From Lt. ventricle aorta From
More informationPERMANENT PACEMAKERS AND IMPLANTABLE DEFIBRILLATORS Considerations for intensivists
PERMANENT PACEMAKERS AND IMPLANTABLE DEFIBRILLATORS Considerations for intensivists Craig A. McPherson, MD, FACC Associate Professor of Medicine Constantine Manthous, MD, FACP, FCCP Associate Clinical
More informationOptical Mapping in a New Guinea Pig Model of Ventricular Tachycardia Reveals Mechanisms for Multiple Wavelengths in a Single Reentrant Circuit
Circulation circ.ahajournals.org Circulation. 1996; 93: 603-613 doi: 10.1161/ 01.CIR.93.3.603 Articles Optical Mapping in a New Guinea Pig Model of Ventricular Tachycardia Reveals Mechanisms for Multiple
More informationPotassium Efflux from Myocardial Cells Induced by Defibrillator Shock
Purdue University Purdue e-pubs Weldon School of Biomedical Engineering Faculty Publications Weldon School of Biomedical Engineering 1986 Potassium Efflux from Myocardial Cells Induced by Defibrillator
More informationChapter 12: Cardiovascular Physiology System Overview
Chapter 12: Cardiovascular Physiology System Overview Components of the cardiovascular system: Heart Vascular system Blood Figure 12-1 Plasma includes water, ions, proteins, nutrients, hormones, wastes,
More informationACTION POTENTIAL TRANSFER AT THE PURKINJE - VENTRICULAR JUNCTION: ROLE OF TRANSITIONAL CELLS
1 of 4 ACTION POTENTIAL TRANSFER AT THE PURKINJE - VENTRICULAR JUNCTION: ROLE OF TRANSITIONAL CELLS Arie O. Verkerk 1, Marieke W. Veldkamp 2, Antoni C.G. van Ginneken 1,2, Ronald Wilders 1,3 1 Department
More informationChapter 13 The Cardiovascular System: Cardiac Function
Chapter 13 The Cardiovascular System: Cardiac Function Overview of the Cardiovascular System The Path of Blood Flow through the Heart and Vasculature Anatomy of the Heart Electrical Activity of the Heart
More informationECG Interpretation Cat Williams, DVM DACVIM (Cardiology)
ECG Interpretation Cat Williams, DVM DACVIM (Cardiology) Providing the best quality care and service for the patient, the client, and the referring veterinarian. GOAL: Reduce Anxiety about ECGs Back to
More informationProlongation of conduction time during premature stimulation in the human atrium is primarily caused by local stimulus response latency
European Heart Journal (1995) 16, 1920-1924 Prolongation of conduction time during premature stimulation in the human atrium is primarily caused by local stimulus response latency B. S. KOLLER, P. E. KARASIK,
More informationTranscoronary Chemical Ablation of Atrioventricular Conduction
757 Transcoronary Chemical Ablation of Atrioventricular Conduction Pedro Brugada, MD, Hans de Swart, MD, Joep Smeets, MD, and Hein J.J. Wellens, MD In seven patients with symptomatic atrial fibrillation
More informationAlterations in electrical coupling between ventricular
Pharmacological Modulation of Cardiac Gap Junctions to Enhance Cardiac Conduction Evidence Supporting a Novel Target for Antiarrhythmic Therapy Benjamin C. Eloff, MS*; Eran Gilat, DSc*; Xiaoping Wan, MD,
More informationMechanism of Ventricular Tachycardia Termination by Pacing at Left Ventricular Sites in Patients with Coronary Artery Disease
Journal of Interventional Cardiac Electrophysiology 6, 35 41, 2002 C 2002 Kluwer Academic Publishers. Manufactured in The Netherlands. Mechanism of Ventricular Tachycardia Termination by Pacing at Left
More informationELECTROCARDIOGRAPHY (ECG)
ELECTROCARDIOGRAPHY (ECG) The heart is a muscular organ, which pumps blood through the blood vessels of the circulatory system. Blood provides the body with oxygen and nutrients, as well as assists in
More informationStretching Cardiac Myocytes: A Finite Element Model of Cardiac Tissue
Megan McCain ES240 FEM Final Project December 19, 2006 Stretching Cardiac Myocytes: A Finite Element Model of Cardiac Tissue Cardiac myocytes are the cells that constitute the working muscle of the heart.
More informationRole of gap junctions in the propagation of the cardiac action potential
Cardiovascular Research 62 (2004) 309 322 www.elsevier.com/locate/cardiores Review Role of gap junctions in the propagation of the cardiac action potential Stephan Rohr* Department of Physiology, University
More informationComputational Modeling of the Cardiovascular System
ibiomep - International Doctoral Programme in Biomedical Engineering and Medical Physics Computational Modeling of the Cardiovascular System Microstructural Basis of Conduction Introduction to Functional
More informationNonuniform Epicardial Activation and Repolarization Properties of in Vivo Canine Pulmonary Conus
Nonuniform Epicardial Activation and Repolarization Properties of in Vivo Canine Pulmonary Conus 233 Mary Jo Burgess, Bruce M. Steinhaus, Kenneth W. Spitzer, and Philip R. Ershler The relation between
More informationECG Interpretation Made Easy
ECG Interpretation Made Easy Dr. A Tageldien Abdellah, MSc MD EBSC Lecturer of Cardiology- Hull University Hull York Medical School 2007-2008 ECG Interpretation Made Easy Synopsis Benefits Objectives Process
More informationAntiarrhythmic Drugs
Antiarrhythmic Drugs DR ATIF ALQUBBANY A S S I S T A N T P R O F E S S O R O F M E D I C I N E / C A R D I O L O G Y C O N S U L T A N T C A R D I O L O G Y & I N T E R V E N T I O N A L E P A C H D /
More informationAtrial Reentry around an Anatomic Barrier with a Partially Refractory Excitable Gap
495 Atrial Reentry around an Anatomic Barrier with a Partially Refractory Excitable Gap A Canine Model of Atrial Flutter Lawrence H. Frame, Richard L. Page, and Brian F. Hoffman From the College of Physicians
More informationRemodeling of Ventricular Conduction Pathways in Healed Canine Infarct Border Zones
Remodeling of Ventricular Conduction Pathways in Healed Canine nfarct Border Zones Robert A. Luke and Jeffrey E. Saffitz Cardiovascular Division and Department ofpathology, Washington University School
More informationCardiac physiology. b. myocardium -- cardiac muscle and fibrous skeleton of heart
I. Heart anatomy -- general gross. A. Size/orientation - base/apex B. Coverings D. Chambers 1. parietal pericardium 2. visceral pericardium 3. Layers of heart wall a. epicardium Cardiac physiology b. myocardium
More informationStep by step approach to EKG rhythm interpretation:
Sinus Rhythms Normal sinus arrhythmia Small, slow variation of the R-R interval i.e. variation of the normal sinus heart rate with respiration, etc. Sinus Tachycardia Defined as sinus rhythm with a rate
More informationElectrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts
LABORATORY INVESTIGATION MYOCARDIAL INFARCTION Electrophysiologic and anatomic basis for fractionated electrograms recorded from healed myocardial infarcts PHYLLIS 1. GARDNER, M.D., PHILIP C. URSELL, M.D.,
More informationLong-Standing Persistent Atrial Fibrillation: Can We Distinguish Ectopic Activity From Reentry by Epicardial Mapping?
Long-Standing Persistent Atrial Fibrillation: Can We Distinguish Ectopic Activity From Reentry by Epicardial Mapping? Running title: de Bakker et al.; Can epicardial mapping reveal the AF mechanism? Jacques
More informationBasic Electrophysiology Protocols
Indian Journal of Cardiology ISSN-0972-1622 2012 by the Indian Society of Cardiology Vol. 15, (3-4), 27-37 [ 27 Review Article Shomu Bohora Assistant Professor, Deptt. of Cardiology, U.N. Mehta Institute
More informationThe Effect of Ischaemic Region Shape on ST Potentials using a Half-Ellipsoid Model of the Left Ventricle
The Effect of Ischaemic Region Shape on ST Potentials using a Half-Ellipsoid Model of the Left Ventricle Author Barnes, Josef, Johnston, Peter Published 2012 Conference Title Computing in Cardiology (CinC)
More informationFREQUENCY COHERENCE MAPPING OF CANINE ATRIAL FIBRILLATION: IMPLICATION FOR ANTI-ARRHYTHMIC DRUG-INDUCED TERMINATION
56 Vol. 5 No. 2 April 2003 FREQUENCY COHERENCE MAPPING OF CANINE ATRIAL FIBRILLATION: IMPLICATION FOR ANTI-ARRHYTHMIC DRUG-INDUCED TERMINATION HAN-WEN TSO', TSAIR KAO', SHIH-AMN CHEN 2, CHING-TAI TAI\
More informationCardiac arrhythmias. Janusz Witowski. Department of Pathophysiology Poznan University of Medical Sciences. J. Witowski
Cardiac arrhythmias Janusz Witowski Department of Pathophysiology Poznan University of Medical Sciences A 68-year old man presents to the emergency department late one evening complaining of increasing
More informationElectrocardiography Biomedical Engineering Kaj-Åge Henneberg
Electrocardiography 31650 Biomedical Engineering Kaj-Åge Henneberg Electrocardiography Plan Function of cardiovascular system Electrical activation of the heart Recording the ECG Arrhythmia Heart Rate
More informationUse of Catheter Ablation in the Treatment of Ventricular Tachycardia Triggered by Premature Ventricular Contraction
J Arrhythmia Vol 22 No 3 2006 Case Report Use of Catheter Ablation in the Treatment of Ventricular Tachycardia Triggered by Premature Ventricular Contraction sao Kato MD, Toru wa MD, Yasushi Suzuki MD,
More informationHow to Ablate Atrial Tachycardia Mechanisms and Approach. DrJo Jo Hai
How to Ablate Atrial Tachycardia Mechanisms and Approach DrJo Jo Hai Contents Mechanisms of focal atrial tachycardia Various mapping techniques Detailed discussion on activation sequence mapping and entrainment
More informationEHRA Accreditation Exam - Sample MCQs Invasive cardiac electrophysiology
EHRA Accreditation Exam - Sample MCQs Invasive cardiac electrophysiology Dear EHRA Member, Dear Colleague, As you know, the EHRA Accreditation Process is becoming increasingly recognised as an important
More informationPlease check your answers with correct statements in answer pages after the ECG cases.
ECG Cases ECG Case 1 Springer International Publishing AG, part of Springer Nature 2018 S. Okutucu, A. Oto, Interpreting ECGs in Clinical Practice, In Clinical Practice, https://doi.org/10.1007/978-3-319-90557-0
More informationVentricular Arrhythmias
Presenting your most challenging cases Venice Arrhythmias Ventricular Arrhythmias Gioia Turitto, MD Presenter Disclosure Information A questionable indication for CRT-D in a patient with VT after successful
More informationBy the end of this lecture, you will be able to: Understand the 12 lead ECG in relation to the coronary circulation and myocardium Perform an ECG
By the end of this lecture, you will be able to: Understand the 12 lead ECG in relation to the coronary circulation and myocardium Perform an ECG recording Identify the ECG changes that occur in the presence
More informationCircus Movement in Rabbit Atrial Muscle as a Mechanism of Tachycardia
Circus Movement in Rabbit Atrial Muscle as a Mechanism of Tachycardia By Maurits A. Allessie, Felix I. M. Bonke, and Francien J. C. Schopman ABSTRACT The isolated left atrium of the rabbit, which showed
More informationSustained monomorphic ventricular tachycardia (VT) due to
Identification of the Ventricular Tachycardia Isthmus After Infarction by Pace Mapping Corinna B. Brunckhorst, MD; Etienne Delacretaz, MD; Kyoko Soejima, MD; William H. Maisel, MD, MPH; Peter L. Friedman,
More informationΦαρμακεσηική αγωγή ζηις ιδιοπαθείς κοιλιακές αρρσθμίες. Άννα Κωζηοπούλοσ Επιμελήηρια Α Ωνάζειο Καρδιοτειροσργικό Κένηρο
Φαρμακεσηική αγωγή ζηις ιδιοπαθείς κοιλιακές αρρσθμίες Άννα Κωζηοπούλοσ Επιμελήηρια Α Ωνάζειο Καρδιοτειροσργικό Κένηρο Όλες οι κοιλιακές αρρσθμίες δεν είναι ίδιες Υπάρτοσν διαθορές ζηον πληθυσμό, ηον μηχανισμό
More informationCirculation: Arrhythmia and Electrophysiology CHALLENGE OF THE WEEK
A 14-year-old girl with Wolff-Parkinson-White syndrome and recurrent paroxysmal palpitations due to atrioventricular reentry tachycardia had undergone two prior failed left lateral accessory pathway ablations
More informationArrhythmia/Electrophysiology
Arrhythmia/Electrophysiology Remodeling in Cells From Different Regions of the Reentrant Circuit During Ventricular Tachycardia Shigeo Baba, MD*; Wen Dun, PhD*; Candido Cabo, PhD; Penelope A. Boyden, PhD
More informationOverdrive pacing of early ischemic ventricular tachycardia: evidence for both reentry and triggered activity
Am J Physiol Heart Circ Physiol 288: H1124 H1130, 2005; doi:10.1152/ajpheart.01162.2003. Overdrive pacing of early ischemic ventricular tachycardia: evidence for both reentry and triggered activity David
More informationPrinciples and Applications of Electrical Circuits and Signal Theories in EP
Principles and Applications of Electrical Circuits and Signal Theories in EP Graydon Beatty, VP Therapy Development Atrial Fibrillation Division, St. Jude Medical, Inc. CardioRhythm 2009 Background Biophysics
More informationJournal of the American College of Cardiology Vol. 37, No. 2, by the American College of Cardiology ISSN /01/$20.
Journal of the American College of Cardiology Vol. 37, No. 2, 2001 2001 by the American College of Cardiology ISSN 0735-1097/01/$20.00 Published by Elsevier Science Inc. PII S0735-1097(00)01133-5 Coronary
More informationMapping Cardiac Pacemaker Circuits: Methodological puzzles of SAN optical mapping
Mapping Cardiac Pacemaker Circuits: Methodological puzzles of SAN optical mapping Igor R. Efimov, Vadim V. Fedorov, Boyoung Joung, and Shien-Fong Lin Journal of American College of Cardiology, 66(18):1976-86,
More informationArrhythmias. 1. beat too slowly (sinus bradycardia). Like in heart block
Arrhythmias It is a simple-dysfunction caused by abnormalities in impulse formation and conduction in the myocardium. The heart is designed in such a way that allows it to generate from the SA node electrical
More informationTitle. CitationJournal of Electrocardiology, 43(5): Issue Date Doc URL. Type. File Information.
Title Pleomorphic ventricular tachycardia originating from Author(s)Yokoshiki, Hisashi; Mitsuyama, Hirofumi; Watanabe, M CitationJournal of Electrocardiology, 43(5): 452-458 Issue Date 2010-09 Doc URL
More informationSudden cardiac death has been described as an electrical
Accelerated Onset and Increased Incidence of Ventricular Arrhythmias Induced by Ischemia in Cx43-Deficient Mice Deborah L. Lerner, MD; Kathryn A. Yamada, PhD; Richard B. Schuessler, PhD; Jeffrey E. Saffitz,
More informationParoxysmal Supraventricular Tachycardia PSVT.
Atrial Tachycardia; is the name for an arrhythmia caused by a disorder of the impulse generation in the atrium or the AV node. An area in the atrium sends out rapid signals, which are faster than those
More information12 Lead ECG. Presented by Rebecca Sevigny BSN, RN Professional Practice & Development Dept.
12 Lead ECG Presented by Rebecca Sevigny BSN, RN Professional Practice & Development Dept. Two Main Coronary Arteries RCA LCA which branches into Left Anterior Descending Circumflex Artery Two Main Coronary
More informationEffects of Elevated Extracellular Potassium on the Stimulation Mechanism of Diastolic Cardiac Tissue
3470 Biophysical Journal Volume 84 May 2003 3470 3479 Effects of Elevated Extracellular Potassium on the Stimulation Mechanism of Diastolic Cardiac Tissue Veniamin Y. Sidorov,* y Marcella C. Woods, z and
More informationECG CONVENTIONS AND INTERVALS
1 ECG Waveforms and Intervals ECG waveforms labeled alphabetically P wave== represents atrial depolarization QRS complex=ventricular depolarization ST-T-U complex (ST segment, T wave, and U wave)== V repolarization.
More informationThe normal atrioventricular (AV) node is able to conduct
Original Article Insights Into Atrioventricular Nodal Function From Patients Displaying Dual Conduction Properties Interactive and Orthogonal Pathways G. Stuart Mendenhall, MD; Andrew Voigt, MD; Samir
More informationThis presentation will deal with the basics of ECG description as well as the physiological basics of
Snímka 1 Electrocardiography basics This presentation will deal with the basics of ECG description as well as the physiological basics of Snímka 2 Lecture overview 1. Cardiac conduction system functional
More informationNEURONS Chapter Neurons: specialized cells of the nervous system 2. Nerves: bundles of neuron axons 3. Nervous systems
NEURONS Chapter 12 Figure 12.1 Neuronal and hormonal signaling both convey information over long distances 1. Nervous system A. nervous tissue B. conducts electrical impulses C. rapid communication 2.
More informationOnset of Induced Atrial Flutter in the Canine Pericarditis Model
JACC Vol. 17, No.5 1223 Onset of Induced Atrial Flutter in the Canine Pericarditis Model AKIHIKO SHIMIZU, MD, AKIRA NOZAKI, MD, YORAM RUDY, PHD, ALBERT L. WALDO, MD, FACC Cleveland, Ohio To test the hypothesis
More informationFull file at
MULTIPLE CHOICE. Choose the one alternative that best completes the statement or answers the question. 1) What electrical event must occur for atrial kick to occur? 1) A) Atrial repolarization B) Ventricular
More informationSpontaneous Termination of Reentry After One Cycle or Short Nonsustained Runs
493 Spontaneous Termination of Reentry After One Cycle or Short Nonsustained Runs Role of Oscillations and Excess Dispersion of Refractoriness Lawrence H. Frame and Edward K. Rhee This study describes
More informationSTRUCTURAL ELEMENTS OF THE NERVOUS SYSTEM
STRUCTURAL ELEMENTS OF THE NERVOUS SYSTEM STRUCTURE AND MAINTENANCE OF NEURONS (a) (b) Dendrites Cell body Initial segment collateral terminals (a) Diagrammatic representation of a neuron. The break in
More informationExtensive evidence supports the concept that dual atrioventricular
Mechanisms Underlying the Reentrant Circuit of Atrioventricular Nodal Reentrant Tachycardia in Isolated Canine Atrioventricular Nodal Preparation Using Optical Mapping Jianyi Wu, Jiashin Wu, Jeffrey Olgin,
More informationDecember 2018 Tracings
Tracings Tracing 1 Tracing 4 Tracing 1 Answer Tracing 4 Answer Tracing 2 Tracing 5 Tracing 2 Answer Tracing 5 Answer Tracing 3 Tracing 6 Tracing 3 Answer Tracing 6 Answer Questions? Contact Dr. Nelson
More informationCreating Order out of Chaos: New Research into Treatment of Atrial Fibrillation
Creating Order out of Chaos: New Research into Treatment of Atrial Fibrillation Peter Spector, MD Professor of Medicine, Director, Cardiac Electrophysiology Fletcher Allen Health Care University of Vermont
More informationParamedic Rounds. Tachyarrhythmia's. Sean Sutton Dallas Wood
Paramedic Rounds Tachyarrhythmia's Sean Sutton Dallas Wood Objectives At the end of this session, the paramedic will be able to: State the key components of the cardiac conduction pathway, along with the
More informationAn activation-repolarization time metric to predict localized regions of high susceptibility to reentry
An activation-repolarization time metric to predict localized regions of high susceptibility to reentry Nicholas Child, Martin J. Bishop, Ben Hanson, Ruben Coronel, Tobias Opthof, Bastiaan J. Boukens,
More informationAcute ischemia-induced gap junctional uncoupling and arrhythmogenesis
Cardiovascular Research 62 (2004) 323 334 Review Acute ischemia-induced gap junctional uncoupling and arrhythmogenesis Joris R. de Groot*, Ruben Coronel Experimental and Molecular Cardiology Group, Department
More informationArrhythmias. Simple-dysfunction cause abnormalities in impulse formation and conduction in the myocardium.
Arrhythmias Simple-dysfunction cause abnormalities in impulse formation and conduction in the myocardium. However, in clinic it present as a complex family of disorders that show variety of symptoms, for
More information798 Biophysical Journal Volume 96 February
798 iophysical Journal Volume 96 February 2009 798 817 Mechanisms of Transition from Normal to Reentrant Electrical ctivity in a Model of Rabbit trial Tissue Interaction of Tissue Heterogeneity and nisotropy
More informationUnderstanding the 12-lead ECG, part II
Bundle-branch blocks Understanding the 12-lead ECG, part II Most common electrocardiogram (ECG) abnormality Appears as a wider than normal S complex Occurs when one of the two bundle branches can t conduct
More informationFactors Determining Vulnerability to Ventricular Fibrillation Induced by 60-CPS Alternating Current
Factors Determining Vulnerability to Ventricular Fibrillation Induced by 60-CPS Alternating Current By Tsuneoki Sugimoto, M.D., Stephen F. School, M.D., and Andrew G. Wallace, M.D. ABSTRACT Very weak,
More informationHuman Anatomy and Physiology II Laboratory Cardiovascular Physiology
Human Anatomy and Physiology II Laboratory Cardiovascular Physiology 1 This lab involves two exercises: 1) Conduction System of the Heart and Electrocardiography and 2) Human Cardiovascular Physiology:
More informationDeterminants of Postrepolarization Refractoriness in Depressed Mammalian Ventricular Muscle
486 Determinants of Postrepolarization Refractoriness in Depressed Mammalian Ventricular Muscle George J. Rozanski, Jose Jalife, and Gordon K. Moe From the Masonic Medical Research Laboratory, Utica, New
More informationSupraventricular Tachycardia (SVT)
Supraventricular Tachycardia (SVT) Daniel Frisch, MD Cardiology Division, Electrophysiology Section Thomas Jefferson University Hospital daniel.frisch@jefferson.edu Short RP Are these the Mid same RP tachycardias?
More informationThe Electrocardiogram
The Electrocardiogram Chapters 11 and 13 AUTUMN WEDAN AND NATASHA MCDOUGAL The Normal Electrocardiogram P-wave Generated when the atria depolarizes QRS-Complex Ventricles depolarizing before a contraction
More informationShock-induced termination of cardiac arrhythmias
Shock-induced termination of cardiac arrhythmias Group members: Baltazar Chavez-Diaz, Chen Jiang, Sarah Schwenck, Weide Wang, and Jinglei Zhang Cardiac arrhythmias, also known as irregular heartbeat, occur
More informationELECTROCARDIOGRAPHY (III) THE ANALYSIS OF THE ELECTROCARDIOGRAM
ELECTROCARDIOGRAPHY (III) THE ANALYSIS OF THE ELECTROCARDIOGRAM Scridon Alina, Șerban Răzvan Constantin Recording and analysis of the 12-lead ECG is part of the basic medical assessment performed for every
More information