Local Refractory Period Research Articles

Correlation relationships of the reentrant ventricular tachycardia circuit

IntroductionA quantitative analysis of the components of reentrant ventricular tachycardia (VT) circuitry could improve understanding of its onset and perpetuation. MethodIn 19 canine experiments, the left anterior descending coronary artery was ligated to generate a subepicardial infarct. The border zone resided at the epicardial surface of the anterior left ventricle and was mapped 3–5 days postinfarction with a 196–312 bipolar multielectrode array. Monomorphic VT was inducible by extrastimulation. Activation maps revealed an epicardial double-loop reentrant circuit and isthmus, causing VT. Several circuit parameters were analyzed: the coupling interval for VT induction, VT cycle length, the lateral isthmus boundary (LIB) lengths, and isthmus width and angle. ResultsThe extrastimulus interval for VT induction and the VT cycle length were strongly correlated (p < 0.001). Both the extrastimulus interval and VT cycle length were correlated to the shortest LIB (p < 0.005). A derivation was developed to suggest that when conduction block at the shorter LIB is functional, the VT cycle length may depend on the local refractory period and the delay from wavefront pivot around the LIB. Isthmus width and angle were uncorrelated to other parameters. ConclusionsThe shorter LIB is correlated to VT cycle length, hence its circuit loop may drive reentrant VT. The extrastimulation interval, VT cycle length, and shorter LIB are intertwined, and may depend upon the local refractory period. Isthmus width and angle are less correlated, perhaps being more related to electrical discontinuity caused by alterations in infarct shape at depth.

Measurement variability of right atrial and ventricular monophasic action potential and refractory period measurements in the standing non-sedated horse

BackgroundIn human and veterinary medicine, monophasic action potential (MAP) analysis and determination of local refractory periods by contact electrode technique gives valuable information about local cardiac electrophysiological properties. It is used to investigate dysrhythmias and the impact of drugs on the myocardium. Precise measurement of total MAP duration is difficult, therefore the MAP duration is usually determined at a repolarization level of 90% (APD90). Until now, no studies are published about the feasibility of this technique in the standing non-sedated horse. In 6 healthy Warmblood horses, on two different days, an 8F quadripolar contact catheter was passed through a jugular introducer sheath and placed under ultrasound guidance at the level of the intervenous tubercle or right atrial free wall (RA), and in the right ventricular apex (RV) to record the MAP. The MAP amplitude and APD90 were measured at a resting sinus rhythm (heart rate of 30-42 bpm) and at pacing cycle lengths (PCL) of 1000 and 600 ms. The effective refractory period (ERP) was determined at PCL of 1000 and 600 ms.ResultsThe overall mean (±SD) APD90 (rest), APD90 (1000) and APD90 (600) were 263 ± 39 ms, 262 ± 41 ms, 236 ± 47 ms for the RA and 467 ± 23 ms, 412 ± 38 ms, 322 ± 29 ms for the RV. The mean ERP1000 and ERP600 were 273 ± 24 ms and 256 ± 22 ms for the RA and 386 ± 40 ms and 293 ± 30 ms for the RV. The measurement variability for the amplitude, APD90 and ERP measurements in the RA ranged between 36 and 44, 9–22 and 7–8%, respectively. The measurement variability for the amplitude, APD90 and ERP measurements in the RV ranged between 49 and 66, 6–7 and 10–12%, respectively.ConclusionsRA and RV MAP duration and ERP can be obtained by a contact electrode in standing non-sedated horses. The measurement variability varies with catheter location.

049 The role of the neural networks in identification and ablation of pulmonary vein ectopic triggers

IntroductionThe cardiac neural network comprises ganglionated plexi (GP) adjacent to each pulmonary vein (PV) which can trigger AV block and PV ectopy. We hypothesised that AV block in response to...

Long-term changes in sequence of atrial activation and refractory periods: No evidence for “atrial memory”

The purpose of this study was to test whether the spatial distribution of the atrial refractory period (AERP) and the vulnerability to atrial fibrillation (AF) are altered by long-term changes in the sequence of atrial activation. The spatial distribution of the AERP plays an important role in AF. Changes in the activation sequence have been postulated to modulate atrial repolarization ("atrial memory"). Six goats were chronically instrumented with epicardial atrial electrodes to determine activation time and AERP at 11 different areas of the right (RA) and left (LA) atrium and the Bachmann bundle. Activation time and AERP were measured during sinus rhythm and during prolonged RA and LA pacing (1 week RA pacing, 2 weeks LA pacing, 1 week RA pacing; 150 bpm). Inducibility of AF was determined by the number of atrial sites where single premature stimuli induced AF paroxysms >1 second. During sinus rhythm (106 +/- 4 bpm), AERP was longest at the Bachmann bundle and shortest at the LA free wall (185 +/- 6 ms and 141 +/- 5 ms, P < .001). In five of six goats, an inverse correlation between local activation time and AERP was found during sinus rhythm (r = -0.53 +/- 0.05; P < .05). The increase in atrial rate during RA and LA pacing caused an overall shortening of AERP from 167 +/- 6 ms to 140 +/- 6 ms (P < .001). However, a switch between long-term RA and LA pacing did not significantly change AERP at any of the 11 atrial regions and had no significant effect on AF inducibility. During sinus rhythm, an inverse relationship exists between the sequence of atrial activation and the local refractory period. However, long-term changes in the sequence of atrial activation do not alter the spatial distribution of AERP or the inducibility of AF.

In vivo recording of monophasic action potentials in awake dogs

Assessment of cardiac repolarization in dogs in vivo is of interest in numerous experimental canine models. Previous studies have used monophasic action potentials (MAPs) to investigate repolarization in vitro and in vivo in anesthetized animal models. Therefore, an approach for recording MAPs in awake dogs without the interference of anesthesia is desirable. We describe an experimental technique to record MAPs in conscious dogs by means of conventional rubber introducers which are implanted into the internal jugular vein. Atrial as well as ventricular MAPs can be simultaneously measured without complications. Pacing thresholds are low and stable over time. Continuous MAP recordings of stable amplitude can be achieved from the same endocardial site for periods up to 1 h. Antegrade and retrograde atrioventricular nodal conduction properties can be assessed. Programmed stimulation can be performed to simultaneously determine local refractory periods and MAP duration at cycle lengths from 500 to 200 ms. In awake, unsedated dogs measuring MAPs via rubber introducers permits safe, long-term recording of MAPs. Such recordings may be useful for safety pharmacologic studies in evaluating cardiovascular and noncardiovascular drugs with respect to their effects on repolarization. In various canine in vivo models including in vivo models of long QT syndrome, heart failures or sudden cardiac death, the present technique permits electrophysiologic measurements without the interference of anesthesia.

Electrophysiological characteristic of a patient exhibiting the short-coupled variant of torsade de pointes

A 41-year-old man was admitted because of syncope. The electrocardiogram showed torsade de pointes (Tdp) with no long QT interval and the coupling interval of the initial beat of Tdp was 240 ms. Heterogeneity of ventricular refractoriness was observed together with shortness of the effective refractory period measured at the right ventricular inflow site where the paced QRS morphology was the same as that of the initial beat of Tdp. Verapamil could suppress frequent ventricular premature complexes with a short coupling interval, which lead to Tdp. Polymorphic ventricular tachycardia was induced by triple ventricular extrastimuli. A pure potassium channel blocker was successful in inhibiting polymorphic ventricular tachycardia inducibility by prolongation of refractoriness. These results suggested that triggered ventricular premature complexes may be represent the initiating mechanism, whereas the shortness of local refractory period and heterogeneity of ventricular refractoriness may play a role in the development and the maintenance of the Tdp.

Focal atrial fibrillation: experimental evidence for a pathophysiologic role of the autonomic nervous system.

Focal paroxysmal atrial fibrillation (AF) was shown recently to originate in the pulmonary veins (PVs) and superior vena cava (SVC). In the present study, we describe an animal model in which local high-frequency electrical stimulation produces focal atrial activation and AF/AT (atrial tachycardia) with electrogram characteristics consistent with clinical reports. In 21 mongrel dogs, local high-frequency electrical stimulation was performed by delivering trains of electrical stimuli (200 Hz, impulse duration 0.1 msec) to the PVs/SVC during atrial refractoriness. Atrial premature depolarizations (APDs), AT, and AF occurred with increasing high-frequency electrical stimulation voltage. APD/AT/AF originated adjacent to the site of high-frequency electrical stimulation and were inducible in 12 of 12 dogs in the SVC and in 8 of 9 dogs in the left superior PV (left inferior PV: 7/8, right superior PV: 6/8; right inferior PV: 4/8). In the PVs, APDs occurred at 13+/-8 V and AT/AF at 15+/-9 V (P < 0.01; n = 25). In the SVC, APDs were elicited at 19+/-6 V and AT/AF at 26+/-6 V (P < 0.01; n = 12). High-frequency electrical stimulation led to local refractory period shortening in the PVs. The response to high-frequency electrical stimulation was blunted or prevented after beta-receptor blockade and abolished by atropine. In vitro, high-frequency electrical stimulation induced a heterogeneous response, with shortening of the action potential in some cells (from 89+/-35 msec to 60+/-22 msec; P < 0.001; n = 7) but lengthening of the action potential and development of early afterdepolar-izations that triggered APD/AT in other cells. Action potential shortening was abolished by atropine. High-frequency electrical stimulation evokes rapid ectopic beats from the PV/SVC, which show variable degrees of conduction block to the atria and induce AF, resembling findings in patients with focal idiopathic paroxysmal AF. The occurrence of the arrhythmia in this animal model was likely due to alterations in local autonomic tone by high-frequency electrical stimulation. Further research is needed to prove absolutely that the observed effects of high-frequency electrical stimulation were caused by autonomic nerve stimulation.

The distribution of refractory periods influences the dynamics of ventricular fibrillation.

The spatial and dynamic properties of ventricular fibrillation (VF) may be random or related to cellular electrical properties of the normal heart. Local activation intervals (AIs) in VF may depend on the local refractory period (RP), and sustained VF may require a steep action potential (AP) restitution curve. In guinea pig hearts, AP durations (APDs) and RPs on the epicardium are shorter at the apex and progressively longer toward the base, producing gradients of RPs that may influence the spatial organization of VF. In the present study, the influence of APDs on VF dynamics is investigated in perfused guinea pig hearts stained with a voltage-sensitive dye by comparing APD gradients to the dynamics of VF elicited by burst pacing. In VF, AIs had no clear periodicity, but average AIs were shorter at the apex (57.5+/-8.1 ms) than the base (76.1+/-1.5 ms, n=6, P<0.05) and had gradients similar to APD gradients (correlation coefficient 0.71+/-0.04). Analysis of local velocity vectors showed no preferential directions, and fast Fourier transform (FFT) power spectra were broad (10 to 24 Hz) with multiple peaks (n=6). However, the selective inhibition of delayed K(+) rectifying currents, I(Kr) (E4031; 0.5 micromol/L, n=3), shifted FFT spectra from complex to a lower dominant frequency (10 Hz) and altered repolarization but retained the correlation between mean AIs and RPs. Thus, VF dynamics are consistent with a multiple wave-make and wave-break mechanism, and the local RP influences VF dynamics by limiting the range of VF frequencies and AIs at each site. The full text of this article is available at http://www.circresaha.org.

In vivo recording of monophasic action potentials in awake dogs--new applications for experimental electrophysiology.

Despite enormous developments in the field of clinical and experimental electrophysiology there is still a gap in evaluating repolarization in the awake animal. Numerous previous studies have used monophasic action potentials (MAP) to assess repolarization in vitro and in vivo in anesthetized animal models. However, an approach for recording MAP in awake dogs without interference of anesthesia has not yet been developed. We developed an experimental technique to record MAP in conscious dogs by means of conventional rubber introducers which were implanted into the internal jugular vein. In seven awake dogs, atrial as well as ventricular MAP were simultaneously measured without complications. Pacing thresholds were low and stable over time ranging from 0.2 to 4.0 mA. The MAP amplitudes ranged from 10 to 30 mV for ventricular and from 5 to 15 mV for atrial MAP. Continuous MAP recordings of stable amplitude could be made from the same endocardial site for periods of up to one hour. Antegrade and retrograde AV-nodal conduction properties could be assessed. Programmed stimulation was performed to simultaneously determine local refractory periods and MAP duration at cycle lengths from 500 to 200 ms. In awake, unsedated dogs the measurement of MAP via rubber introducers permits safe, long-term recording of MAP. Such recordings may be useful for safety pharmacological studies in evaluating cardiovascular and non-cardiovascular drugs with regard to their effects on repolarization. In various canine in vivo models including in vivo models of long QT syndrome, heart failure or sudden cardiac death, the present technique permits electrophysiological measurements without interference of anesthesia.

Electrophysiologic effects of the new I(Ks)-blocking agent chromanol 293b in the postinfarction canine heart. Preserved positive use-dependence and preferential prolongation of refractoriness in the infarct zone.

Aim of the present study was to investigate site- and rate dependent effects of the IKs-blocking agent chromanol 293b on conduction and refractoriness in normal, infarcted, and transitional regions of in-situ canine hearts. In five dogs with subacute myocardial infarction, three-dimensional mapping was performed after insertion of 6 x 6 needle electrodes in the left ventricle. Before and after application of chromanol 293b (10 mg/kg), activation patterns and local refractory periods (ERPs) at pacing intervals of 300, 500 and 850 ms were obtained for the surviving epicardial muscle layer of the infarct zone (IZ) and for epi-, endo-, and midmyocardial muscle layers of both the normal zone (NZ) and the border zone (BZ) separating normal and infarcted areas. At baseline, both the NZ and the BZ exhibited uniform ERPs throughout the ventricular wall. Epicardial ERPs were longer in the IZ than in the NZ, and intermediate in the BZ. Chromanol 293b did not affect total activation times. However, at fast heart rates regional areas of slow conduction occurred. Chromanol 293b ubiquitously prolonged local ERPs, most markedly in the IZ. A preferential effect on individual muscle layers of the NZ or BZ and, thus, drug-induced transmural dispersion of ERP could not be observed. Again ubiquitously, the effect on ERP was more pronounced at faster than at slower heart rates, that is, positive use-dependent. At a basic cycle length of 300 ms, chromanol 293b prolonged local ERPs in the IZ by 46 +/- 24 %, in the BZ by 34 +/- 26%, and in the NZ by 20 +/- 17% (p < or = 0.05). At least in theory, the electrophysiologic properties of chromanol 293 b, that is, preferential prolongation of refractoriness in ischemic myocardium, more pronounced at faster than at slower heart rates, but homogeneously throughout the intact ventricular wall, appear to be favorable. Whether this translates into a clinical benefit, particularly in the treatment of ischemia-related ventricular tachyarrhythmias, remains to be determined.

Multisite pacing for prevention of atrial tachyarrhythmias: potential mechanisms

OBJECTIVESTo determine the effects of single-, dual-, triple- and quadruple-site atrial pacing on atrial activation and refractoriness in normal canine hearts.BACKGROUNDMultisite pacing has been suggested to be superior to single-site pacing for prevention of atrial tachyarrhythmias. However, the underlying electrophysiological mechanisms are undetermined at the moment, as is the rationale for the selection of pacing locations and the number of pacing sites.METHODSIn 13 normal beagle dogs, an epicardial multielectrode (128 bipoles) and a multiplexer mapping system were used to reconstruct epicardial atrial activation patterns obtained during simultaneous stimulation from up to four electrodes located in the high and low right and left atrium, respectively. For all pacing modes (single-, dual-, triple- and quadruple-site pacing), total activation times and local effective refractory periods at eight randomly selected sites as well as local recovery intervals were determined. In a subgroup of five dogs, total epicardial activation times were also obtained during single-site septal stimulation (septal group).RESULTSActivation times and local recovery intervals were minimized by triple-site stimulation, whereas a fourth site did not produce further shortening. Septal stimulation produced epicardial activation times comparable to quadruple-site stimulation. Local refractory periods and their dispersion always remained unaffected. Functional conduction blocks apparent during single-site were found to resolve during multisite stimulation.CONCLUSIONSMultisite pacing can prevent functional conduction blocks by multidirectional excitation and a reduction in total activation time. Triple-site and, possibly, septal pacing modes are expected to be most efficient because both minimize total activation times and maximize the multidirectionality of excitation. In spite of unaffected local refractory periods, the shortening of local recovery intervals might homogenize atrial repolarization and, thus, contribute to the preventive effects of multisite pacing.

QT interval dispersion: Dispersion of ventricular repolarization or dispersion of QT interval?

The QT interval (QTI) has long been useful as a clinical index of the duration of ventricular repolarization, particularly as a marker of prolonged repolarization and its well-established association with arrhythmogenic cardiac states. Likewise, inhomogeneity (dispersion) of repolarization has been linked definitively to increased susceptibility to reentrant arrhythmias. Recent studies have reported the use of QTI dispersion as a meaningful clinical index to identify patients at risk, but the interpretation of the measurement has been controversial. A Langendorff-perfused, isolated canine heart suspended in a torso-shaped, electrolytic tank filled with NaCl-sucrose solution was used to investigate the relationship between body surface QTIs and ventricular repolarization measured directly from the cardiac surface by using activation-recovery intervals, which have been documented to reflect the duration of local action potentials as well as local refractory periods. The data showed poor correlation between cardiac surface activation-recovery intervals and QTIs, as well as the insensitivity of QTIs to regional repolarization shortening in the presence of prolonged repolarization elsewhere. Furthermore, the data confirmed that torso tank QTI dispersion does not reflect directly the full range of measured ventricular repolarization inhomogeneity. It is concluded that body surface QTI dispersion is not a reliable index of repolarization dispersion.

Regional and functional factors determining induction and maintenance of atrial fibrillation in dogs.

The present study was designed to determine the factors governing the ability of premature beats at various atrial sites to initiate atrial fibrillation (AF) and the determinants of the duration of AF in dogs at 1-10 Hz. The site of atrial extrasystoles determined their ability to induce AF. Regional differences in AF inducibility were due to differences in local refractoriness. Premature beats initiated AF by blocking in regions of greater refractoriness, causing macroreentrant activation with subsequent disorganization producing fibrillation. The atrial refractory period and wavelength during rapid 1:1 atrial pacing were weak predictors of AF duration (r = 0.24 and 0.23, respectively), which depended strongly on variability in regional refractoriness measured by the standard deviation in local refractory periods (r = 0.80, P < 0.001) and on the heterogeneity of activation during AF (r = 0.74, P < 0.001). Thus, premature beats cause AF by initiating a single macroreentrant cycle that degenerates into multiple wavefronts, regional refractoriness is the primary determinant of AF induction by premature beats, and variability in refractoriness may be an important determinant of the ability of AF to sustain itself.

Effect of altered activation sequence on epicardial QRST area and refractory period in dogs.

We investigated the effects of activation sequence on cardiac surface QRST areas and refractory periods in experiments on dogs. Right and left ventricular pacings were performed, and the pacing site was altered every 6 minutes. After 4 minutes of a given pacing, 54 unipolar electrograms distributed over the entire cardiac surface were recorded. Next, refractory periods at electrode sites near pacing electrodes were measured. Paired right ventricular/left ventricular (RV/LV) pacing data were obtained six or seven times in each sample. Although the QRST isoarea maps during the two activation orders were qualitatively similar, it was recognized consistently from the right ventricle-left ventricle difference map that leads around the RV free wall had positive values and that leads around the LV free wall and apex had negative values. Compared with the same leads at RV and LV pacing, QRST areas were larger when pacing sites were near the leads. The local QRST areas of individual leads at which we measured local refractory period were consistently larger during drive from proximal pacing sites than during drive from distant pacing sites. Refractory periods were consistently longer during proximal pacing than during distal pacing, and there was a positive correlation between change in local QRST area and change in refractory period (r = 0.64) during altered activation sequence, whereas there was an inverse correlation between change in QRST area and change in refractory period (r = -0.91) during localized myocardial warming. Both local QRST areas and local refractory periods were dependent on the activation sequence, and there was a positive correlation between QRST areas and refractory periods during various activation sequences compared with localized myocardial warming.

Electrophysiological effects of flecainide in a canine 7 day old myocardial infarction model

Flecainide has been reported to be effective in suppressing chronic ventricular arrhythmias in clinical studies, but the electrophysiological mechanisms of its action are not understood. We therefore studied its effects on re-entrant ventricular arrhythmias in eight dogs with 7 day old infarction. Epicardial mapping and local refractory periods were obtained using 48 channel bipolar electrodes attached to the epicardium. Epicardial conduction velocity was significantly depressed by flecainide (2 mg.kg-1 intravenously), from 49.3 (SD 11.9) cms-1 to 35.3(11.2) cm s-1 (p less than 0.01). Flecainide prolonged effective refractory periods (ERP) in the normal, border and infarct zones: normal (n = 93), from 189.5 (15.9) to 219.3 (17.7) ms, p less than 0.01; border (n = 54) from 187.4(24.0) to 225.2 +/- 32.5 ms, p less than 0.01; and infarct (n = 93), from 197.7 (30.6) to 247.1 (34.2) ms, p less than 0.01. However, the percent change in refractoriness was greater in the infarct zone than in the normal zone, at 25.7(17.1)% v 16.2 (10.3)%, p less than 0.01. Furthermore, an area of functional unidirectional conduction block developed within the infarct zone where the maximal dispersion of ERP was observed. Inducible sustained ventricular tachycardia (SVT) was prevented in one dog and slowed (300 to 150 beats.min-1) in another by flecainide, while ventricular fibrillation remained inducible in one dog. Pro-arrhythmic effects were observed in two of five dogs without inducible SVT. In conclusion, flecainide significantly depressed conduction velocity and prolonged local refractoriness in the epicardial myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of local disparity in conduction and recovery time on ventricular vulnerability to fibrillation

Summary In experiments on 16 mongrel dogs, conduction time (CT), local refractory periods (RP), and recovery time (RT) of conducted beats were measured in the ventricles under local coronary perfusion and under systemic intravenous infusion with potassium chloride or epinephrine. The values of these parameters found in the locally perfused and in the non-perfused areas and the degree of local dispersion of these values were correlated with ventricular fibrillation thresholds. Regardless of potassium or epinephrine infusion, ventricular vulnerability to fibrillation was significantly lower with local infusions than with systemic infusions. It was found that changes of CT, RP, and RT in either direction would occur with increased and decreased fibrillation thresholds, and they were not directly correlated to ventricular vulnerability to fibrillation. The local dispersion of these parameters between the perfused and non-perfused areas, however, was always increased when ventricular vulnerability was high, and decreased when ventricular vulnerability was low. These results are strong evidence supporting the importance of local dispersion in excitability. The local dispersion was best represented by local variation in the RT of conducted beats, which under all experimental conditions correlated best with ventricular vulnerability. The other electrophysiological parameters seem to be of importance for the ventricular vulnerability when they contribute to an increased or decreased local dispersion of excitability.

The effect of acute coronary artery occlusion on subepicardial transmembrane potentials in the intact porcine heart.

Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.

Electrophysiologic effects of partial coronary occlusion and reperfusion

Electrophysiologic changes caused by partial coronary occlusion have not previously been examined. In nine dogs, refractory periods and conduction times were determined using the extrastimulus method after a 50 percent reduction in coronary blood flow. In another five dogs, ventricular automaticity was studied after the production of complete heart block. After 5 minutes of partial coronary occlusion the refractory period in the ischemic zone shortened from 164.6 ± 4.2 (mean ± standard error of the mean) to 149.6 ± 5.8 msec ( P < 0.001); after 60 minutes it shortened further to 142.5 ± 5.6 msec, resulting in a dispersion of refractoriness. Intramyocardial conduction time from the ischemic to the non-ischemic zone was prolonged from 48.6 ± 1.6 to 60.0 ± 3.3 msec ( P < 0.01), whereas conduction time from the nonischemic to the ischemic zone remained unchanged. No significant changes were observed in ventricular automaticity after partial coronary occlusion (idioventricular rate 56.0 ± 6.4 versus 51.2 ± 6.6 beats/min). Reperfusion 1 hour after partial occlusion resulted in a return of the refractory period and conduction time to preocclusion values, but there were no changes in idioventricular rate. Thus, after a 50 percent reduction in coronary blood flow, the decrease in local refractory period and prolongation of conduction time result in underlying electrical instability predisposing to reentrant arrhythmias whereas automaticity is unchanged. These abnormalities are fully abolished when reperfusion is instituted after 60 minutes of partial coronary occlusion.

Confinement of premature impulses in functional compartments of regions of the A-V conducting system.

The local refractory periods of the multiple branches of the distal A-V conducting system progressively increase from proximal to distal, reaching a maximum a few millimetres proximal to the termination of a given tract of conducting tissue in muscle, and progressively decreasing beyond the point of maximum duration. The multiple areas of maximum local refractory periods function collectively to provide a limiting segment, or gate, which determines the functional refractory period of preparations of large segments of A-V conducting tissue. Artificial or natural changes in the refractory period of a single tract of conducting tissue alter the functional properties of such preparations. Reversal of the changes in, or ablations of, the single abnormal tracts of tissue reverses the changes in functional refractory period of the entire preparation. These observations may relate to the way in which local cardiac disease may cause re-entrant arrhythmias.

Electrophysiological propertiesf the canine peripheral A-V conducting system.

Action potential durations and local refractory periods were mapped along the course of canine conducting tissue from bundle branches to the termination of false tendons in ventricular muscle. Standard microelectrode techniques were used. Areas of maximum action potential duration, which coincided with areas of maximum local refractory periods, were consistently found 2 to 3 mm proximal to the termination of conducting fibers in muscle. The refractory periods at the areas of maximum action potential duration were quantitatively identical in the multiple false tendons of a segment of the conducting system, providing a uniform functional limit for the propagation of premature impulses across the distal end of the conducting system of the segments studied. It was demonstrated that appropriately timed premature impulses could be confined within conducting tissue either proximal or distal to the area of maximum action potential duration. This occurred when the area of maximum duration was still refractory, after other areas of the conducting system had recovered excitability. In most preparations, maximum action potential durations and functional refractory periods across distal false tendons were longer in tissue from the right side than from the left side of the conducting system.