Ventricular tachyarrhythmia initiation in a canine model of recent myocardial infarction. Comparison of unipolar cathodal, anodal and bipolar stimulation

Ventricular tachyarrhythmia initiation was compared using unipolar cathodal, anodal and bipolar programmed stimulation at 21 sites in 5 normal adult mongrel dogs and 67 noninfarct sites in 16 dogs 3-5 days after experimental myocardial infarction. For this purpose, the minimum number of extrastimuli required for tachyarrhythmia initiation was determined in each pacing mode using twice cathodal threshold current for the drive beats and all extrastimuli except the last. The current and pacing mode were varied for the last extrastimulus (S2, S3 or S4). In the 5 normal dogs, ventricular fibrillation was reproducibly inducible from only 1/21 sites, and only in the cathodal mode. In 15/16 (94%) of the myocardial infarction dogs, a sustained ventricular tachycardia or ventricular fibrillation could be reproducibly initiated with either one (4 dogs), two (5 dogs) or three extrastimuli (6 dogs). Diastolic excitability thresholds were 0.08 +/- 0.03, 0.30 +/- 0.17, and 0.09 +/- 0.04 mA (median +/- SD) for unipolar cathodal, anodal and bipolar pacing, respectively (p less than 0.001 for anodal vs. cathodal and bipolar). The median absolute current required for ventricular tachyarrhythmia initiation was also highest with anodal pacing (0.72 +/- 0.77 mA), versus both the cathodal and anodal modes (0.18 +/- 0.28 and 0.20 +/- 0.28 mA, respectively, each p less than 0.001) but was comparable in all three modes relative to the threshold current (2.0, 2.4 and 2.6 mA for cathodal, anodal and bipolar pacing, respectively) required for initiation. Overall, ventricular tachyarrhythmia initiation was concordant in all three modes at 58/67 (87%) sites and discordant at only 9/67 (13%) sites (p less than 0.001). Moreover, there was no difference in either the pattern of arrhythmia initiated in each of the pacing modes with respect to ventricular tachycardia versus ventricular fibrillation, or in the median current required to initiate ventricular tachycardia (0.30 +/- 0.36 mA) versus ventricular fibrillation (0.31 +/- 0.44 mA; p greater than 0.1). Thus, ventricular tachyarrhythmia initiation was comparable in all three pacing modes with respect to overall success rate, number of ventricular extrastimuli required and the pattern of ventricular tachyarrhythmia initiated. Bipolar pacing with similar size anodal and cathodal electrodes appear to be appropriate for electrophysiologic ventricular tachyarrhythmia studies and are not likely to induce spurious arrhythmias resulting from stimulation at the anodal pole.     

Comparison of bipolar and unipolar programmed electrical stimulation for the initiation of ventricular arrhythmias: significance of anodal excitation during bipolar stimulation

To determine if anodal excitation during bipolar stimulation facilitates the initiation of sustained monomorphic ventricular tachycardia, nonsustained polymorphic ventricular tachycardia, or repetitive ventricular responses, both bipolar and cathodal unipolar programmed ventricular stimulation with one to three extrastimuli delivered during ventricular pacing at two rates from the right ventricular apex were performed in 28 patients evaluated for spontaneous sustained ventricular tachycardia or ventricular fibrillation (11 patients), nonsustained tachycardia (eight patients), or syncope (nine patients). In 25 patients a hexapolar pacing catheter was used to record local endocardial activation times adjacent to the cathode and anode and ventricular excitation during bipolar stimulation was defined as predominantly anodal, cathodal, or simultaneous at both anode and cathode. When bipolar and unipolar stimulation were compared there was no difference in the incidence of initiating sustained monomorphic ventricular tachycardia (57% vs 57%), nonsustained polymorphic ventricular tachycardia (14% vs 14%), or repetitive ventricular responses (21% vs 21%), although the response to bipolar vs unipolar stimulation was not concordant in every patient. Evidence of anodal excitation was observed in 11 (44%) patients but did not indicate increased risk of initiation of any ventricular arrhythmia, despite the fact that it was associated with shortening of the ventricular effective refractory period by 5.2 +/- 8.7 msec (p less than .05) during bipolar as opposed to unipolar stimulation. We conclude that unipolar and bipolar stimulation produce a similar incidence of initiation of arrhythmia, despite the frequent occurrence of anodal excitation during bipolar stimulation. Thus, the risk of initiation of nonspecific ventricular arrhythmias during programmed stimulation is unlikely to be reduced by the use of unipolar stimulation.     

Limitations of bipolar and unipolar conditioning stimuli for inhibition in the human heart

Noncapturing, conditioning electrical stimuli (Sc) delivered within the ventricular refractory period can prolong refractoriness and prevent later stimuli from eliciting a propagated response (inhibition). The purpose of this study was to further define the spatial effects of Sc, to determine if the effects of Sc can be enhanced by the use of unipolar as opposed to bipolar stimulation, and to evaluate the effect of Sc on the physiologic spread of excitation during atrioventricular reentry tachycardia. In 23 patients the right ventricular refractory period was determined before and after the introduction of bipolar, unipolar cathodal, and unipolar anodal noncapturing Sc with pulse widths of 2 or 9 msec and strengths of twice diastolic threshold and 10 MA. Pacing and conditioning stimuli were delivered at the same site and at sites separated by 3 mm. During ventricular pacing both bipolar and unipolar Sc prolonged the ventricular refractory period by greater than or equal to 10 msec in 22 of 23 patients when both Sc and pacing stimuli were delivered to the same site. However, when Sc was delivered 3 mm away from the pacing stimuli, the ventricular refractory period increased by greater than or equal to 10 msec in only 1 of 17 patients who received bipolar Sc and in none of 13 patients who received unipolar Sc. In seven patients bipolar conditioning stimuli were delivered as close as possible to the atrial insertion of an accessory atrioventricular connection during circus movement tachycardia with a well-localized accessory pathway. Sc did not terminate or slow tachycardia in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Vulnerability of the right ventricle to cathodal,anodal, and bipolar stimulation at double diastolic threshold strength

Summary The repetitive ventricular response (RVR) to three stimulation techniques (bipolar, cathodal and anodal) was investigated in 35 patients. 26 patients suffered from coronary heart disease and 9 patients from dilative cardiomyopathy. The stimulation study was performed at a ventricular driving rate of 120/min with one and two premature ventricular extrastimuli. We used rectangular impulses of 1.8 ms duration at duable diastolic threshold strength. RVR was scored as follows: 0: no RVR, 1: one nonstimulated RVR, 2: two nonstimulated RVR, 3: three nonstimulated RVR, 4: four to ten nonstimulated RVR, 5: more than ten nonstimulated RVR lasting less than 2 minutes, 6: sustained ventricular tachycardia or ventricular fibrillation. We found that with unipolar anodal stimulation the diastolic threshold was significantly greater and the effective refractory period of the right ventricle was significantly shorter as compared to the other stimulation techniques. Between the three different electrode configurations there were no significant differences concerning the number of consecutive ventricular depolarizations following premature stimulation. Conclusion: the phenomenon of RVR is not influenced by the stimulation technique (bipolar, cathodal and anodal) at double diastolic threshold.Supported by the Robert-Müller-Stiftung     

Anodal stimulation as a cause of pacemaker-induced ventricular fibrillation

A review of animal investigations suggests that pacemaker-induced ventricular fibrillation usually occurs at the anode, and in fact is difficult to evoke at the cathode. A search of the literature showed that every documented episode of pacemaker-induced ventricular tachycardia/fibrillation in humans has been with a bipolar electrode system. Since the problem most often occurs during temporary pacing associated with myocardial infarction, bipolar catheter electrodes should not be used for temporary pacing, and the use of unipolar (cathodal) pacing systems should increase the safety of electrical pacing.     

Effect of pacing current strength on indexes of myocardial activation in humans: influence of chronic infarction and polarity of pacing

The effects of current strength (threshold to 20 mA) and pacing polarity (bipolar versus unipolar) on indexes of ventricular activation during endocardial pacing (cycle length 400 to 500 ms) from 10 normal and 17 abnormal left ventricular sites were assessed in 19 patients. Abnormal sites were infarcted and demonstrated an electrogram duration greater than 70 ms and amplitude less than 3 mV during sinus rhythm. Bipolar pacing was performed from poles 1 (cathode) and 3 (1 cm interelectrode distance) of a quadripolar catheter. Unipolar cathodal pacing was performed from the tip electrode (pole 1). Local activation was indexed by the interval from the pacing stimulus to 1) the onset of the QRS complex, 2) the largest rapid deflection of the local electrogram, and 3) the end (total duration) of the local electrogram recorded from poles 2 and 4 of the quadripolar catheter used for left ventricular pacing. Distant activation was indexed by the interval from pacing stimulus to electrograms recorded at the right ventricular apex and outflow tract. Bipolar and unipolar pacing of normal sites produced a modest homogeneous reduction of all activation times by 3 to 11 ms (median) with increments in current strength from threshold (0.8 mA) to 20 mA. Bipolar pacing of abnormal sites showed marked (up to 110 ms) and heterogeneous changes in local (median 22 to 30 ms) as well as distant (median 14 to 23 ms) activation times with increases in current strength from threshold (2.7 mA) to 20 mA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of Interelectrode Distance on the Bipolar Strength-Interval Relationship and Ventricular Effective Refractory Period in Humans

Effect of Interlectrode Spacing The purpose of this study was to compare the effects of interelectrode distaices of 1 cm and 0.5 cm on the ventricular effective refractory period (VERP) and the strength-interval relationship during bipolar cathodal pacing. A quadripolar electrode catheter with an interelectrode spacing of 0.5 cm was positioned at the right ventricular apex in 30 subjects, and the VERP was measured in 2-msec steps at twice the late diastolic threshold using bipolar cathodal pacing, first with an electrode spacing of I cm, then 0.5 cm. With the technique used in this study, there was up to 4 msec of variability in the measured VERP. Therefore, a change in the VERP of at least 6 msec was required before concluding that the interelectrode distance had affected the measured VERP In 15 subjects (group 1), the VERP was not affected by a change in electrode spacing; in nine subjects (group 2) the VERP was 6–10 msec longer with the 0.5 cm spacing than with the 1-cm spacing, and in six subjects (group 3) the VERP was 6–12 msec longer with the 1.0-cm spacing than with the 0.5-cm spacing. Determination of unipolar strength-interval curves in ten other subjects demonstrated that anodal curves can be distinguished from cathodal curves by the presence of an early diastolic dip and by the occurrence of the ascent of the curve at a longer extrastimulus coupling interval. These features were used as markers of an anodal contribution to the bipolar strength-interval curves in groups 1, 2, and 3. In subjects in whom there was a difference in the VERP with the two electrode spacings, an anodal contribution to the bipolar strength interval curve was always identifiable in the curve generated with the electrode spacing that had yielded the longer VERP With the bipolar configuration that yielded the longer VERP, the unipolar stimulation threshold at the anode was always ≤ 1.6 mA and was always lower than the anodal threshold of the bipolar configuration that yielded the shorter VERP. In conclusion, the VERP may either lengthen or shorten by up to 10–12 msec when the interelectrode distance is changed from 1 to 0.5 cm during bipolar cathodal pacing. The effect of electrode spacing on the measured VERP is attributable to position-dependent effects on the unipolar anodal stimulation threshold. A lower anodal threshold may result in a greater degree of anodal contribution during bipolar pacing, manifest by the occurrence of the ascent of the strength-interval curve later in diastole and a corresponding increase in the VERP measured at a current strength of twice the late diastolic threshold. (J Cardiovasc Electrophysiol, Vol. 1. pp. 103–115, April 1990)     

Contribution of the anode to ventricular excitation during bipolar programmed electrical stimulation

Anodal excitation may contribute to the initiation of ventricular arrhythmias during bipolar pacing in the canine ventricle. To determine if anodal excitation occurs during bipolar programmed ventricular stimulation in humans, ventricular electrograms adjacent to the anode and cathode were recorded using a specially designed hexapolar electrode catheter in 10 patients. Single extrastimuli were delivered during ventricular pacing at stimulus strengths slightly above the late diastolic threshold and at 2 to 5 times late diastolic threshold. Evidence of anodal excitation was observed in 18 of the 52 combinations (35%) of stimulus strengths and electrode configurations tested, and occurred in 9 of the 10 patients; it consisted of earliest ventricular activation adjacent to the anode (8 patients) or simultaneous activation at the anode and cathode (3 patients). This occurred either with premature stimuli (3 patients) or during the basic drive and extrastimuli (6 patients). Comparison of local activation times during unipolar pacing supported an anodal contribution to excitation during bipolar pacing and suggested that inhomogenous conduction delays were not responsible for these findings. Thus, anodal excitation occurs frequently during bipolar programmed stimulation and produces marked changes in local myocardial activation, which may potentially influence the initiation of ventricular arrhythmias.     

Reverse polarity pacing: the hemodynamic benefit of anodal currents at lead tips for cardiac resynchronization therapy

Background: Myocardial depolarization can be achieved with currents of either anodal or cathodal polarity. In contrast to conventional cathodal pacing, anodal pacing initially hyperpolarizes tissue and improves myocardial contractility in animal models.
Methods and Results: In 13 patients undergoing cardiac resynchronization therapy (CRT) device implantation, we compared the mean left ventricular outflow velocity-time integral (LV-VTI) for anodal and cathodal polarities in three different pacing configurations. Intraoperative continuous-wave Doppler measurements were taken at a fixed interrogation angle, while polarities were switched during unipolar left ventricular, unipolar biventricular, and shared-coil biventricular pacing. Comparisons used identical pacing rates, intervals, and stimulus strengths. Patients had a mean ejection fraction of 0.18 ± 0.08 and a mean QRS duration of 140 ± 34 ms. All capture thresholds were less than 4.5 volts at a pulse width of 0.4 ms. Data were suitable for analysis in 37 of the 39 pairs of Doppler measurements. Anodal polarity significantly increased average LV-VTI in 36 of these 37 comparisons. The mean increase in LV-VTI for each configuration with anodal versus cathodal polarity was 2.8 ± 2.6 cm (P < 0.001). The combined mean LV-VTI for all configurations was similarly higher for anodal polarity (24.4 ± 11.7 cm) versus cathodal polarity (21.7 ± 10.9 cm; P < 0.001).
Conclusion: Anodal pacing polarity significantly improves a measure of LV function compared to traditional cathodal currents. Anodal pacing, which can be achieved by a simple reversal of pacing circuit polarity, may represent an important therapeutic addition to future resynchronization devices.     

Effect of increased current, multiple pacing sites and number of extrastimuli on induction of ventricular tachycardia

Reproduction of spontaneously occurring ventricular tachycardia (VT) and induction of previously undocumented VT were studied prospectively in 98 patients: 48 with documented sustained VT or ventricular fibrillation, 25 with nonsustained or exercise-induced VT, and 25 with no documented VT. Patients received 1 to 4 ventricular extrastimuli and ventricular burst pacing at 2 right ventricular (RV) sites, first at twice late diastolic threshold, and then at 10 mA using a prospective, tandem study design. Spontaneously occurring VT was reproduced in 37 of 48 patients (77%) at twice late diastolic threshold and in 1 other patient (2%) at 10 mA. VT was reproduced at both RV sites in 17 of 48 patients (35%) and at 1 site in 20 of 48 patients (42%) at twice late diastolic threshold. A previously undocumented VT was induced in 7 of 25 patients (28%) with no documented VT at twice diastolic threshold and 14 of 25 patients (56%) at 10 mA. A previously undocumented VT was induced in 33 of 73 patients (45%) with a history of sustained or nonsustained VT at twice late diastolic threshold and in 47 of 73 patients (64%) at 10 mA. In patients with documented sustained VT, the use of up to 4 ventricular extrastimuli at multiple RV sites increases the sensitivity of the test. In patients without documented VT, the induction of previously undocumented VT with more than 3 ventricular extrastimuli limits the specificity of the test. Increased current provides only a slight advantage over 4 ventricular extrastimuli at twice late diastolic threshold in terms of reproduction of spontaneously occurring VT, but leads to a marked increase in induction of previously undocumented VT.     

Effects of high stimulation current on the induction of ventricular tachycardia

Programmed stimulation at 2 right ventricular sites with 1 to 3 extrastimuli was performed at current strengths of twice diastolic threshold (1.0 +/- 0.2 mA, mean +/- standard deviation) and 10 mA in 41 patients undergoing an electrophysiologic study because of sustained ventricular tachycardia (VT) (11 patients), nonsustained VT (19 patients) or unexplained syncope (11 patients). In 26 patients, VT was not induced by programmed stimulation at twice diastolic threshold. Programmed stimulation at 10 mA induced VT or ventricular fibrillation in 16 of these 26 patients (62%). In 4 of 16 patients, the coupling intervals of the extrastimuli that induced VT/ventricular fibrillation at 10 mA were all equal to or longer than the shortest coupling intervals resulting in ventricular capture at twice diastolic threshold. Fifteen patients had inducible VT at twice diastolic threshold. Programmed stimulation at 10 mA induced a similar VT in 12 of these patients, but resulted in no VT induction in 3 of 15 patients (20%), despite ventricular capture at the same coupling intervals that had induced VT at twice diastolic threshold. This study shows that programmed stimulation at a high current strength may either facilitate or prevent induction of VT. Facilitation of VT induction usually is attributable to a shortening of ventricular refractoriness and the ability of extrastimuli at 10 mA to capture the ventricle at shorter coupling intervals than possible at twice diastolic threshold. However, in 25% of cases, the facilitation of VT induction by 10-mA stimuli is not explained by a shortening of ventricular refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular fibrillation during programmed ventricular stimulation: Incidence and clinical implications

Ventricular fibrillation occurred in 10 (3.3 percent) of 300 patients consecutively studied with programmed ventricular stimulation. One hundred twenty-five of these patients were studied with double ventricular extrastimuli including 68 patients with and 57 patients without documented or suspected ventricular tachycardia or fibrillation, or both. Ventricular fibrillation did not develop in response to a single ventricular extrastimulus delivered during sinus rhythm, ventricular pacing or ventricular tachycardia or in response to ventricular pacing at cycle lengths of 300 msec or greater and occurred only in response to double ventricular extrastimuli. All 10 patients who manifested ventricular fibrillation during programmed stimulation were in the group of patients with suspected or documented ventricular tachycardia or fibrillation. Ventricular fibrillation was initiated in seven patients with double ventricular extrastimuli delivered during sinus rhythm or ventricular pacing and in three patients with double ventricular extrastimuli delivered during ventricular tachycardia. Four patients had spontaneous conversion to sinus rhythm and the remainder underwent defibrillation without sequelae. Recurrent ventricular fibrillation occurred clinically in 7 of the 10 patients. This study suggests that ventricular fibrillation occurs uncommonly during programmed ventricular stimulation and only in response to double ventricular extrastimuli in patients in whom spontaneous episodes are likely to occur.     

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination

Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. In conclusion: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Programmed electrical stimulation studies for ventricular tachycardia induction in humans. I. The role of ventricular functional refractoriness in tachycardia induction

Closely coupled extrastimuli are frequently necessary to induce ventricular tachycardia at electrophysiologic study. Although induction usually requires propagated extrastimuli, systematic evaluations of minimal coupling intervals have focused on nonpropagated measures (effective refractory periods) rather than on propagated measures (functional refractory periods). The effects of procedural factors on ventricular functional refractory periods were examined in 10 patients. Like the effective refractory period, the functional refractory period shortens with rapid pacing cycle lengths (281 +/- 12 ms at a cycle length of 600 ms; 260 +/- 15 ms at a cycle length of 400 ms) and with multiple extrastimuli (279 +/- 16 ms with one extrastimulus; 214 +/- 16 ms with two extrastimuli). The effects of multiple extrastimuli exceed those of shortening pacing cycle length. Unlike the effective refractory period, the functional refractory period is affected by recording site (increasing as the distance from the pacing site increases) but is not affected by increasing the stimulus intensity above twice diastolic threshold (282 +/- 14 ms at 2 times threshold; 282 +/- 13 ms at 16 times threshold) or by increasing the pulse width above 2 ms (282 +/- 13 ms at a pulse width of 2 ms; 282 +/- 14 ms at a pulse width of 5 ms). The effect of varying stimulus intensity on ventricular tachycardia induction was examined in a second group of 11 patients with documented, spontaneous ventricular tachycardia. No change in ventricular tachycardia inducibility accompanied changes in stimulus intensity from 2 to 10 times threshold.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms and relevance of arrhythmias induced by high-current programmed ventricular stimulation

Programmed ventricular stimulation was performed at 10 mA with up to 3 extrastimuli in 15 patients studied for indications other than sustained ventricular tachycardia and with no sustained arrhythmias induced at twice diastolic threshold. Stimulation with 10 mA produced 6 new instances of ventricular fibrillation (VF), 1 of which may have been clinically relevant. No sustained ventricular tachycardia was induced. VF was induced with triple extrastimuli in 5 of 6 cases. The increased arrhythmogenicity of 10-mA stimulation was related to shortened ventricular refractory periods (S2 267 +/- 21 vs 231 +/- 22 ms, p less than 0.0001; S3 217 +/- 15 vs 178 +/- 15 ms, p less than 0.0005) and did not occur without at least 2 extrastimulus coupling intervals being less than was possible at twice diastolic threshold. Stimulation with 10 mA also resulted in greater increments in extrastimulus local conduction time (27 +/- 19 vs 54 +/- 15 ms, p less than 0.001) and intraventricular conduction time (27 +/- 17 vs 45 +/- 18 ms, p less than 0.005) as coupling intervals were shortened from 360 ms to just beyond ventricular refractoriness. VF was induced more frequently in patients with cardiomyopathy (p less than 0.05). Thus, the increase in arrhythmogenicity with 10-mA stimulation with triple extrastimuli is predominantly manifest as VF, which occurs with considerable frequency and is of uncertain clinical significance. This technique should be used with great caution, and only after other stimulation modalities have been attempted.     

Uni- and bipolar pacing threshold measurements with capturecontrol, a new automatic pacemaker function for capture verification. Comparison of the automatic and the manual pacing threshold measurement

It is mandatory in pacemaker patients to determine the pacing threshold at each follow-up visit. To facilitate the pacing threshold measurements, complete automatic pacemaker tests are being developed. A new pacemaker algorithm for automatic capture verification (Capturecontrol) detects the presence of the evoked response signal 70-100 ms after the pacing pulse. The aim of this study was to determine the uni- and bipolar pacing thresholds using this automatic pacemaker function and compare them with the manually determined threshold. The study included 14 patients with the DDD pacemaker Logos (Biotronik) connected to the high-ohmic ventricular pacing lead Synox SX 60-BP (Biotronik). At predischarge and 8, 14, 20 and 26 weeks after implantation the uni- and bipolar pacing thresholds were assessed manually and with the automatic pacemaker function at 0.4 ms duration. Mean pacing thresholds determined with the automatic pacemaker function were not different from the manually measured values. This applied to uni- and bipolar pacing. Seventy percent of all unipolar and 67% of all bipolar measurements had no deviation. A deviation of 0.1 V between manual and automatic threshold measurement was observed in 25% (unipolar) and 28% (bipolar), respectively. A 0.2-volt difference occurred in 3% in the unipolar measurements. Deviations >/=0.3 V were found in 2% of all unipolar and in 5% of all bipolar measurements. In conclusion, automatic pacing threshold measurements using the Capturecontrol algorithm were similar compared to the manually determined thresholds. The excellent agreement between the two methods was observed for bipolar as well as unipolar pacing and on condition that all patients had a high-ohmic ventricular pacing lead. Therefore, fewer requirements are necessary for Capturecontrol than for presently available systems. Such pacemaker functions can help to speed up the measurements during follow-up visits.     

Local effects of electrical and mechanical stimulation on the recovery properties of the canine ventricle

The effects of electrical stimulation on local recovery properties of the canine ventricle were studied. Ventricular excitability was examined by an analysis of unipolar or bipolar strength-interval curves, and the effective refractory period was derived from the steep portion of the curve. Conduction times of all propagated responses to testing stimuli were recorded. When ventricular driving and testing sites were the same, effective refractory periods were significantly shorter (probability [p] < 0.001), conduction times longer (p < 0.001) and anodal dip thresholds lower (p < 0.001) than during atrial drive. However, as ventricular driving and testing sites were separated, effective refractory periods increased and conduction times shortened. At interelectrode distances of greater than 15 mm, both effective refractory periods and conduction times remained constant and similar to those observed during atrial drive. Effective refractory periods measured at the ventricular drive electrode shortened by 8.2 percent (p < 0.001) when the driving stimulus was twice threshold and by 15.4 percent (p < 0.001) when 10 times threshold. At a distance of 15 mm from the driving sites, the effective refractory period was not significantly shortened when testing stimuli of twice threshold intensity were used and was reduced by only 8.1 percent (p < 0.002) when stimuli 10 times threshold were used. Shortening of the effective refractory period near the ventricular driving site was accentuated by short coupling intervals. When ventricular drive was accomplished using mechanical impulses delivered to the epicardium, effective refractory periods during atrial and ventricular drive were virtually the same, regardless of the proximity of ventricular driving and testing sites.Thus, shortening of the effective refractory period and prolonged conduction in the vicinity of the driving electrode are a function of stimulus intensity, distance from the driving site and time. These local alterations in the recovery properties of the ventricle provide conditions that may be favorable for the induction of reentrant arrhythmias.     

Effects of procainamide on strength-interval relations in normal and chronically infarcted canine myocardium

The effects of procainamide on strength-interval relations in normal and chronically infarcted canine myocardium were determined in nine adult mongrel dogs susceptible to sustained ventricular tachyarrhythmias. The dogs were studied at 3 to 30 days after two stage occlusion and reperfusion of the mid left anterior descending coronary artery. Unipolar cathodal stimulation (pulse duration 2 ms, drive cycle length 300 ms) was used to evaluate excitability and refractoriness at a total of 19 normal and 22 infarct sites both before and 15 to 30 minutes after intravenous infusion of procainamide, 20 to 25 mg/kg body weight. The electrophysiologic effects of procainamide were evaluated at the time of the plateau phase of procainamide's antiarrhythmic activity in this model. At normal sites, procainamide had only a minimal effect on the mean diastolic excitability threshold (increased from a mean [± standard deviation]of 0.07 ± 0.02 to 0.08 ± 0.02 mA [probability (p) = not significant (NS)], the mean effective refractory period (increased from 137 ± 10 to 139 ± 11 ms [p = NS]) and the mean ventricular refractory period at twice diastolic threshold (increased from 156 ± 12 to 163 ± 16 ms [p <0.01]). At infarct sites, the mean diastolic excitability threshold was similarly unchanged after procainamide (from 0.57 ± 1.13 to 0.57 ± 1.09 mA [p = NS]), but both the mean effective refractory period (from 142 ± 17 to 159 ± 27 ms [p <0.001]) and the mean ventricular refractory period at twice diastolic threshold (from 166 ± 25 to 187 ± 33 ms [p <0.001]) were moderately prolonged. In addition, dispersion of refractoriness between normal and infarct sites as well as within areas of infarcted myocardium was often either unchanged or increased rather than decreased by procainamide.

Thus, the antiarrhythmic activity of procainamide in this canine model of chronic myocardial infarction was not explained by an effect on the excitability or refractoriness of normal myocardium, by changes in the diastolic excitability of infarcted tissue or by an effect on the dispersion of refractoriness. The most prominent effect of procainamide was to decrease the excitability of abnormal myocardium during the relative refractory period and to prolong the refractoriness of abnormal myocardium.     

Termination of ventricular tachycardia: Role of tachycardia cycle length

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79%) and cardioversion was required in 29 patients (21% ). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 62 (63%), and 7 of 16 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 6 patients (86%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (76%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35%). The ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30%) procainamide increased the tachycardia cycle length by 49 ± 42 ms (p < 0.01) and did not modify the mode of termination. In 6 patients (26%) procainamide increased cycle length by 142 ± 108 ms (p < 0.01), but termination was more difficult. In 10 patients (44%) procainamide increased the cycle length by 138 ± 110 ms (p < 0.001) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.     

Improved method for evaluating ventriculoatrial conduction before implantation of atrial-sensing dual chamber pacemakers

Pacemaker-mediated tachycardia may occur when a spontaneous ventricular premature depolarization is retrogradely conducted to the atrium with a ventriculoatrial (VA) interval that exceeds the atrial refractory period of an atrial-sensing dual chamber pacemaker. Previous methods for evaluating VA conduction have failed to predict clinical occurrences of pacemaker-mediated tachycardia. In this study, maximal VA intervals after ventricular extrastimuli during atrial or atrioventricular (AV) sequential pacing were compared with intervals measured by the standard method of ventricular pacing. VA intervals were 201 +/- 53 ms during ventricular pacing and 224 +/- 52 ms after ventricular extrastimuli during atrial pacing (p = NS). VA intervals were 305 +/- 77 ms after ventricular extrastimuli during AV sequential pacing and were longer than VA intervals during ventricular pacing (p less than 0.001) or after ventricular extrastimuli during atrial pacing (p less than 0.01). Thus, the ventricular extrastimulus technique during AV sequential pacing reveals substantially longer VA intervals than does ventricular pacing and explains why pacemaker-mediated tachycardia might occur when pacemaker atrial refractory periods are designed or programmed according to VA intervals measured only during ventricular pacing.