Importance of the pacing mode in the initiation of ventricular tachyarrhythmia in a canine model of chronic myocardial infarction

The use of unipolar anodal or bipolar pacing, as compared with unipolar cathodal pacing, purportedly increases the likelihood of inducing inadvertent ventricular fibrillation in susceptible patients. In this study, the ability to initiate sustained ventricular tachycardia or fibrillation with unipolar cathodal, unipolar anodal and bipolar pacing modes was compared using programmed ventricular stimulation at 82 subendocardial periinfarction sites in 11 dogs with chronic myocardial infarction. The late diastolic excitability threshold was significantly higher and the ventricular refractory period was significantly shorter (p less than 0.001) with anodal pacing (mean 0.62 mA, 156 ms, respectively) than with pacing in either the cathodal (0.12 mA, 174 ms) or the bipolar (0.13 mA, 173 ms) mode. At a current intensity twice that of the excitability threshold, the introduction of one or two extrastimuli induced ventricular tachycardia and ventricular fibrillation comparably among the three pacing modes. However, when three extrastimuli were used, ventricular fibrillation was induced with anodal pacing twice as frequently (50 [61%] of 82 sites) as with either of the other two pacing modes (each 23 [28%] of 82 sites, p less than 0.001), whereas the induction of ventricular tachycardia remained comparable with anodal pacing (15 [18%] of 82 sites) and cathodal and bipolar pacing (each 14 [17%] of 82 sites). Furthermore, a similarly high incidence of inducibility of ventricular fibrillation was observed with both cathodal pacing (56 [68%] of 82 sites) and bipolar pacing (40 [49%] of 82 sites) when an increased current equal to twice the anodal excitability threshold (1.23 mA) was used.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Comparison of effects of three anesthetic agents on induction of ventricular tachycardia in a canine model of myocardial infarction

The effects of three anesthetic agents on the inducibility of ventricular tachycardia by programmed stimulation were investigated in dogs with a surgically induced left ventricular infarct. Endocardial catheter electrodes were placed at the right ventricular apex under general anesthesia at least 2 weeks after infarction, and the dogs were allowed to recover for 24 hours before undergoing programmed stimulation in the conscious state on two occasions 2 hours apart. A protocol of programmed stimulation with up to seven ventricular extrastimuli was used. In 15 animals, ventricular tachycardia was inducible on both occasions with 3.4 +/- 0.4 (mean +/- SEM; range, 1-5) extrastimuli. Two hours after baseline conscious induction, the dogs were anesthetized with either halothane, pentobarbital, or a fixed combination of fentanyl-droperidol plus nitrous oxide. Halothane prolonged the PR interval from 99 +/- 4 to 117 +/- 6 msec (p = 0.001) and the ventricular effective refractory period from 140 +/- 4 to 157 +/- 6 msec (p = 0.008). The ability to induce ventricular tachycardia was abolished in five of 10 animals (p less than 0.05). In the animals that remained inducible, the cycle length of tachycardia increased from 153 +/- 10 to 168 +/- 10 msec (p = 0.015), while the number of extrastimuli required was unaltered. Pentobarbital prolonged the PR interval from 104 +/- 6 to 124 +/- 6 msec (p = 0.004) and the QTc interval from 270 +/- 10 to 310 +/- 6 msec (p = 0.006). Ventricular tachycardia remained inducible in only six of 10 dogs (p less than 0.05) with no change in cycle length or the number of extrastimuli required. Ventricular fibrillation was inducible in an additional three dogs with a number of extrastimuli similar to that required to induce ventricular tachycardia before anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Late potentials on the signal-averaged electrocardiogram after canine myocardial infarction: correlation with induced ventricular arrhythmias during the healing phase

Signal-averaged electrocardiograms (ECGs) and programmed ventricular stimulation were serially performed in 12 dogs (3 weeks of age) after experimental anteroapical myocardial infarction. At electrophysiologic study, sustained ventricular tachyarrhythmia was induced in seven dogs on at least one occasion. Of a total of 39 electrophysiologic studies, sustained monomorphic ventricular tachycardia was induced in seven studies and ventricular fibrillation in eight studies. In the remaining studies, no ventricular arrhythmia could be induced with triple ventricular extrastimuli. There was considerable day to day variability in the response to programmed stimulation and the results of the signal-averaged ECG. The signal-averaged QRS complex was significantly longer in dogs with inducible ventricular tachycardia or fibrillation (61 +/- 5 versus 57 +/- 3 ms, p = 0.02), had a lower terminal QRS amplitude (24 +/- 20 versus 46 +/- 33 microV, p = 0.04) and a longer late potential duration (19 +/- 4 versus 15 +/- 3 ms, p = 0.003) compared with that in animals with no inducible ventricular arrhythmia. Late potentials were defined as a total QRS duration greater than 58 ms, a terminal QRS amplitude less than 20 microV and a late potential duration greater than 18 ms. Using this definition, late potentials were seen in two distinct phases--immediately after coronary ligation and then beyond the first 72 h after infarction. The appearance of late potentials coincided with a change in arrhythmia inducibility from no ventricular arrhythmia to initiation of sustained monomorphic ventricular tachycardia. There is a close relation between inducibility of ventricular tachycardia in experimental canine myocardial infarction and the appearance of late potentials on the surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of isoproterenol on induction of ventricular tachyarrhythmias in the normal and infarcted canine heart

The influence of isoproterenol on induction of ventricular arrhythmias was evaluated in 10 normal dogs and 17 dogs with experimentally induced myocardial infarction. Programmed stimulation (using up to 6 extrastimuli) was performed before and then during infusion of isoproterenol (2 micrograms/minute followed by 4 micrograms/minute). Isoproterenol facilitated induction of sustained monomorphic ventricular tachycardia (cycle length 163 +/- 26 msec) in 5 of the 10 animals with no inducible baseline arrhythmia (P less than 0.05). Isoproterenol did not affect cycle length or the number of extrastimuli required in animals with baseline ventricular tachycardia (cycle length 158 +/- 15 msec before versus 163 +/- 17 msec during isoproterenol, P = 0.3; extrastimuli 3.8 +/- 0.6 before versus 3.8 +/- 0.4 during isoproterenol infusion, P = 0.3). Isoproterenol did not significantly facilitate induction of ventricular fibrillation in either normal dogs or those studied after production of myocardial infarction. We conclude that infusion of isoproterenol increases the incidence of inducible ventricular tachycardia in the infarcted heart, but does not facilitate the induction of ventricular fibrillation in infarcted or normal hearts, despite the use of an aggressive protocol for programmed stimulation. Isoproterenol is, therefore, a safe and useful adjunct to programmed stimulation in this setting.     

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     

Proarrhythmic effects of antiarrhythmic drugs in patients with malignant ventricular arrhythmias evaluated by electrophysiologic testing

The provocation or worsening of arrhythmias by antiarrhythmic regimens was evaluated in patients with malignant ventricular arrhythmias undergoing electrophysiologic studies. In 314 patients with sustained or nonsustained ventricular tachycardia or ventricular fibrillation, 801 drug studies were performed using a standard protocol of programmed electrical stimulation. The criteria for proarrhythmia were: 1) initiation of sustained ventricular tachyarrhythmia in a patient in whom only nonsustained tachycardia was induced at baseline; 2) conversion of a sustained tachycardia that could be terminated by programmed electrical stimulation at baseline to one that required cardioversion for termination during drug therapy; 3) initiation of a sustained tachyarrhythmia by a less aggressive mode of stimulation than was required at baseline; and 4) development of spontaneous or incessant ventricular tachycardia. Proarrhythmia criterion 1 occurred during 20 (18%) of 118 studies and at least once in 15 (28%) of 54 patients. Criterion 2 was met during 39 (7%) of 578 studies and at least once in 29 (13%) of 220 patients. Criterion 3 was achieved during 135 (20%) of 687 studies in patients with sustained ventricular tachyarrhythmias at baseline. Criterion 4 occurred during 9 (1%) of 801 drug studies. In 40 patients in whom well tolerated ventricular tachycardia was initiated with fewer extrastimuli during drug study than at baseline, the drug was continued and the patients were followed up. The recurrence rate of tachycardia was the same in these patients as in 73 patients followed up on regimens on which the number of extrastimuli required for initiation was not reduced.(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.     

Can potentially significant polymorphic ventricular arrhythmias initiated by programmed stimulation be distinguished from those that are nonspecific?

Polymorphic ventricular arrhythmias (PVAs) initiated by programmed electrical stimulation may be a nonspecific response or evidence of ventricular electrical instability. To determine if PVAs initiated in patients with spontaneous sustained ventricular tachycardia or fibrillation differ from those which are clearly a nonspecific response in structurally normal hearts, the initiation, characteristics, and relationship to ventricular repolarization of PVAs greater than five beats in duration were evaluated in 32 patients without structural heart disease and in 36 patients with spontaneous sustained ventricular arrhythmias more than 9 days after myocardial infarction. Patients received one to four extrastimuli during sinus rhythm and right ventricular pacing. In a comparison with patients who completed the same steps (defined by the basic drive cycle length and number of extrastimuli) in the stimulation protocol, there was no difference in the cumulative risk of initiation of a PVA between the patients with and those without heart disease at any step. This risk was 51% vs 38% for patients who received two or fewer extrastimuli at four basic cycle lengths (p = NS). PVAs were initiated by the same mean number of extrastimuli (2.3 +/- 0.5 vs 2.6 +/- 0.9 p NS) with the same degree of prematurity in both groups. Forty-four percent of the PVAs in the myocardial infarction group had a cycle length greater than 250 msec or a coupling interval of the first tachycardia beat to its initiating stimulus greater than 320 msec as opposed to only one (6%) in the group without heart disease (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (less than or equal to 2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTs]) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 11 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (greater than 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.     

Electrophysiologic and anatomic characteristics of ventricular tachycardia induced at the right ventricular outflow tract but not at the apex.

The site of ventricular stimulation is an important variable in the initiation of ventricular tachycardia (VT) by programmed ventricular stimulation. Among 169 patients studied consecutively, 17 (10%) had ventricular tachycardia induced by programmed electrical stimulation from the right ventricular outflow tract but not from the apex. Fourteen of these 17 patients had had prior myocardial infarction (12 had inferior, and two had both inferior and anterior myocardial infarction), two had a dilated cardiomyopathy, and one had a localized cardiomyopathy. Fourteen patients had echocardiograms suitable for analysis. Of these, 12 had posterior/inferior ventricular wall motion abnormalities located at the base of the heart. The ventricular effective refractory periods from the right ventricular outflow tract and right ventricular apex were 237 +/- 4 and 244 +/- 5 msec, respectively (p less than 0.05, mean +/- SEM). Induced VT had a cycle length of 229 +/- 4 msec and had the morphology of right bundle branch block in 12 patients, of left bundle branch block in three patients, and had both morphologies in two patients. In 14 patients the axis was superior. VT was initiated with two extrastimuli in 15 patients and with burst right ventricular pacing in two patients. Similar pacing techniques with identical pacing intervals did not induce VT at the right ventricular apex in 14 of these 17 patients. Further, among the 15 patients whose VT was induced at the right ventricular outflow tract with two extrastimuli, neither burst pacing (n = 13) nor two extrastimuli introduced at faster paced rates (n = 12) induced VT at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Electrophysiologic study of the left ventricle: indications and safety.

Eighty patients (69 with documented or suspected recurrent ventricular tachycardia or fibrillation, ten with left bundle-branch block, and one with the Wolff-Parkinson-White syndrome) underwent both right ventricular and left ventricular programmed electrical stimulation, including ventricular pacing and the introduction of one or two ventricular extrastimuli or electrode catheter mapping of the left ventricle (or both). Left ventricular catheters were introduced precutaneously via the femoral artery (of 61 patients, one required secondary repair) or via brachial arteriotomy (of 19 patients, two required secondary repair). All patients received an intravenously administered bolus of hep arin (5,000 units) following the insertion of the left ventricular catheter and then 1,000 units/hr after the first hour of study. No patients had cerebrovascular, systemic thromboembolic, or cardiac sequelae. In four (12 percent) of 34 patients with inductible ventricular tachycardia, programmed electrical stimulation of the left ventricle was required for initiation. Extensive left ventricular endocardial mapping was performed in 45 patients. Our experience suggests that (1) electrophysiologic study of the left ventricle can be performed safely, (2) programmed electrical stimulation of the left ventricle is indicated when a suspected ventricular tachyarrhythmia cannot be induced from the right ventricle, and (3) endocardial mapping of the left ventricle is indicated when surgery is being considered to abolish recurrent sustained ventricular tachycardia.     

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.     

A new protocol of programmed stimulation for assessment of predisposition to spontaneous ventricular arrhythmias

We have devised a simple method for identifying predispositionto spontaneous sustained ventricular fibrillation (VF) and tachycardia(VT). A standardized protocol of programmed stimulation wasapplied to 111 control subjects without ventricular diseaseand with no history of VF or VT (Group I) and to 27 patientswith previous myocardial infarction and documented spontaneous(in the absence of evidence of further acute myocardial ischaemia)VF or VT (Group II). The stimulation protocol consisted of singleand paired ventricular extrastimuli introduced during ventriculardrive at the right ventricular apex and ouflow tract, at twicediastolic threshold current intensity and at 20 mA. None ofthe Group I subjects exhibited VF or sustained (more than 10s) VT. In contrast sustained arrhythmias were induced in 24(89%) of Group II patients. We conclude: In our study population,initiation of a sustained ventricular tachyarrhythmia at programmedstimulation was both a sensitive (89%) and specific (100%) indicatorfor predisposition to spontaneous VF and VT.     

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)     

Atrial Burst Pacing with Biphasic and Monophasic Waveforms for Atrial Fibrillation

Background: Biphasic pacing is a novel mode of pacing that was suggested to increase cardiac conduction velocity as compared with cathodal monophasic pacing. We aimed to evaluate the safety and efficacy of rapid atrial pacing to convert atrial fibrillation (AF) to normal sinus rhythm. Methods: Multiple biphasic (anodal/cathodal), reverse biphasic (cathodal/anodal), and monophasic (cathodal) atrial pacing therapies were performed among 12 patients undergoing left atrial catheter ablation for AF. The efficacy end point was successful conversion of AF to sinus rhythm, and safety end point no induction of ventricular arrhythmias. Patients were paced at three cycle lengths (100, 200, and 333 msec) for 60 seconds at three locations (right and left atrial appendages and coronary sinus). Results: Among the 66 biphasic (anodal/cathodal) pacing procedures one procedure in a patient with chronic AF, which involved pacing at the left atrial appendage with a cycle length of 200 msec, led to conversion of AF to sinus rhythm. None of the 66 monophasic pacing procedures or the 66 reverse biphasic (cathodal/anodal) pacing procedures was associated with AF termination. None of the biphasic pacing procedures was associated with induction of ventricular arrhythmias. Conclusions: Rapid atrial pacing using a variety of waveforms at the cycle length and output used in the current study was found to be safe. There was a single success in converting a chronic AF to sinus rhythm. Ann Noninvasive Electrocardiol 2012;17(1):22–27     

Effects of atrial pacing, isoprenaline and lignocaine on experimental polymorphous ventricular tachycardia

In 22 anaesthetised dogs, iv, administration of quinidine sulphate (30 mg X kg-1) over 5 min produced bradycardia and marked prolongation of the QT interval. Right ventricular extrastimulations, four times diastolic threshold, provoked polymorphous ventricular tachycardia in 18 dogs, and typical torsade de pointes was observed in four of these 18 dogs. Ventricular flutter was induced in another four dogs. In one of these 22 dogs, double stimuli were required to induce ventricular tachyarrhythmias, in 19 dogs triple stimuli, and in two dogs quadruple stimuli. Using this experimental model, effects of interventions including atrial pacing, isoprenaline, and lignocaine on the QT interval and induction of polymorphous ventricular tachycardia by extrastimuli were studied. Atrial pacing shortened QT interval only slightly and did not prevent induction of polymorphous ventricular tachycardia in nine dogs studied. Isoprenaline infusion definitely shortened QT interval, and in four out of nine dogs triple stimuli could not elicit polymorphous ventricular tachycardia. By contrast, although the QT interval was not shortened, lignocaine was effective in preventing induction of polymorphous ventricular tachycardia by triple stimuli in three out of nine dogs. These results indicate atrial pacing is an ineffective means of preventing induction of polymorphous ventricular tachycardia by extrastimuli in dogs with a long QT interval, but that isoprenaline and lignocaine are effective in some dogs.