Effectiveness of Ibutilide in Cardioversion of Persistent Atrial Fibrillation in Patients with Dual Chamber Stimulation

Aim of the study: To evaluate the effectiveness of Ibutilide in cardioversion of persistent atrial fibrillation in patients with sinus node disease wearing a dual chamber pacemaker and to assess the potential role of overdrive ventricular pacing in prevention of drug related proarrhythmia. Methods and Results: Fifty-three sinus node disease patients (35 males; mean age 75 ± 9.5 years), implanted with a dual chamber pacing system, with persistent atrial fibrillation, lasting for 328 ± 416 days, received 1–2 mg of intravenous Ibutilide. Pacing mode was programmed in VVI at 90 ppm, in order to suppress spontaneous ventricular activity. All patients were monitored for 4 hours. Late occurrence of ventricular arrhythmias was evaluated using the pacemaker memory. Ventricular pacing threshold, spontaneous electrogram amplitude and pacing impedance were measured before and after Ibutilide infusion. Cardioversion to sinus rhythm occurred in twenty-two patients (41.5%). Treatment success was significantly related to shorter atrial fibrillation duration. Paced QT interval duration increased from 412 ± 36 ms to 481 ± 40 ms (p < 0.0001), without differences between responders and non responders; QRS width did not change significantly (from 152 ± 25 ms to 161 ± 25 ms; p = n.s.). No early or late episodes of sustained or non sustained polymorphic ventricular tachycardia were observed. Pacing and sensing threshold did not show any significant variation. Conclusions: Ibutilide showed a good effectiveness in treating persistent atrial fibrillation in paced patients. Overdrive ventricular pacing may have played a role in preventing drug induced ventricular proarrhythmia. No adverse effect on pacing threshold was observed.     

Induction of clinical ventricular tachycardia using programmed stimulation: value of third and fourth extrastimuli

Initiation of ventricular tachycardia (VT) by right ventricular extrastimulation was analyzed in 142 consecutive patients, 53 with electrocardiographically documented episodes of spontaneous VT or ventricular fibrillation (VF) and 68 with no spontaneous VT or VF; 21 patients with a history of sudden death but no documented arrhythmia were excluded from further analysis. All patients received 1 to 4 extrastimuli (S2, S3, S4 and S5) during pacing at fixed cycle lengths of 600 or 500 msec at 1 or 2 right ventricular sites. Clinical VT was reproduced by extrastimulation in 28 of 43 patients (65%) with sustained VT and in 0 of 10 patients with nonsustained VT. Clinical VT was induced by S2 or S3 in 16 patients and by S4 or S5 in 12 patients. Ventricular burst pacing reproduced clinical VT in 3 other patients. Nonclinical VT, which was most often polymorphic and nonsustained, was induced in 24 of 121 patients (20%), in 11 by S2 or S3 and in 13 by S4 or S5. Ventricular burst pacing induced nonclinical VT in 4 other patients. In patients with spontaneous sustained VT, the use of S4 and S5 in the right ventricle increases the yield of inducible clinical VT compared with use of S2 and S3 alone, but at a cost of increased induction of nonclinical VT. Frequent induction of nonclinical VT limits the interpretation of the results of such stimulation in patients without previously documented VT.     

Relation of the endocardial and epicardial ventricular fibrillation thresholds of the right and left ventricles

Ventricular fibrillation thresholds were measured on the endocardium and epicardium of the right or left ventricle, or both, in 13 dogs. The electrodes, introduced through a right or left atriotomy to avoid injury to the ventricles, were aligned opposite and parallel to each other on the endocardium and epicardium. The ventricular fibrillation threshold was measured during atrial pacing by delivering a train of impulses to the ventricle during the vulnerable period after every 12th paced complex in 1 milliampere (mA) increments of current until fibrillation ensued. The mean (± standard deviation) right ventricular epicardial and endocardial fibrillation thresholds were 18.3 ± 5.3 and 17.6 ± 5.3 mA, respectively, (values not significantly different). However, the fibrillation threshold of 36.1 ± 9.5 mA in the left ventricular epicardium was significantly higher than the value of 20.7 ± 9.4 mA on the left ventricular endocardium. These data suggest that the proximity of the fibrillating electrodes and Purkinje network may be a factor in the measurement of ventricular vulnerability.     

Bradycardia pacing-induced short-long-short sequences at the onset of ventricular tachyarrhythmias: a possible mechanism of proarrhythmia?

OBJECTIVES: The purpose of this study was to characterize interactions between normal pacing system operation and the initiating sequence of ventricular tachycardia (VT)/ventricular fibrillation (VF). BACKGROUND: Abrupt changes in ventricular cycle lengths (short-long-short, S-L-S) might initiate VT/VF. The S-L-S sequences might be passively permitted or actively facilitated by bradycardia pacing. METHODS: Initiating sequences of 1,356 VT/VF episodes in the PainFree Rx II (n = 634) and EnTrust Trial (n = 421) were analyzed with stored electrograms and by pacing mode (DDD/R, VVI/R, and Managed Ventricular Pacing [MVP]). Interactions between pacing and VT/VF initiation were classified as: non-pacing associated, pacing associated, pacing permitted, and pacing facilitated. RESULTS: Non-pacing associated (no pacing, no S-L-S) and pacing associated (ventricular pacing without S-L-S) onset accounted for 44.0% and 29.8% of all VT/VF, respectively. Pacing permitted (S-L-S sequences without ventricular pacing) episodes accounted for 6.4% (DDD/R), 20.0% (MVP), and 25.6% (VVI/R) of 1,356 VT/VF episodes. Pacing facilitated onset (S-L-S sequences actively facilitated by ventricular pacing including the terminal beat after a pause) accounted for 8.2% (MVP), 9.4% (VVI/R), and 14.8% (DDD/R) of 1,356 VT/VF episodes. Pacing facilitated S-L-S VT/VF occurred in 2.6% (MVP), 3.3% (VVI/R), and 5.2% (DDD/R) of patients with episodes and was the sole initiating sequence in approximately 1% of patients. Pause durations during pacing facilitated S-L-S differed between modes (DDD/R 793 +/- 172 ms vs. MVP 865 +/- 278 ms vs. VVI/R 1180 +/- 414 ms, p = 0.002). The majority of these episodes were monomorphic VT. CONCLUSIONS: Ventricular tachycardia/VF in some implantable cardioverter-defibrillator patients might be initiated by S-L-S sequences that are actively facilitated by bradycardia pacing operation and might constitute an important mechanism of ventricular proarrhythmia.     

Mechanism of ventricular vulnerability to single premature stimuli in open-chest dogs

To determine the mechanism of ventricular vulnerability to electrical stimulation, we simultaneously recorded from 120 transmural electrodes in a 35 X 20 X 5-mm portion of right ventricular infundibulum in seven dogs. Baseline pacing (S1) was performed from outside the mapped region followed by single premature stimulation (S2) of increasing strength at the center of the mapped region. In five of six episodes of ventricular fibrillation and 26 of 30 episodes of repetitive responses, complete reentrant pathways were observed. Earliest activation following S2 was not at the site of S2 stimulation but was at a point between the S1 and S2 sites of stimulation. Activation spread away from the early site toward the opposite side of the mapped region around the sides of an arc of block near the S2 site to form a "figure-of-eight." The activation fronts coalesced to activate the region around the S2 site last and, if the difference in times between activation at the early site and near the S2 site was large, reentered the tissue toward the S1 site. Ventricular refractory periods were determined in four dogs following S1 pacing; the regions with the greatest nonuniformity in the dispersion of refractoriness were not the regions of unidirectional block after S2 stimulation. Thus, 1) ventricular fibrillation and repetitive responses induced electrically with S1 and S2 stimuli at different ventricular sites arise by figure-of-eight reentry, 2) this reentry is caused by the ability of S2 stimulation both to prolong refractoriness near the S2 site and to initiate a propagated response in the region between the S1 and S2 sites, and 3) a nonuniform dispersion of refractoriness is not crucial for the electrical induction of reentry leading to ventricular fibrillation or repetitive responses when S1 and S2 stimuli are given at different locations on the right ventricular outflow tract.     

Ventricular arrhythmias induced by appropriate antibradycardia pacing in patients with implantable defibrillators]

INTRODUCTION AND OBJECTIVES: The induction of ventricular arrhythmias by appropriate antibradycardia ventricular pacing in patients with implantable cardioverter defibrillators has been reported in only a few cases. The aim of this study was to assess the incidence, characteristics and management of these episodes. METHODS: The follow-up records of 180 patients with implantable cardioverter defibrillators with intracardiac electrogram storage were reviewed. Pacing induced episodes were defined as those occurring immediately after an appropriate paced stimulus in a patient with sporadic paced beats. We assessed the number and type of episodes, mode of onset, therapy administered and the efficacy of different prevention measures. RESULTS: Pacing induced episodes were found in 9 patients (5%). Seven received device administered therapy which was effective in all cases. One to 95 episodes were observed per patient, of which 138 were monomorphic ventricular tachycardias and 20 polymorphic ventricular tachycardia/ventricular fibrillation episodes. All were induced by a paced ventricular beat after a post-extrasystolic pause or after long RR intervals during atrial fibrillation. Pacing induced arrhythmias were prevented by changing the pacing rate or hysteresis in 3 out of 6 patients and by decreasing the stimulus energy in 3 out of 3. Antibradycardia pacing function was disabled in 4 patients. CONCLUSIONS: Ventricular arrhythmias induced by appropriate antibradycardia ventricular pacing are relatively common in patients with implantable cardioverter defibrillators. Effective prevention can be achieved in most cases by changing the pacing rate or the pacing stimulus energy, however in selected cases the antibradycardia function may be disabled.     

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.     

Effects of ventricular fibrillation and defibrillation on pacing threshold in the anesthetized dog

The effects of transthoracic and internal defibrillation on the bipolar ventricular pacing threshold in 20 anesthetized dogs were examined. Ventricular pacing was accomplished with a computer-controlled, constant voltage pacemaker that permitted rapid determination of pacing threshold. Defibrillation at various energy levels was administered during ventricular pacing and after ventricular fibrillation of 5, 15, 30, 45, 60 or 120 s duration in the 20 dogs. Defibrillation during pacing or within 15 s after initiation of ventricular fibrillation did not significantly increase threshold, regardless of defibrillation energy or mode of delivery. Defibrillation after ventricular fibrillation lasting greater than or equal to 30 s increased (p less than 0.05) threshold determined 6 s after defibrillation. The increase in threshold (in volts) determined 6 s after defibrillation was an exponential function of fibrillation duration (30 s = 0.30 +/- 0.09 V; 45 s = 0.53 +/- 0.13 V; 60 s = 2.24 +/- 1.05 V), but was independent of defibrillation energy or mode of delivery. Threshold returned to control values 15 to 30 s after defibrillation. Cardiopulmonary bypass to maintain coronary perfusion prevented the increase in pacing threshold even after ventricular fibrillation of up to 2 min duration. Pacing threshold is not increased by transthoracic or internal defibrillation, but is increased by ventricular fibrillation of sufficient duration to create substantial myocardial hypoxemia.     

Transvenous pacing in the presence of acute right ventricular infarction.

Ventricular tachycardia and ventricular fibrillation are very frequent during transvenous pacing in the presence of acute right ventricular infarction. An acceptable pacing threshold is not usually achieved. A relatively high pacing threshold should, therefore, be accepted in these cases with minimum catheter manipulation. Invisible or very small pacing spikes, increased time intervals between the spike and paced QRS, atypical QRS configurations and sensing failure are frequent in these cases.     

A model of chronic ischemic arrhythmias: The relation between electrically inducible ventricular tachycardia,ventricular fibrillation threshold and myocardial infarct size

To study the relation between inducible ventricular tachycardia and ventricular vulnerability, myocardial infarction was created in 22 closed chest mongrel dogs by inflating a balloon catheter in the left anterior descending coronary artery for 2 hours. The presence of inducible ventricular tachycardia was determined by programmed electrical stimulation of the right ventricle in each dog before and 4 days after infarction, using a transvenous electrode catheter and a “clinical” stimulation protocol. In each dog the repetitive ventricular response threshold and the ventricular fibrillation threshold were measured before and 4 days after infarction.Ventricular tachycardia was not inducible in any dog before infarction. After infarction, sustained ventricular tachycardia was inducible in 10 (45 percent) of 22 dogs and nonsustained tachycardia in an additional 4 dogs (18 percent). Ventricular fibrillation threshold was greatly reduced 4 days after infarction in dogs with inducible sustained tachycardia (mean ± standard deviation 29 ± 11 to 10 ± 5 mA, p < 0.001); the mean threshold did not change significantly in dogs without inducible sustained tachycardia. Both the ventricular fibrillation threshold and mean ventricular repetitive response threshold were reduced in the dogs with sustained ventricular tachycardia; neither was significantly altered in the dogs without sustained tachycardia. The magnitude of change in the two thresholds frequently differed; hence, a correlation was weak between the control and postinfarction repetitive response/fibrillation threshold ratio (r = 0.41). Postmortem measurement of infarct size demonstrated an association between this measurement and the presence of inducible ventricular tachycardia. Sustained ventricular tachycardia was not inducible in the presence of a small infarct.It is concluded that: (1) Inducible ventricular tachycardia on the 4th day after myocardial infarction is associated with a considerable decrease in the ventricular fibrillation threshold; (2) changes in the repetitive response and fibrillation thresholds after myocardial infarction may not be parallel, complicating the use of the repetitive ventricular response threshold as a substitute for the ventricular fibrillation threshold in the postinfarction state; (3) a large infarct predisposes the heart to electrically inducible sustained ventricular tachycardia.     

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.     

Pacing following shocks stronger than the defibrillation threshold: impact on defibrillation outcome

INTRODUCTION: A recent study of shocks near defibrillation threshold (DFT) strength demonstrated that at least three rapid cycles always occur after failed shocks but not after successful shocks, suggesting that the number and rapidity of postshock cycles are important in determining defibrillation success. To test this hypothesis, rapid pacing was performed following a shock stronger than the DFT that by itself did not induce rapid cycles and ventricular fibrillation (VF). METHODS AND RESULTS: Epicardial activation was mapped in six pigs using a 504-electrode sock. The DFT was determined by an up/down protocol with S1 shocks (right ventricle-superior vena cava, biphasic). Ten shocks that were 100 to 200 V above the DFT (aDFT) were delivered after 10 seconds of VF to confirm they always defibrillated. Then, S2, S3, etc., pacing at 5 to 10 times diastolic threshold was performed from the left ventricular apex after aDFT shocks during VF. First, the postshock interval after aDFT shocks was scanned with an S2 stimulus to find the shortest S1-S2 coupling interval (CI) that captured. This was repeated for S3, S4, etc., until VF was induced. To induce VF after aDFT shocks, three pacing stimuli (S2, S3, S4) with progressively shorter CIs were always required; S2 or S2,S3 never induced VF. For the S2-S4 cycles, the intercycle interval was shorter (P < 0.01), and the wavefront conduction time was longer (P < 0.01) for episodes in which VF was induced (n = 57) than for episodes in which it was not (n = 60). Following the S4 cycle that induced VF, two types of spontaneous activation patterns appeared: focal (88%) and reentrant (12%). CONCLUSION: VF induction after aDFT shocks always required at least three rapid successive paced-induced cycles. Thus, the number and rapidity of the first several postshock cycles rather than just the first postshock cycle may be determining factors for defibrillation outcome.     

Ventricular fibrillation threshold in canine hearts with quinidine induced prolonged QT interval: effects of atrial pacing, isoproterenol, and lignocaine

Ventricular fibrillation threshold was determined using a train of pulses, 4 ms in duration, delivered at 10 ms intervals, in 20 anaesthetised dogs receiving toxic doses of quinidine sulphate (30 mg X kg-1) injected intravenously over 5 min to prolong the QT interval. The effects of atrial pacing, isoproterenol, and lignocaine on ventricular fibrillation threshold were investigated. Quinidine administration lowered the mean(SD) threshold from 14.7(5.1) to 8.8(3.6) mA (n = 20, p less than 0.001). Atrial pacing shortened the mean(SD) basic cycle length from 652 to 400 ms and the QT interval (378(28) vs 334(19) ms, n = 8, p less than 0.01) but did not alter the mean(SD) threshold (7.0(2.3) vs 7.5(1.5) mA). Isoproterenol infusion to maintain basic cycle length at 421(23) ms shortened the mean(SD) QT interval to 291(14) ms (p less than 0.001) and increased the mean(SD) threshold to 13.6(5.9) mA (n = 8, p less than 0.01). Lignocaine (plasma concentration 1.36 micrograms X ml-1) increased the mean(SD) threshold from 10.9(3.4) to 16.7(6.7) mA (n = 7, p less than 0.02) without affecting basic cycle length and QT interval. Thus atrial pacing shortened the QT interval slightly but did not make the canine heart with a quinidine induced prolonged QT interval less vulnerable to electrically induced ventricular fibrillation, whereas both isoproterenol and lignocaine did, although they affected basic cycle length and QT interval differently.     

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)     

Electrophysiologic characteristics at initiation of ventricular tachycardia and ventricular fibrillation in a canine infarct model

Local ventricular activation time and the conduction time during sinus rhythm at the induction of ventricular tachycardia (VT) and ventricular fibrillation (VF) were investigated using a canine model of chronic myocardial infarction. Of 26 dogs studied, 15 had inducible VT, 10 had inducible VF, and 1 had no inducible arrhythmias. Bipolar local ventricular electrograms were recorded during sinus rhythm from 136 sites in 10 dogs with VT and 164 sites in 11 dogs with VF. Mean activation time in dogs with inducible VT was significantly longer than in dogs with inducible VF. Furthermore, simultaneous local ventricular electrograms were recorded during the induction of VT (74 episodes) or VF (38 episodes) from the infarct border zone at the endocardium (B-EN), the epicardium (B-EP), and normal sites (N-EN, N-EP). During VT induction, the activation time at N-EN and N-EP was significantly longer than during VF induction (N-EN: 94 ± 21, 70 ± 19 ms; N-EP: 83 ± 21, 64 ± 10 ms; p < 0.05). Conduction time was measured at the initiation of VT or VF induced by orthodromic or antidromic pacing. The conduction times of the last paced beat between N-EN and B-EP (35 ± 11, 62 ± 24 ms), N-EN and N-EP (35 ± 12, 14 ± 13 ms), B-EN and B-EP (16 ± 10, 38 ± 25 ms), and B-EP and N-EP (77 ± 27, 44 ± 12 ms) were significantly different in dogs with inducible VT (p < 0.05), but not in dogs with VF. Dispersion of effective refractory period was also observed in dogs with VT. Percent infarct in inducible VT was larger than in inducible VF (VT: 16 ± 5%; VF: 10 ± 2%; p < 0.001). These studies suggest that dogs with inducible VT have prolonged ventricular activation time and significantly different bidirectional conduction time during VT induction. This may serve as a substrate for reentry.     

The effect of heart rate on the termination of electrically induced ventricular fibrillation in the isolated perfused rat heart

Ventricular fibrillation (VF) which is normally sustained in large animals and humans, is transient in small animals. The purpose of the present study was to evaluate the possible effect of changing cardiac rate on spontaneous ventricular defibrillation. In isolated perfused rat heart, VF was electrically induced during normal spontaneous rhythm of the heart at normal rate and at various ventricular pacing rates. It was found that: 1) Electrically induced VF in isolated perfused, non-ischemic rat heart spontaneously terminated in 88% of the hearts; 2) Ventricular pacing rhythm of spontaneous rate plus 10% caused VF to be sustained in 26% of the hearts (which defibrillated spontaneously during normal rates); 3) Ventricular pacing at 200% of the basic rate led to sustained VF in about half the VF episodes (14 out of 33, p less than 0.005). In the remainder, which defibrillated spontaneously, a sustained VF could be achieved by further increase in ventricular pacing rate; 4) Slow pacing rate, as a result of the surgical production of atrioventricular (A-V) block, enhanced the probability of spontaneous defibrillation (21 of 21 episodes after slow pacing vs 24 of 34 episodes following pacing at previous normal sinus rhythm, p less than 0.05). Selective modulation of conduction velocity, refractory period or both, achieved by changes in ventricular pacing rate was assumed to play an important role in determining whether electrically-induced VF would be transient or sustained.     

Sensitivity of an automatic external defibrillator for ventricular tachyarrhythmias in patients undergoing electrophysiologic studies

An automatic advisory external defibrillator (AED) was activated during all arrhythmias occurring at the time of 77 electrophysiologic studies in 45 patients. Sustained ventricular tachycardia (VT) occurred during 55 studies in 31 patients and nonsustained VT was induced during 10 studies in 9 patients. Ventricular fibrillation was induced 5 times in 5 patients and atrial arrhythmias with a rapid ventricular response occurred during 7 studies in 4 patients. The AED detection algorithm advised "shock" during 36 of 55 (65%) episodes of sustained VT and all 5 episodes of ventricular fibrillation. The device correctly advised "shock" for all 6 episodes of nonsustained VT that spontaneously terminated after analysis was complete. Thus, the sensitivity of the device for all ventricular arrhythmias analyzed was 47 of 66 (71%). The device recommended "shock" for all 31 episodes of rapid VT and 1 of 2 episodes of atrial fibrillation associated with systemic hypotension (32 of 33, 97%). The 19 episodes of VT for which "no shock" was advised were comparatively slow and were hemodynamically well tolerated. The device recommended "no shock" during all 21 episodes of normal sinus rhythm and all 20 episodes of rapid atrial pacing (cycle length 400 ms) analyzed. "No shock" was advised during 4 episodes of sustained narrow QRS complex supraventricular tachycardia and 4 brief episodes of nonsustained VT that terminated before analysis was complete. Thus, in this study the specificity of the AED for wide complex tachycardias was 100%.     

慢性心力衰竭对兔心室肌电重构的影响

探讨慢性心力衰竭 (简称慢性心衰 )对兔心室肌电重构的影响及其与室性快速性心律失常的关系。 30只家兔随机分成两组 :实验组 2 0只 ,由阿霉素静脉注射 ( 8周 )引起慢性心衰 ;对照组 10只。所有家兔在麻醉开胸后进行电生理检查 :右室心尖部心外膜 2 5 0ppm快速起搏 ,每次持续 10min ,然后停止 1min ,如此重复 6次。其间若诱发出室性快速性心律失常 ,电生理实验便提前终止。分别在起搏前及每次 10min快速起搏后测定心室有效不应期(V ERP)、心室单相动作电位 (MAP)复极 90 %时间 (V MAPD90 )及右室心尖部和左室心底部MAP去极化 10 %处的时差 (CTARV BLV)。结果 :6次右室快速起搏后 ,实验组与对照组V ERP和V MAPD90 均延长 ,但与对照组相比 ,实验组V ERP显著延长的时间提前 (第 3次 10min快速起搏时vs第 5次 10min快速起搏时 ) ,延长的幅度增大 (平均每次 10min快速起搏延长V ERP :9.70msvs 2 .87ms ,P <0 .0 0 1) ;V MAPD90 明显延长的时间提前 (第 3次 10min快速起搏时vs第 4次 10min快速起搏时 ) ;CTARV BLV 延长的幅度增大 ( 1.5 0msvs 0 .6 0ms ,P <0 .0 1) ;诱发出心室颤动 (简称室颤 )的时间提前 (第 3次 10min快速起搏完成时 :35 .3 %vs 0 ,P =0 .0 4) ;室颤总诱发率增高 ( 70 .6 %vs 2 0 .0 % ,P     

Significance of pacing cycle lengths in manifest entrainment of orthodromic circus movement tachycardia by ventricular pacing

The physiology of entrainment of orthodromic circus movement tachycardia (CMT) was studied using ventricular pacing during 18 episodes of induced CMT in 7 patients with atrioventricular (AV) accessory pathways. The first paced impulse was delivered as late as possible in the tachycardia cycle (mean 88 +/- 5% of the spontaneous cycle length [CL]). Entrainment was demonstrated by the following criteria: 1:1 retrograde conduction via the accessory pathway; capture of atrial, ventricular and His bundle electrograms at the pacing rate; and resumption of tachycardia at its previous rate after cessation of pacing. The number of ventricular paced impulses ranged from 5 to 14 (mean 8 +/- 3), and entrainment occurred in 2 to 7 paced cycles (mean 4 +/- 2). Orthodromic activation of a major part of the reentry circuit (manifest entrainment) was demonstrated during 9 episodes by the occurrence of His bundle electrogram preceding the first CMT QRS at the time anticipated from the last paced beat. In the 9 other episodes, persistent retrograde His bundle activation and AV nodal penetration by each paced impulse caused a delay (mean 79 +/- 25 ms) in activation of the His bundle preceding the first CMT QRS after the last paced beat. The mean pacing CL achieving manifest entrainment was 92 +/- 3% of the tachycardia CL, compared with 84 +/- 3% for retrograde AV nodal penetration (p less than 0.01). In conclusion, manifest entrainment of orthodromic CMT can be demonstrated by ventricular pacing at very long CLs; shorter CLs may cause CMT termination due to retrograde AV nodal penetration.     

Preimplant left ventricular end-diastolic dimension and body weight independently associate with paced QRS duration in patients receiving right ventricular apical pacing for complete atrioventricular block

Background:

Paced QRS duration, a good marker of ventricular asynchrony while pacing, has been accepted as a valuable predictor of new‐onset heart failure in patients receiving right ventricular apical pacing. But nowadays we have little evidence for predicting paced QRS duration before the implantation.

Hypothesis:

There might be relationships between paced QRS duration and demographic characteristics, clinical features such as comorbidities, native QRS duration, or preimplant cardiac size. The purpose of this article was to identify potential predictors of paced QRS duration in patients receiving right ventricular apical pacing for complete atrioventricular block.

Methods:

One hundred seventy patients with right ventricular apical pacing for complete atrioventricular block were divided into 2 groups according to whether the paced QRS duration was longer than 170 ms or not. Demographic characteristics, clinical features, electrocardiogram and echocardiography before implantation, and electrocardiogram immediately after implantation, were retrospectively recorded.

Results:

Preimplant left ventricular end‐diastolic dimension (LVEDD) and body weight were found to be independently associated with the paced QRS duration. Although both of them had low sensitivity and specificity in predicting paced QRS duration longer than 170 ms, the specificity could increase to 81.2% when they were combined.

Conclusions:

Both preimplant LVEDD and body weight independently associate with paced QRS duration in patients receiving apical pacing for complete atrioventricular block. Although whether they really have an effect on new‐onset heart failure still needs to be verified, and these findings might be a good indication. Copyright © 2010 Wiley Periodicals, Inc. The authors have no funding, financial relationships, or conflicts of interest to disclose.