Optical mapping of the functional reentrant circuit of ventricular tachycardia in acute myocardial infarction.

OBJECTIVES: We used optical mapping to characterize the reentrant circuit of ventricular tachycardia (VT) during acute myocardial infarction (MI) in isolated canine left ventricular preparations. BACKGROUND: The nature of the reentrant circuit that underlies VT during acute MI is not well understood. METHODS: Using optical mapping in isolated canine left ventricular preparations, we characterized the reentrant circuit of monomorphic VT (mean cycle length 245.3 +/- 15.6 ms, n = 7) induced by programmed stimulation during acute MI. RESULTS: Optical mapping during VT revealed a functional reentrant circuit consisting of four components: (1) a protected isthmus located between the infarction area and the functional line of block; (2) an entrance site located at one end of the isthmus; (3) an exit site located at the other end of the isthmus; and (4) an outer loop consisting of nonischemic normal tissue, connecting the exit and entrance sites. Rate-dependent slow conduction within the border zone was associated with significant changes (n = 6) in action potential amplitude (99.1 +/- 0.4 vs 71.4 +/- 0.6 mV, P < .01), maximal diastolic potential (-80.6 +/- 0.2 vs -65.4 +/- 0.6 mV, P < .05), action potential duration at 90% repolarization (APD(90); 188.4 +/- 1.0 vs 164.3 +/- 3.1 ms, P < .05), and dV/dt (302.4 +/- 7.9 vs 168.5 +/- 3.6 V/s, P < .05). Compared to preparations with no inducible VT (n = 7), formation of a functional line of block was the key mechanism for initiation of functional reentry in preparations with VT. When comparing preparations with sustained and nonsustained VT, preservation of slow conduction over the isthmus was the key component for maintenance of sustained VT. CONCLUSIONS: The reentrant circuit of monomorphic VT in the setting of acute MI involved both the infarction border zone and nonischemic normal tissue. The underlying mechanism is related to the presence of rate-dependent slow conduction and the development of a functional line of block in the border zone.     

Dissociation of membrane potential and intracellular calcium during ventricular fibrillation

Membrane potential and intracellular calcium during VF. INTRODUCTION: The cardiac action potential (AP) and the intracellular Ca transient (CaT) are closely associated under normal physiological conditions, but not during ventricular fibrillation (VF). The purpose of this study was to determine whether this dissociation is directly related to the fast activation rate during VF. METHODS AND RESULTS: We optically mapped AP and CaT simultaneously in nine isolated rabbit hearts. Pinacidil, a K(ATP) channel opener, was used to shorten the action potential duration (APD) in order to capture tissue at fast pacing rates or to induce ventricular tachycardia (VT) comparable to VF activation rates. Mutual information (MI) was used to calculate the degree of AP and CaT coupling. Pinacidil (40 microM) infusion significantly shortened APD. The CL of VF without pinacidil averaged 77+/-13 ms, whereas the shortest CL achieved during VT under pinacidil infusion was 76 ms. MIs during fast pacing (1.13+/-0.15 bits) and fast VT (0.88+/-0.18 bits) were higher than those during baseline VF (0.39+/-0.11 bits), VF with pinacidil infusion (0.21+/-0.07 bits) and VF after pinacidil washout (0.36+/-0.15 bits). MIs during fast pacing or fast VT were higher than that of VFs at comparable dominant frequencies. CONCLUSIONS: CaT is closely associated with the AP during fast pacing and fast VT, but not during VF. The reduced MI during VF is not secondary to the fast rate of activation.     

A mechanism of transition from ventricular fibrillation to tachycardia : effect of calcium channel blockade on the dynamics of rotating waves

Abbreviation of the action potential duration and/or effective refractory period (ERP) is thought to decrease the cycle length of reentrant arrhythmias. Verapamil, however, paradoxically converts ventricular fibrillation (VF) to ventricular tachycardia (VT), despite reducing the ERP. This mechanism remains unclear. We hypothesize that the size and the dynamics of the core of rotating waves, in addition to the ERP, influence the arrhythmia manifestation (ie, VF or VT). The objectives of this study were (1) to demonstrate functional reentry as a mechanism of VF and VT in the isolated Langendorff-perfused rabbit heart in the absence of an electromechanical uncoupler and (2) to elucidate the mechanism of verapamil-induced conversion of VF to VT. We used high-resolution video imaging with a fluorescent dye, ECG, frequency and 2-dimensional phase analysis, and computer simulations. Activation patterns in 10 hearts were studied during control, verapamil perfusion (2x10(-6) mol/L), and washout. The dominant frequency of VF decreased from 16.2+/-0.7 to 13.5+/-0.6 Hz at 20 minutes of verapamil perfusion (P<0.007). Concomitantly, phase analysis revealed that wavefront fragmentation was reduced, as demonstrated by a 3-fold reduction in the density of phase singularities (PSs) on the ventricular epicardial surface (PS density: control, 1.04+/-0.12 PSs/cm(2); verapamil, 0.32+/-0.06 PSs/cm(2) [P=0.0008]). On washout, the dominant frequency and the PS density increased, and the arrhythmia reverted to VF. The core area of transiently appearing rotors significantly increased during verapamil perfusion (control, 4.5+/-0.6 mm(2); verapamil, 9.2+/-0.5 mm(2) [P=0.0002]). In computer simulations, blockade of slow inward current also caused an increase in the core size. Rotating waves underlie VF and VT in the isolated rabbit heart. Verapamil-induced VF-to-VT conversion is most likely due to a reduction in the frequency of rotors and a decrease in wavefront fragmentation that lessens fibrillatory propagation away from the rotor.     

Mechanisms underlying the development of ventricular fibrillation during early myocardial ischemia

The mechanisms underlying the development of ventricular fibrillation (VF) during early myocardial ischemia were assessed by use of a computerized three-dimensional mapping system capable of recording simultaneously from 232 intramural recording sites throughout the entire feline heart in vivo. Occlusion of the proximal left anterior descending coronary artery led to ventricular tachycardia (VT), which degenerated to VF in 1-5 minutes in four of 15 animals. Normal sinus beats immediately preceding the initiation of VT leading to VF demonstrated delayed activation (total activation time 133 +/- 14 msec), which was not significantly different from the activation time for normal sinus beats immediately preceding nonsustained VT (149 +/- 7 msec). Most of the conduction delay occurred in the subendocardial and midmyocardial regions in both groups. Initiation of VT leading to VF occurred by intramural reentry in three of the four cases. In one case, a mechanism responsible for the initiation of VT could not be assigned. The coupling interval of the initiating beats of VT ultimately leading to VF (210 +/- 15 msec) did not differ from that of nonsustained VT. Maintenance of the VT that led to VF was due primarily to intramural reentry (84% of cases) involving multiple activation sites in and around the border region of the ischemic zone. Nonreentrant mechanisms, arising in the subendocardium and subepicardium, also contributed to the maintenance of VT before development of VT. The transition from VT to VF was due exclusively to intramural reentry with initiation of the reentrant beats in the subendocardium and, occasionally, the subepicardium. Acceleration of the tachycardia by intramural reentry, along with very rapid and inhomogeneous recovery of excitability (as low as 50-60 msec), led to increased functional block and conduction delay. As a result, the total activation time for a given beat exceeded the coupling interval for that beat and led to the multiple reentrant circuits and multiple simultaneous activations characteristic of VF. Thus, the initiation and maintenance of VT leading to VF during early ischemia is due to intramural reentry, although nonreentrant mechanisms also contribute. However, the development of VF is due to continued intramural reentry and rapid recovery of excitability.     

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.     

Comparison of coupling intervals that induce clinical and nonclinical forms of ventricular tachycardia during programmed stimulation

Coupling intervals of extrastimuli that induced 57 previously documented unimorphic ventricular tachycardias (VTs) were compared with coupling intervals that induced 57 episodes of polymorphic VT or ventricular fibrillation (VF) in patients without a documented or suspected history of polymorphic VT or VF. Programmed stimulation was performed with the patient in the drug-free state, with 1 to 3 extrastimuli and 2 basic drive cycle lengths (600 or 500 ms, and 400 ms) at 2 right ventricular sites; stimuli were twice diastolic threshold. The mean coupling intervals of the first, second and third extrastimuli that induced nonclinical VT/VF (241 +/- 19, 185 +/- 19 and 173 +/- 24 ms, respectively, mean +/- standard deviation) were significantly shorter than the corresponding coupling intervals that induced the clinical VTs (266 +/- 25, 228 +/- 32 and 214 +/- 27 ms, respectively, p less than 0.001 for each). Regardless of the basic drive cycle length, the shortest coupling interval required to induce a clinical VT was 180 ms. Depending on the drive cycle length, 29 to 70% of nonclinical VT/VF induced by 3 extrastimuli required a coupling interval of less than 180 ms to induce. Therefore, a lower limit of coupling intervals may be identified below which only nonclinical VT/VF is induced by programmed stimulation. Restriction of coupling intervals to this lower limit may allow for significant improvement in specificity without compromise in the sensitivity of programmed ventricular stimulation protocols.     

Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart

Reentrant ventricular tachycardia (VT) is the most common sustained arrhythmia leading to ventricular fibrillation (VF). However, despite more than a century of research, the mechanism(s) of the conversion from reentrant VT to VF have not been elucidated. Based on their different electrocardiographic appearance, reentrant VT and VF have traditionally been thought of as resulting from two widely different mechanisms. Whereas VT is seen as a rapid but well organized process whereby the excitation wave rotates about a single well-defined circuit, fibrillation has been described as turbulent cardiac electrical activity, resulting from the random and aperiodic propagation of multiple independent wavelets throughout the cardiac muscle. Recently, the application of concepts derived from the theory of non-linear dynamics to the problem of wave propagation in the heart and the advent of modern high-resolution mapping techniques, have led some investigators to view VT and VF in terms of a single mechanism, whereby the self-organization of electrical waves forms 'rotors' that give rise to rapidly rotating spiral waves and results in either VT or VF, depending on the frequency of rotation and on the interaction of wave fronts with the cardiac muscle. As such, monomorphic VT is thought to result from a stationary rotor, whose frequency of rotation is within a range that allows 1:1 excitation of both ventricles. On the other hand, VF is thought to result from either a single rapidly drifting rotor, or a stationary rotor whose frequency of excitation is exceedingly high, thus resulting in multiple areas of intermittent block and giving rise to complex patterns of propagation with both deterministic and stochastic components. This article reviews the prevailing theories for the maintenance of VF, and discusses recently proposed mechanisms underlying transitions between VT and VF.     

Both Purkinje cells and left ventricular posteroseptal reentry contribute to the maintenance of ventricular fibrillation in open-chest dogs and swine: effects of catheter ablation and the ventricular cut-and-sew operation.

BACKGROUND: Radiofrequency catheter ablation (RFCA) targeting the left ventricular posteroseptum (LVPS) and posterior papillary muscle (PPM) terminates or prevents ventricular fibrillation (VF) in rabbit and dog hearts. However, whether the mechanism of VF maintenance is reentry or focal Purkinje firing is unclear. METHODS AND RESULTS: In the present study the effects of RFCA (endocardial ablation of PPM+LVPS in 7 dogs and 7 swine), left ventricular anterolateral wall ablation (LVAL in 7 dogs), and the cut-and-sew operation (CSO: along the left ventricular posterior wall (LVPW) beside PPM in 7 swine) on VF inducibility were compared. (1) VF inducibility was decreased from 100+/-0% to 21.9+/-31.2% (p<0.0001) by PPM+LVPS endocardial ablation, but not by LVAL ablation in dogs. (2) LVPW CSO reduced VF inducibility (100+/-0% to 43.6+/-9.5%, p<0.0001) in swine. (3) In contrast to the canine Purkinje network, which is mostly localized to the subendocardium, the swine Purkinje network extends to the subepicardial layer with a higher density (p<0.001). CONCLUSION: Both PPM+LVPS ablation (Purkinje destruction) in dogs and LVPW CSO (blocking reentry) in swine reduce VF inducibility, suggesting that in both species focal firing from the Purkinje network and reentry around the PPM contributes to the maintenance of VF.     

Clinical study of late potentials--comparison of late potentials in myocardial infarction, cardiomyopathy and idiopathic ventricular tachycardia

Late potentials (LPs) were studied using the signal averaging technique in 80 patients with myocardial infarction (MI), idiopathic cardiomyopathy (CM) and idiopathic ventricular tachycardia (IVT). In MI, LP duration was 28.4 +/- 12.6 ms in the sustained VT group (I; 8 cases); 18.6 +/- 9.0 ms in the non-sustained VT group (II; 11 cases); and 14.4 +/- 8.6 ms in the non-VT group (III; 21 cases); (p less than 0.05 in I vs II, p less than 0.01 in I vs III and not significant in II vs III). In CM, it was 33.7 +/- 13.0 ms in group I (6 cases); 20.1 +/- 5.9 ms in group II (12 cases); and 7.1 +/- 9.2 ms in group III (14 cases); (p less than 0.01 in I vs II, I vs III and II vs III). The LP duration in IVT (8 cases) was 15.6 +/- 10.4 ms, which was significantly shorter than that of group I in MI and CM (p less than 0.05 vs MI and p less than 0.01 vs CM). Late potential duration was also compared between a pacing-inducible VT group and a non-inducible VT group. The mean value of LP duration in the inducible VT group of MI was significantly longer than that in the non-inducible group (27.8 +/- 3.9 ms in 4 cases vs 17.3 +/- 2.5 ms in 4 cases, p less than 0.05). However, there was no significant difference in LP duration between the inducible and non-inducible groups of CM (22.0 +/- 11.0 ms in 5 cases vs 22.2 +/- 13.6 ms in 5 cases).(ABSTRACT TRUNCATED AT 250 WORDS)     

A Comparison of Chronaxies for Ventricular Fibrillation Induction, Defibrillation, and Cardiac Stimulation: Unexpected Findings and Their Implications

Introduction: A low-energy (≤ 4 J) cardioversion shock (LEC) either terminates reentrant ventricular tachycardia (VT) or accelerates it to ventricular fibrillation (VF). Optimization of the duration and amplitude of LEC shocks could improve the success rate of VT termination without VF induction.
Methods and Results: In order to learn how LEC shocks may be optimized, we used an animal model to compare the strength-duration curve for VF induction and the strength-duration curve for cardiac stimulation via the shock coil. Conventional implantable cardioverter-defibrillator (ICD) leads were implanted in 12 narcotized pigs from 20 kg to 25 kg in weight. Stimulation, VF induction, and defibrillation pulses were delivered by custom-designed stimulators at preset pulse durations and amplitudes. The corresponding hyperbolic strength-duration curves were constructed using the least-squares fit method and averaged for all the animals. The mean chronaxie for stimulation via the shock coil of 0.23 ms was significantly shorter than both defibrillation (4.8 ms) and VF induction (3.1 ms) chronaxie values. At a shock duration of 0.3 ms or less, the mean VF-induction threshold amplitude exceeded 300 V.
Conclusion: It may be reasonable to study whether LEC pulses from 0.25 ms to 0.30 ms in duration and up to 250 V in amplitude would increase therapeutic yield in VT termination without VF induction in humans. Contrary to the current belief, the discrepancy between defibrillation and stimulation chronaxie is not caused by different electrode size. We postulate that the time constant of the fast sodium channel reactivation may be the underlying reason.     

Distribution of excitation frequencies on the epicardial and endocardial surfaces of fibrillating ventricular wall of the sheep heart

Tissue heterogeneities may play an important role in the mechanism of ventricular tachycardia (VT) and fibrillation (VF) and can lead to a complex spatial distribution of excitation frequencies. Here we used optical mapping and Fourier analysis to determine the distribution of excitation frequencies in >20 000 sites of fibrillating ventricular tissue. Our objective was to use such a distribution as a tool to quantify the degree of organization during VF. Fourteen episodes of VT/VF were induced via rapid pacing in 9 isolated, coronary perfused, and superfused sheep ventricular slabs (3x3 cm(2)). A dual-camera video-imaging system was used for simultaneous optical recordings from the entire epi- and endocardial surfaces. The local frequencies of excitation were determined at each pixel and displayed as dominant frequency (DF) maps. A typical DF map consisted of several (8.2+/-3.6) discrete areas (domains) with a uniform DF within each domain. The DFs in adjacent domains were often in 1:2, 3:4, or 4:5 ratios, which was shown to be a result of an intermittent Wenckebach-like conduction block at the domain boundaries. The domain patterns were relatively stable and could persist from several seconds to several minutes. The complexity in the organization of the domains, the number of domains, and the dispersion of frequencies increased with the rate of the arrhythmia. Domain patterns on the epicardial and endocardial surfaces were not correlated. Sustained epicardial or endocardial reentry was observed in only 3 episodes. Observed frequency patterns during VT/VF suggest that the underlying mechanism may be a sustained intramural reentrant source interacting with tissue heterogeneities.     

Triphasic waveforms are superior to biphasic waveforms for transthoracic defibrillation: experimental studies

OBJECTIVES: Our objective was to evaluate the efficacy of triphasic waveforms for transthoracic defibrillation in a swine model. BACKGROUND: Triphasic shocks have been found to cause less post-shock dysfunction than biphasic shocks in chick embryo studies. METHODS: After 30 s of electrically induced ventricular fibrillation (VF), each pig in part I (n = 32) received truncated exponential biphasic (7.2/7.2 ms) and triphasic (4.8/4.8/4.8 ms) transthoracic shocks. Each pig in part II (n = 14) received biphasic (5/5 ms) and triphasic shocks (5/5/5 ms). Three selected energy levels (50, 100, and 150 J) were tested for parts I and II. Pigs in part III (n = 13) received biphasic (5/5 ms) and triphasic (5/5/5 ms) shocks at a higher energy (200 and 300 J). Although the individual pulse durations of these shocks were equal, the energy of each pulse varied. Nine pigs in part I also received shocks where each individual pulse contained equal energy but was of a different duration (biphasic 3.3/11.1 ms; triphasic 2.0/3.2/9.2 ms). RESULTS: Triphasic shocks of equal duration pulses achieved higher success than biphasic shocks at delivered low energies: <40 J: 38 +/- 5% triphasic vs. 19 +/- 4% biphasic (p < 0.01); 40 to <50 J: 66 +/- 7% vs. 42 +/- 7% (p < 0.01); and 50 to <65 J: 78 +/- 4% vs. 54 +/- 5% (p < 0.05). Shocks of equal energy but different duration pulses achieved relatively poor success for both triphasic and biphasic waveforms. Shock-induced ventricular tachycardia (VT) and asystole occurred less often after triphasic shocks. CONCLUSIONS: Triphasic transthoracic shocks composed of equal duration pulses were superior to biphasic shocks for VF termination at low energies and caused less VT and asystole.     

Localization of the isthmus in reentrant circuits by analysis of electrograms derived from clinical noncontact mapping during sinus rhythm and ventricular tachycardia

INTRODUCTION: New methods for electrogram analysis accurately estimated reentrant circuit isthmus location and shape in a canine model. It was hypothesized that these methods also would locate reentrant circuits causing clinical ventricular tachycardia (VT). METHODS AND RESULTS: Intracardiac electrogram recordings, obtained with a noncontact mapping system, were analyzed retrospectively from 14 patients with reentrant VT who had undergone successful radiofrequency ablation for prevention of VT initiation. Unipolar electrograms from 256 uniformly distributed endocardial sites were reconstructed by mathematical transformation. Twenty-seven tachycardias were mapped; 15 (in 11 patients) had a complete endocardial reentrant circuit with a figure-of-eight conduction pattern. During sinus rhythm, the location and axis of the slowest and most uniform conduction in the region of latest endocardial activation (the primary axis), the limits of which were defined as boundaries with >15 ms difference in electrogram duration between contiguous recordings, identified the location and shape of the reentrant circuit isthmus with a mean sensitivity compared with activation mapping of 79.3% and a mean specificity of 97.6%. The midpoint of a theoretical "estimated best ablation line" drawn perpendicular to the primary axis of activation, spanning the estimated isthmus location was within 1.3 +/- 0.2 cm (mean distance +/- SD) of the actual ablation site that terminated tachycardia. Analysis of VT electrograms, based on time shifts in the far-field component of the local electrogram when cycle length changed (piecewise linear adaptive template matching [PLATM] method) in 5 of the cases, accurately estimated the time interval between activation at the recording site and the circuit isthmus slow conduction zone where the effective ablation lesion had been placed, which is proportional to the distance between the two locations (mean difference compared with activation mapping: +/-37.3 ms). CONCLUSION: In selected patients with VT who have a complete endocardial circuit, isthmus location and shape can be discerned by analysis of sinus rhythm or tachycardia electrograms, and an effective ablation site can be predicted without the need to construct activation maps of reentrant circuits.     

Mechanical interruption of postinfarction ventricular tachycardia as a guide for catheter ablation

BACKGROUND: Mechanical trauma has been described as a helpful guide for ablation of atrial tachycardias and accessory pathways. In postinfarction ventricular tachycardia (VT), the reentrant circuit is partly endocardial and therefore may be susceptible to catheter trauma. OBJECTIVES: The purpose of this study was to determine the prevalence and significance of VT termination resulting from catheter trauma. METHODS: A consecutive series of 39 patients (mean age 68 +/- 7 years, ejection fraction 0.25 +/- 0.02) underwent left ventricular mapping for postinfarction VT. Mapping was performed during 62 hemodynamically tolerated VTs (mean cycle length 451 +/- 88 ms). Only hemodynamically tolerated VTs that did not terminate spontaneously and VTs that were reproducibly inducible were included in the study. VT termination was considered mechanical only if it was not caused by a premature depolarization. RESULTS: In 13 of 62 VTs (21%) in 8 of 39 patients (21%), either VT terminated during catheter placement at a particular site (n = 7) or a previously reproducibly inducible VT became no longer inducible with the mapping catheter located at a particular site (n = 6). The stimulus-QRS interval was significantly shorter at sites where mechanical trauma affected the reentrant circuit compared with sites having concealed entrainment (102 +/- 56 ms vs 253 +/- 134 ms, P = .003). At the site that was susceptible to mechanical trauma, the pace map was identical or highly similar in 13 of 13 VTs. After radiofrequency ablation at these sites, the targeted VTs were no longer inducible. No patient had recurrence of the targeted VT during a mean follow-up of 15 +/- 11 months. CONCLUSIONS: Catheter contact at a critical endocardial site can interrupt postinfarction VT or prevent its induction. Radiofrequency ablation at sites of mechanical termination of VT has a high probability of success.     

Quantification of activation patterns during ventricular fibrillation in open-chest porcine left ventricle and septum

BACKGROUND: A single stationary mother rotor has been hypothesized to be responsible for maintenance of ventricular fibrillation (VF) in the guinea pig. Previous studies have pointed to the ventricular septum as a possible location for a mother rotor in the pig heart. OBJECTIVES: The purpose of this study was to test the hypothesis that a mother rotor is located in the septum. METHODS: In seven open-chest pigs, we mapped the first 20 seconds of electrically induced VF simultaneously from the posterior left ventricle (LV) and right side of the septum with two electrical arrays. Each array contained 504 electrodes (21 x 24) spaced 2 mm apart in the LV and 1.5 mm apart in the septum. RESULTS: The percentage of VF wavefronts that formed reentrant circuits was significantly lower in the septum (1% +/- 1% [mean +/- SD]) than in the LV (2% +/- 1%). The peak frequency during VF also was significantly smaller in the septum (8.6 Hz +/- 3.0 Hz) than in the LV (10.4 Hz +/- 3.4 Hz). The mean direction of spread of activation of VF wavefronts was away from the region where the posterior LV free wall intersects the posterior septum in both the LV and septum. CONCLUSIONS: The lower incidence of reentry and lower peak frequency in the mapped region of the septum than in the LV indicate that a mother rotor is not present in swine on the RV side of the septum. The mean directions of the VF activation sequences in the LV and septum suggest that if a mother rotor is present during the first 20 seconds of VF, it exists where the posterior LV free wall joins the septum, the region where the posterior papillary muscle inserts.     

High-current stimuli to the spared epicardium of a large infarct induce ventricular tachycardia.

BACKGROUND. Previous studies have demonstrated that both ventricular tachycardia (VT) and ventricular fibrillation (VF) may begin as figure-eight reentry: VT with a longer cycle length from spared tissue adjacent to an infarct by programmed stimulation and VF with a shorter cycle length from noninfarcted tissue by a large premature S2 stimulus. These results suggest that the type of tissue or cycle length of the arrhythmia rather than the mode of induction determines whether the figure eight becomes sustained VT or degenerates into VF. Thus, a protocol similar to that by which a VF threshold is determined may induce VT rather than VF when performed in the spared tissue over an infarct. METHODS AND RESULTS. In 10 dogs, 4 days after occlusion-reperfusion of the left anterior descending coronary artery, 10 S1 stimuli were delivered from a total of 34 right and left ventricular sites outside the infarct. An epicardial S2 stimulus over the infarct was increased in 10-mA steps and introduced in diastole at decreasing cycle lengths of 5 msec until VT or VF was induced. Sustained monomorphic figure-eight VT was induced from 24 S1 sites and VF from nine (p = 0.03). The mean cycle lengths for the initial six arrhythmic cycles was 152 +/- 33 msec for VT and 115 +/- 13 msec for VF (p less than 0.001). Mean transmural infarct extent was 80% in five dogs with only VT, 63% in three dogs with both VT and VF, and 15% in two dogs with only VF. Different morphologies of VT were induced by changing the S1 site, the S2 strength, or the S1S2 coupling interval. In 25 of the 34 arrhythmias, the central part of the initial figure-eight pathway was oriented opposite the S1 activation sequence in that region. CONCLUSIONS. A large S2 stimulus over a nontransmural infarct induces VT if the spared myocardium is thin. This study introduces a useful technique for inducing sustained monomorphic VT in which the location and direction of the figure-eight pathway are known a priori and in which different morphologies of sustained VT can be produced by changing the S1 site.     

Mechanisms determining sudden death. A cooperative study of 69 cases recorded using the Holter method

A cooperative study involving 23 centres enabled review of 69 cases of sudden death occurring less than one hour after onset of symptoms recorded by the Holter method and not related to recent, clinically documented myocardial infarction or to class IV cardiac failure. The 15 cases of asystole (22 p. cent) were observed in elderly patients (73.3 +/- 2.7 years) whose known ischaemic heart disease (12/15) was confirmed in 10 cases as the direct cause by the preceding acute ST changes. In 2 cases, death resulted from AV block presumed to be iatrogenic. The 13 episodes of torsades de point (19 p. cent) occurred mainly in younger women (58.8 +/- 6 years) without apparent cardiac disease (8 cases) and were provoked by a Group IA antiarrhythmic drug (7 cases) or by hypokalemia (3 cases). Apart from 1 case of congenital long QT syndrome, slowing of the sinus rhythm was observed (78.3 +/- 2.6 to 60.2 +/- 2.7 bpm, p less than 0.001) in the 3 hours preceding these episodes, and ventricular bigeminy with a long coupling interval was recorded in the lasts seconds before the torsades. The 41 (59 p. cent) cases of ventricular fibrillation (VF) were observed in men aged 64.9 +/- 2 years with coronary artery disease (39/41). However signs of acute ischaemia were only found in 5 cases. The VF was primary in 8 cases and secondary to ventricular tachycardia (VT in 33 cases). An acceleration of the cardiac rhythm (83.3 +/- 3.4 to 90 +/- 4.1 bpm, p less than 0.01) was recorded in the hour preceding VF and other arrhythmias were common: atrial tachycardia (4 cases), atrial extrasystoles (4 cases), a new type of ventricular extrasystoles (VES). The VF and VT were preceded by a long cycle in 17 cases. The first complex was different from previous VES in 10 cases and identical to the previous VES in 16 cases; in 4 cases this feature could not be identified and in 11 cases there were no premonitory VES. The coupling interval of the initial VES was shorter than that of the most premature preceding VES (368 +/- 13 ms vs 442 +/- 19 ms, p less than 0.001), especially in primary VF (335 +/- 9 ms, N = 8) compared to polymorphic VT (360 +/- 12 ms, N = 11) or monomorphic VT (384 +/- 18 ms N = 22).(ABSTRACT TRUNCATED AT 250 WORDS)     

Incidence of nonsustained and sustained ventricular tachyarrhythmias in patients with an implantable cardioverter defibrillator

INTRODUCTION: Nonsustained ventricular tachycardia (NSVT) is a frequent phenomenon in some patients with heart disease, but its association with sustained ventricular tachycardias (ventricular tachycardia [VT]/ventricular fibrillation [VF]) is still not clear. The aim of this study was to determine whether NSVT incidence was associated with sustained VT/VF in patients with an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: Retrospective data analysis was conducted in 923 ICD patients with a mean follow-up of 4 months. NSVT and sustained VT/VF were defined as device-detected tachycardias. The incidence rates of NSVT and sustained VT/VF as well as ICD therapies were determined as episodes per patient. The NSVT index was defined as the product of NSVT episodes/day times the mean number of beats per episode, i.e., total beats/day. The NSVT index peak was defined as the highest value on or prior to the day with sustained VT/VF episodes. Patients (n = 393) with NSVT experienced a higher incidence of sustained VT/VF (17.2 +/- 63.0 episodes/patient) and ICD therapies (15.2 +/- 61.4 episodes/patient) than patients (n = 530) without NSVT (sustained VT/VF: 0.5 +/- 6.6 and therapies: 0.5 +/- 5.6; P < 0.0001). Approximately 74% of NSVT index peaks occurred on the same day or <3 days prior to sustained VT/VF episodes. The index was higher for peaks < or =3 days prior to the day with sustained VT/VF (94.3 +/- 140.1 total beats/day) than for peaks >3 days prior to the day with sustained VT/VF (32.7 +/- 55.9 total beats/day; P < 0.0001). CONCLUSION: ICD patients with NSVT represent a population more likely to experience sustained VT/VF episodes with a temporal association between an NSVT surge and sustained VT/VF occurrence.     

Signal averaged ECG and mechanisms of sudden death

The aim of signal averaged electrocardiography is to detect late potentials (LP) which are markers of ventricular tachycardia. As sudden death is often due to ventricular fibrillation which can complicate ventricular tachycardia, some workers have suggested that the presence of LP may increase the risk of sudden death. We analysed the results of signal averaged ECG in 17 subjects who died suddenly and compared them with 8 patients who died from ventricular tachycardia. These two groups of patients were part of a general population of 450 subjects who underwent programmed ventricular stimulation and signal averaged ECG by Simson's method (25 Hz filter). Three parameters of this ECG were analysed: total QRS duration (Dur QRS), amplitude of the signal 40 ms before its termination (V 40), and the duration of the terminal activity less than 40 microV (Dur LP). The criteria of diagnosis of Lp were: Dur QRS greater than or equal to 120 ms, V 40 less than or equal to 20 microV, Dur LP greater than or equal to 40 ms. The results of signal averaged ECG of patients who died suddenly were different to those of patients who died from VT: Dur QRS 116 +/- 40 vs 140 +/- 25 ms, V 40 27 +/- 24 vs 7 +/- 8 microV, Dur LP 39 +/- 27 vs 59 +/- 14 ms. Only 8 patients who died suddenly had LP (47%) whereas all patients who died of VT had LP. A correlation was observed between the presence of LP and 2 factors: the LV ejection fraction which was significantly lower in patients with LP (28 +/- 8 vs 46 +/- 19%) and the results of programmed ventricular stimulation: patients with induced sustained VT less than 270/mn usually had LP (15/16). LP were usually absent (4/6) in cases of ventricular flutter (VT greater than or equal to 270/mn) or induced VF. The presence of LP in 2 patients could signify a risk of developing VT later on. In conclusion, 9/17 patients who died suddenly did not have LP. The risk of sudden death due to primary VF or V flutter cannot be predicted. Other causes of VF are even harder to identify.     

Dysrhythmias after direct-current cardioversion

The success rate of direct-current (DC) countershocks and postshock arrhythmias are of concern for the design of automatic devices. Results of 112 DC shocks for induced ventricular tachycardia/fibrillation (VT/VF) (n = 99) or atrial fibrillation (AF) were analyzed. Clinical and arrhythmia characteristics were related to the success rate of DC shocks as well as postshock arrhythmias. Sixty-one patients were men and 14 were women; mean age was 52 +/- 15 years. Coronary artery disease was present in 56 patients and cardiomyopathy in 4. The other patients had no apparent structural heart disease. The success rate of transchest DC shocks for VT and VF were identical. The first DC shock interrupted 80% of VT and VF episodes. All episodes were terminated by 4 or fewer DC shocks. A single DC shock changed morphologic pattern or rate of 4 episodes of VT. Asystole after VT/VF (1,900 +/- 960 ms) was longer than after atrial fibrillation (1,150 +/- 470 ms, p less than 0.01). VT/VF recurred (within 3 minutes) after 26 of 99 initially successful DC shocks, requiring repeat shocks in 2 cases. Sinus bradycardia (n = 18) or high degree atrioventricular block (n = 11) necessitated rate support pacing in 10 patients. Antiarrhythmic drugs did not prevent postshock tachycardias, but facilitated the development of bradycardias. In conclusion, reliable and continuous analysis of cardiac rhythm after discharge is mandatory to enable automatic devices to correct unsuccessful discharges or recurring VT/VF. In addition, demand pacing capability is desirable to prevent severe bradycardia after DC shocks in patients receiving antiarrhythmic drugs.