Double-wave reentry as a mechanism of acceleration of ventricular tachycardia

By using a Langendorff-perfused ring of anisotropic rabbit epicardium, sustained reentrant ventricular tachycardia with a cycle length of 168 +/- 13 msec (n = 26) was induced by programmed electrical stimulation. Continuous left ventricular epicardial mapping with 256 simultaneously recorded unipolar electrograms demonstrated that the tachycardia was based on circuital movement of the impulse around a fixed obstacle. Because of the anisotropic properties of the myocardium, the circuit consisted of a ring with segments in which the circulating wave propagated slowly (20 +/- 2 cm/sec) or faster (62 +/- 4 cm/sec). This was related to transverse or longitudinal propagation in relation to fiber direction. In six of 26 experiments, sudden acceleration in rate of the tachycardia was observed during programmed electrical stimulation. This acceleration was caused by the occurrence of double-wave reentry (two successive waves traveling in the same direction and using the same circuit). In one of the experiments, induction of double-wave reentry was only possible at basal conditions but not after the administration of a class III antiarrhythmic drug. In a seventh experiment, induction of double-wave reentry became possible after the administration of a class IC antiarrhythmic drug. Because conduction velocity around the ring was depressed during acceleration, the total revolution time of the circuit during double-wave reentry was about 120% of that during single-wave reentry. Ventricular tachycardias in which double-wave reentry could be elicited had longer cycle lengths (197 +/- 11 vs. 156 +/- 8 msec, p less than 0.001) and larger excitable gaps (71 +/- 16 vs. 28 +/- 5 msec, p less than 0.001) than those not showing this phenomenon. Double-wave reentry might have important clinical implications in understanding ventricular tachycardia acceleration during programmed electrical stimulation, proarrhythmic effects of drugs, and pathophysiology of rapid ventricular tachycardias.     

Sustained bundle branch reentry as a mechanism of clinical tachycardia

The incidence of sustained bundle branch reentrant (BBR) tachycardia as a clinical or induced arrhythmia or both continues to be underreported. At our institution, BBR has been the underlying mechanism of sustained monomorphic ventricular tachycardia in approximately 6% of patients, whereas mechanisms unrelated to BBR were the cause in the rest. Data gathered from 20 consecutive patients showed electrophysiologic characteristics that suggest this possibility. These include induction of sustained monomorphic tachycardia with typical left or right bundle branch block morphology or both and atrioventricular dissociation or ventriculoatrial block. On intracardiac electrograms, all previously published criteria for BBR were fulfilled, and in addition, whenever there was a change in the cycle length of tachycardia, the His to His cycle length variation produced similar changes in ventricular activation during subsequent complexes with no relation to the preceding ventricular activation cycles. Compared with patients with ventricular tachycardia due to mechanisms unrelated to BBR, patients with BBR had frequent combination of nonspecific intraventricular conduction defects and prolonged HV intervals (100% vs. 11%, p less than 0.001). When this combination was associated with a tachycardia showing a left bundle branch block pattern, BBR accounted for the majority compared with mechanisms unrelated to BBR (73% vs. 27%, p less than 0.01). The above finding in patients with dilated cardiomyopathy should raise the suspicion of sustained BBR because dilated cardiomyopathy was observed in 95% of the patients with BBR. Twelve of the 20 patients were treated with antiarrhythmic agents, and the other eight were managed by selective catheter ablation of the right bundle branch with electrical energy. Our data suggest that sustained BBR is not an uncommon mechanism of tachycardia; it can be induced readily in the laboratory and is amendable to catheter ablation by the very nature of its circuit. The clinical and electrophysiologic features outlined in this study should enable one to correctly diagnose this important arrhythmia.     

Reflected reentry in nonhomogeneous ventricular muscle as a mechanism of cardiac arrhythmias

Arrhythmogenesis in ventricular muscle exhibiting nonhomogeneous excitability was studied in isolated tissues from feline and canine hearts. Longitudinal bundles were mounted in a three-chambered bath and simultaneous transmembrane recordings were obtained from fibers in each chamber. Nonhomogeneous excitability was established by depressing only the central segment (1 to 2 mm wide) with high-K+ Tyrode's solution, which induced discontinuity of propagation associated with step delays mediated by electrotonic current flowing through the depressed zone. When transmission delays were long, activity distal to the site of block returned to proximal tissue as one of two forms of reflected reentry, each elicited by a different mechanism. Type I reflection, occurring with antegrade delays of 30 to 60 msec, was characterized by an early secondary depolarization due to electrotonic spread of currents from delayed responses in the depressed segment. Type II reflection evolved with delays greater than 90 msec and was manifest as a closely coupled regenerative action potential that developed independently of a pacemaker mechanism and of slow but continuous conduction. We conclude that delayed activation of excitable elements, which occurs when propagation is discontinuous, may lead to rhythm disturbances of focal origin that are mediated by electrotonic interactions across a zone of depressed tissue.     

Role of anatomic architecture in sustained atrial reentry and double potentials.

To determine the role of anatomic architecture in atrial flutter, electrophysiologic findings were correlated with anatomic features in a modified model of atrial flutter with ligation of the crista terminalis. Crista ligation in the middle right atrium prolonged intraatrial conduction time in a rate-dependent manner in 12 dogs, particularly in the low right atrium. With burst atrial pacing, unidirectional block occurred either in the low right atrium or in the interatrial septal region near the superior vena cava, leading to initiation of atrial flutter. Atrial activation mapping revealed a slow conduction area in the low right atrium where conduction had been delayed by crista ligation. On the intact tissues between the venae cavae, double potentials were recorded, a finding indicative of functional block in the center of the reentrant circuit. The interdeflection time of double potentials changed with the activation sequence of atrial flutter. This change could be explained by assuming that the functional center of the reentrant circuit leaned on the right atrial free wall side. Anatomic study demonstrated that areas of slow conduction, unidirectional block, and functional block in the center of the reentrant circuit were closely related to the location of the intact crista terminalis. In conclusion, the intact portion of the crista terminalis played an important role in the genesis of atrial flutter after blockage of longitudinal conduction through the crista.     

Role of wavelength adaptation in the initiation, maintenance, and pharmacologic suppression of reentry

INTRODUCTION: The stability of reentry is thought to depend on a critical balance between the spatial extent of refractory tissue in a reentrant wave (i.e., wavelength lambda) and the reentrant path length. Because considerable evidence suggests that lambda changes continuously in space and time during abrupt rate changes associated with the onset of tachycardia, we hypothesized that beat-by-beat adaptation of A to the dimensions of the reentrant path plays a central role in the mechanism of initiation of reentry. METHODS AND RESULTS: To investigate the dynamic relationship between lambda and path length during initiation of reentry, optical mapping with voltage-sensitive dyes was used in a guinea pig model of reentrant ventricular tachycardia (VT). In this model, a computer-guided laser obstacle precisely controlled the position and dimensions of the reentrant path. Under control perfusion and after addition of 15 microM d-sotalol, lambda was monitored during steady-state pacing, premature stimulation, and the initiating beats leading to nonsustained and sustained VT. During control perfusion, reentrant VT was reproducibly induced in 8 of 8 hearts, whereas in the presence of d-sotalol, reentry could only be initiated in 1 of 8 hearts due primarily to the failure of lambda to adapt to the reentrant path length. During successful initiation of VT, a consistent sequence was observed. The sequence was characterized by antidromic and orthodromic propagation around both sides of the anatomic obstacle, followed by unidirectional block of the antidromic impulse and persistence of reentry only if the A of the orthodromic impulse adapted to the reentrant path (lambda < path length). d-Sotalol prevented initiation of VT by altering lambda adaptation of the orthodromic wave; however, it failed to terminate ongoing VT because reverse use-dependence developed after several beats of tachycardia. CONCLUSION: In an experimental model where lambda, path length, and cellular action potentials were monitored during initiation of reentry, we found that, in contrast to termination, the initiation of reentry and the transition from nonsustained to sustained VT is strongly dependent on beat-to-beat adaptation of lambda to the dimensions of the reentrant path.     

The mechanism of paroxysmal supraventricular tachycardia--PSVT due to peri-AV nodal reentry

To evaluate the role of perinodal tissue in the genesis of atrioventricular (AV) nodal reentry, echo beats were induced by programmed stimulation in nine superfused rabbit AV nodal preparations which included the crista terminalis (CT) input, interatrial septal (IAS) input and perinodal atrial tissues in addition to the AV node. Two patterns of AV reentry were observed: In six preparations, premature response was blocked within the AV node, but anterograde conduction continued along the perinodal fibers and entered the AV node by way of another input region. Reentry occurred via retrograde nodal conduction to the initial input and subsequently conducted within the perinodal region. In three preparations, premature beat elicited by CT stimulation was blocked in the perinodal tissues near the CT, conducted slowly in an anterograde fashion through the AV node. To complete the reentry circuit, it exited at the IAS region and conducted in retrograde fashion via the perinodal tissues to reenter the node at the CT. Moreover, in four other preparations, surgical interruption of the perinodal tissue prevented reinitiation of reentrant phenomena. Thus, the critical role of the perinodal tissues as a necessary link in AV nodal reentry was demonstrated in this preparation.     

Impact of thromboischemic reentry mechanism of coronary thrombosis and microembolism in acute myocardial infarction

It has been suggested that the thromboischemic reentry mechanism (TRM) is responsible for washing platelet aggregates out of the coronary vessels during the early phase of acute myocardial infarction (AMI). This might account for the observation of Schwartz, who reported the presence of multiple microthrombi in the subendocardial blood vessels following AMI but found only a few thrombotic occlusions in the main coronary arteries. This washing-out of the vessel (due to reperfusion waves) intermittently releases myoglobin into the serum and is responsible for the "staccato phenomenon." We examined a group of 177 patients with a mean age of 66.1 years, whose sudden death was definitely of cardiac origin. Infarction was confirmed in 84.7% of the subjects (fresh infarct: 23.7%; fresh infarct with scarring: 25.9%; scarring alone: 35.0%; no change in myocardium: 15.2%). In other words, 49.7% of all postmortem subjects (88 cases) showed fresh infarction. Opening the coronary arteries longitudinally revealed only 7 thrombi in these 88 cases, i.e., 7.9% of all fresh infarcts. These observations confirm those of Roberts (8.5%) and Friedmann (4%).     

Bundle branch reentry tachycardia: a possible mechanism of flecainide proarrhythmia effect

A 42-year old man with non-obstructive myocardiopathy complicated by paroxysmal atrial fibrillation treated with amiodarone (200 mg per day) received flecainide in daily doses of 400 mg for undocumented palpitations. Ten syncopes and numerous malaises occurred during the following two months. Electrophysiological testing was performed, showing prolongation of HV to 80 ms and discreet widening of QRS to 100 ms. Programmed atrial stimulation failed to demonstrate a second degree subnodal block and to induce tachycardia. In contrast, ventricular stimulation elicited a critical SH delay (260 ms), always followed by a left delay-type complex preceded by His bundle deflection which suggested reentry within the His-Purkinje system. Three extrasystoles on imposed rhythm started sustained ventricular tachycardia with the same 270 ms cycle morphology and reproducing the symptoms. Each V wave was preceded by an H potential, with HV varying from 100 to 300 ms. Three weeks after flecainide was discontinued, HV was 60 ms, and no ventricular tachycardia could be triggered by programmed stimulation. The patient remained symptom-free throughout the 5-month follow-up. This case illustrates the proarrhythmic effect of the flecainide-amiodarone combination. The mechanism of provoked tachycardia probably involves ventricular reentry through the His bundle branches, induced by a critical depression of conduction below the His bundle.