Supernormal Conduction Research Articles

Physiologic Variants of Cardiac Conduction (Aberration, Gap, Supernormal Conduction).

Wide QRS complexes during supraventricular rhythms can be caused by fixed bundle branch block, functional (intermittent) bundle branch block, preexcitation, or toxic/metabolic causes. Functional bundle branch block can be caused by long-short aberrancy (usually physiologic), or acceleration/deceleration dependent aberrancy (usually pathologic). Electrocardiogram criteria have been proposed to differentiate aberration from ventricular tachycardia; they are not always accurate. The gap phenomenon "paradox" is that with increasingly premature extrastimuli, progressive proximal conduction delay allows time for distal recovery of excitability. Supernormal conduction may explain unusual conduction phenomena in patients with abnormal His-Purkinje function or poorly conducting accessory pathways.

547 Supernormal conduction of an accessory pathway: the case of a young sportsman

Abstract Aims Ventricular pre-excitation is defined by the presence of all of the following electrocardiographic criteria: PQ interval duration ≤120 ms, QRS duration ≥120 ms, and presence of δ wave (defined as initial ‘slurring’ of the QRS complex). Ventricular pre-excitation together with the presence of symptoms (orthodromic and/or antidromic atrioventricular reentry tachycardia, atrial fibrillation) defines Wolff–Parkinson–White (WPW) syndrome. The anatomical substrate of ventricular pre-excitation consists of an extranodal accessory atrio-ventricular connection: the so-called Kent bundle. Such pathways can have antegrade, retrograde, or mixed conductive properties. Accessory pathways endowed with anterograde conductive capability may be responsible for manifest, intermittent, or non-manifest ventricular pre-excitation depending on whether it is respectively always visible on the ECG, not always visible on the ECG and not visible on the ECG even though the pathway has the ability to antegrade conduction. The rare phenomenon of supernormal conduction of anomalous pathways is part of the manifest pre-excitation, which represents the topic of the case reported below. Methods and results We report the clinical case of a young not agonist sportsman undergoing an electrophysiological study (SEF) because of he is suffering from ventricular pre-excitation. The SEF did not showed the inducibility of arrhythmias and, at the same time, apparently it showed low risk characteristics of the pathway even during adrenergic stimulus. However, a careful study, performed with atrial stimulation with couplings up to refractoriness of the atrioventricular node revealed supernormal conduction properties of the Kent bundle which proved to have high risk characteristics according to current guidelines and, therefore, was effectively treated with catheter ablation. Conclusions This case invites us to careful studying of accessory pathways properties, especially since, although rare, they may possess supernormal conduction characteristics capable of determining high ventricular rates in the case of sustained atrial tachyarrhythmias, especially in conditions of adrenergic hyperactivity.

Physiologic Variants of Cardiac Conduction (Aberration, Gap, Supernormal Conduction).

Wide QRS complexes during supraventricular rhythms can be caused by fixed bundle branch block, functional (intermittent) bundle branch block, preexcitation, or toxic/metabolic causes. Functional bundle branch block can be caused by long-short aberrancy (usually physiologic), or acceleration/deceleration dependent aberrancy (usually pathologic). Electrocardiogram criteria have been proposed to differentiate aberration from ventricular tachycardia; they are not always accurate. The gap phenomenon "paradox" is that with increasingly premature extrastimuli, progressive proximal conduction delay allows time for distal recovery of excitability. Supernormal conduction may explain unusual conduction phenomena in patients with abnormal His-Purkinje function or poorly conducting accessory pathways.

Wolff-Parkinson-White pattern on alternate beats: What is the mechanism?

The Holter electrocardiogram from an asymptomatic man shows intermittent preexcitation. At the lowest rates all the QRS complexes display a WPW pattern. As the rate increases, preexcitation fails to occur and all the QRS complexes become persistently narrow. With a further increase in sinus rate the WPW occurs on alternate beats and this alternation is maintained for a while. A careful analysis of the accessory pathway conduction in relation to sinus-cycle length and morphology of the prior beat strongly supports the supernormal conduction through the Kent bundle associated with linking as the key mechanism underlying the preexcitation on alternate beats.

ECG quiz – Where is the block?

A 68 year-old man presented with palpitations. A standard 12‑lead ECG was performed and demonstrated significant conduction disease. Using findings on the index and prior ECGs, we review the differential diagnoses for his conduction abnormality. We discuss the possibility of phase III delay, phase IV delay, and “supernormal conduction” to explain the ECG findings. We explore each of these phenomena and review their relative likelihood as it applies to the case presented.

Abstract 16378: Increased Extracellular Sodium and Calcium Modify the Extracellular Potassium and Cardiac Conduction Velocity Relationship in a Langendorff-perfused Guinea Pig Heart

Background: Previous studies have demonstrated a biphasic relationship between extracellular potassium (K o ) and cardiac conduction velocity (CV). With moderate hyperkalemia, CV increases in what is referred to as supernormal conduction, but further increases in K o lead to severe conduction slowing and asystole. We recently demonstrated that altering extracellular sodium (Na o ) and extracellular calcium (Ca o ) modulates CV dependence on gap junctions (GJs). We have also shown that increasing Na o and Ca o can attenuate conduction loss caused by global ischemia ischemia. The purpose of this study was to determine if increasing Na o and Ca o would alter the K o -CV relationship and preserve CV at high K o . Hypothesis: Increasing Na o and Ca o will mitigate conduction slowing and the incidence of asystole associated with severe hyperkalemia in conditions of both normal and uncoupled GJs. Methods: Langendorff-perfused guinea pig hearts were optically mapped to measure CV. Na o was set to 145 or155mM and Ca o to 1.25 or 2.0mM. K o was varied from 4.6, 6.4, 8, to 10 mM in each experiment. Perfusion order was blinded and randomized. GJs were inhibited using carbenoxolone. Results: A biphasic K o -CV relationship was observed under all conditions. Maximum CV was achieved at either 6.4 or 8.0mM K o followed by a decrease in CV with increased K o . Importantly, the degree of CV slowing in the presence of 10mM K o was significantly reduced with the 155mM Na o / 2.0mM Ca o perfusate compared to all other Na o /Ca o combinations. Carbenoxolone reduced CV across all K o , but did not alter the K o -CV relationship. With 145mM Na o / 1.25mM Ca o , all hearts became asystolic at K o =10.0mM. Increasing Na o and Ca o significantly reduced the incidence of asystole at K o =10.0mM. Conclusions: Elevating Na o and Ca o preserves CV during severe hyperkalemia with or without strong GJ coupling. Increasing Na o and Ca o significantly reduces the incidence of asystole during severe hyperkalemia. These data suggest that non-linear and combinatorial effects of sodium, calcium, and GJ uncoupling can differentially modulate cardiac conduction during hyperkalemic perfusion. These results have important implications for cardioplegic arrest and ischemic heart disease when potassium and calcium homeostasis are disrupted.

Tachycardia cycle length alternans in orthodromic reciprocating tachycardia due to mutually dependent dual AV node physiology and retrograde supernormal conduction.

Tachycardia cycle length alternans in orthodromic reciprocating tachycardia due to mutually dependent dual AV node physiology and retrograde supernormal conduction.

The Role of Membrane Capacitance in Cardiac Impulse Conduction: An Optogenetic Study With Non-excitable Cells Coupled to Cardiomyocytes.

Non-excitable cells (NECs) such as cardiac myofibroblasts that are electrotonically coupled to cardiomyocytes affect conduction velocity (θ) by representing a capacitive load (CL: increased membrane to be charged) and a resistive load (RL: partial depolarization of coupled cardiomyocytes). In this study, we untangled the relative contributions of both loading modalities to NEC-dependent arrhythmogenic conduction slowing. Discrimination between CL and RL was achieved by reversibly removing the RL component by light activation of the halorhodopsin-based hyperpolarizing membrane voltage actuator eNpHR3.0-eYFP (enhanced yellow fluorescent protein) expressed in communication-competent fibroblast-like NIH3T3 cells (3T3HR cells) that served as a model of coupled NECs. Experiments were conducted with strands of neonatal rat ventricular cardiomyocytes coated at increasing densities with 3T3HR cells. Impulse conduction along preparations stimulated at 2.5 Hz was assessed with multielectrode arrays. The relative density of 3T3HR cells was determined by dividing the area showing eYFP fluorescence by the area covered with cardiomyocytes [coverage factor (CF)]. Compared to cardiomyocytes, 3T3HR cells exhibited a depolarized membrane potential (−34 mV) that was shifted to −104 mV during activation of halorhodopsin. Without illumination, 3T3HR cells slowed θ along the preparations from ∼330 mm/s (control cardiomyocyte strands) to ∼100 mm/s (CF = ∼0.6). Illumination of the preparation increased the electrogram amplitudes and induced partial recovery of θ at CF > 0.3. Computer simulations demonstrated that the θ deficit observed during illumination was attributable in full to the CL represented by coupled 3T3HR cells with θ showing a power-law relationship to capacitance with an exponent of −0.78 (simulations) and −0.99 (experiments). The relative contribution of CL and RL to conduction slowing changed as a function of CF with CL dominating at CF ≤ ∼0.3, both mechanisms being equally important at CF = ∼0.5, and RL dominating over CL at CF > 0.5. The finding that RL did not affect θ at CFs ≤ 0.3 is explained by the circumstance that, at the respective moderate levels of cardiomyocyte depolarization, supernormal conduction stabilized propagation. The findings provide experimental estimates for the dependence of θ on membrane capacitance in general and suggest that the myocardium can absorb moderate numbers of electrotonically coupled NECs without showing substantial alterations of θ.

SUPERNORMAL CONDUCTION: A RARE CASE OF ABERRANCY

Supernormal conduction(SNC) is a rare phenomenon where intermittent narrow QRS complexes can occur despite underlying bundle branch block(BBB) at a slower rate. Cellularly, this occurs if the ventricular rate is just beyond the effective refractory period of the septal myocardium, while at the same

Food deprivation and prior anoxic coma have opposite effects on the activity of a visual interneuron in the locust

We compared how different metabolic stressors, anoxic coma and food deprivation, affected signaling in neural tissue. We used the locust’s Descending Contralateral Movement Detector (DCMD) interneuron because its large axon, high firing frequencies, and rapid conduction velocity make it energetically expensive. We exposed locusts to a 30min anoxic coma or 1day of food deprivation and found contrasting effects on signaling within the axon. After a prior anoxic coma, the DCMD fired fewer high-frequency (>200Hz) action potentials (APs) (Control: 12.4±1.6; Coma: 6.3±0.9) with a reduction in axonal conduction velocity (CV) at all frequencies (∼4–8%) when presented with a standard looming visual stimulus. Prior anoxic coma was also associated with a loss of supernormal conduction by reducing both the number of supernormal APs and the firing frequency with the highest CV. Initially, food deprivation caused a significant increase in the number of low- and high-frequency APs with no differences observed in CV. After controlling for isolation, food deprivation resulted in an increase in high-frequency APs (>200Hz: Control: 17.1±1.7; Food-deprived: 19.9±1.3) and an increase in relative conduction velocity for frequencies >150Hz (∼2%). Action potentials of food-deprived animals had a smaller half-width (Control: 0.45±0.02ms; Food-deprived: 0.40±0.01ms) and decay time (Control: 0.62±0.03ms; Food-deprived: 0.54±0.02ms). Our data indicate that the effects of metabolic stress on neural signaling can be stressor-dependent.

Ventriculoatrial Intervals ≤70 ms in Orthodromic Atrioventricular Reciprocating Tachycardia.

Although a ventriculoatrial interval (VAI) of ≤70 ms is used to distinguish atrioventricular nodal reentrant tachycardia from orthodromic atrioventricular reciprocating tachycardia (AVRT), a VAI of ≤70 ms is sometimes observed in cases of AVRT. The study aimed to evaluate the short VAI that is seen in AVRT and to understand its underlying mechanism. Electrophysiologic studies of 46 consecutive patients with AVRT involving an accessory pathway (AP) were examined retrospectively. AP was right sided in seven patients and left sided in 39. A VAI (interval from QRS onset to the earliest intracardiac atrial electrogram recorded by any mapping catheter during AVRT) ≤70 ms during AVRT (short VAI) was observed in eight patients: six with a left lateral AP and two with a left posteroseptal AP. During AVRT involving a left-sided AP, the QRS-V interval (from the earliest QRS onset to the local ventricular electrogram at a site which showed earliest atrial electrogram recorded from the coronary sinus catheter) was significantly shorter (37 ± 7 ms vs 54 ± 13 ms, P = 0.001) and supernormal conduction (QRS duration or the QRS-V interval shortening by ≥10 ms during AVRT) was more frequently seen (63% vs 6%, P = 0.02) in the short VAI group than in the normal VAI group. Furthermore, these parameters were shown to be determinants for short VAI. A short VAI is sometimes observed during AVRT involving a left-sided AP. The short VAI may be caused by rapid propagation or supernormal conduction between the proximal Purkinje-muscle junction and basal left ventricular myocardium.

Normality that is abnormal

Supernormal conduction is defined as better-than-expected conduction in patients with depressed conduction during a short interval in the ventricular cycle. It is mainly observed in long-duration electrocardiogram (ECG) assessments. Its occurrence during 12-lead ECG is uncommon and its interpretation demands knowledge on electrophysiological alterations that are hard to understand. By reporting this case we aim to propose a rationale sequence that should be considered when facing an ECG with these same features, which would enable a greater accuracy to make a definitive diagnosis.

Supernormal and alternating conduction in intermittent bundle branch block and intermittent or concealed ventricular preexcitation. Electrophysiological study, mechanisms and clinical considerations

Supernormal and alternating conduction are not rare in clinical arrhythmology, detectable at various levels of the conduction system in different pathophysiological conditions, and often associated, so as to justify the search for a possible link between them. In order to define a possible relationship between supernormal and alternating conduction, the electrophysiological data of two patient groups were analyzed. Group 1 included 9 patients with intermittent bundle branch block in the presence of supernormal conduction through the pathological branch. Group 2 included 16 patients with ventricular preexcitation, intermittent or concealed, in the presence of supernormal conduction through the atrioventricular accessory pathway. In group 1, 8 patients had a phase 3 and 1 patient a phase 3 and phase 4 bundle branch block. In all 9 patients, the area of phase 3 block was interrupted by a window of unexpected conductivity detectable by atrial premature stimulation. In 7/9 cases, by modulating the atrial rate, alternating conduction through the branch was observed, and the cardiac cycle of occurrence of the phenomenon was in the range of supernormal conduction in 6/7 cases. In group 2, 11 patients showed conduction through the accessory pathway only for a narrow range of cardiac cycles, during atrial premature stimulation. One patient had a prolonged accessory pathway refractory period (phase 3 block), but a window of unexpected supernormal conduction within the refractory zone was observed at atrial premature stimulation. Another patient presented a tachycardia and bradycardia-dependent block along the accessory pathway (phase 3 and phase 4 block) and the phase 3 block area was interrupted by a window of supernormal conduction. In the other three cases, supernormal conduction was manifested as unexpected resumption of conductivity through the accessory pathway for atrial cycles more precocious than the actual duration of its effective refractoriness. By modulating the atrial rate, alternating conduction through the accessory pathway was observed in 13/16 cases, and the cardiac cycle at which this phenomenon appeared falling in the range of supernormal conduction in 11/13 cases. It can be hypothesized that supernormal conduction is in relation with the presence of a phase of supernormal excitability experimentally demonstrated in the late phase of repolarization of cardiac cells, and that supernormal and alternating conduction are related phenomena, so that the evidence on ECG of alternating conduction through a pathological branch or an atrioventricular accessory pathway can be considered as a marker of the presence of supernormal conduction through the structure.

Supernormal Conduction and Suppression of Spatially Discordant Alternans of Cardiac Action Potentials.

Spatially discordant alternans (DA) of action potential durations (APD) is thought to be more pro-arrhythmic than concordant alternans. Super normal conduction (SNC) has been reported to suppress formation of DA. An increase in conduction velocity (CV) as activation rate increases, i.e., a negative CV restitution, is widely considered as hallmark of SNC. Our aim in this study is to show that it is not an increase in CV for faster rates that prevents formation of DA, rather, it is the ratio of the CV for the short relative to the long activation that is critical in DA suppression. To illustrate this subtlety, we simulated this phenomenon using two approaches; (1) by using the standard, i.e., S1S2 protocol to quantify restitution and disabling the slow inactivation gate j of the sodium current (INa), and (2) by using the dynamic, i.e., S1S1 protocol for quantification of restitution and increasing INa at different cycle lengths (CL). Even though both approaches produced similar CV restitution curves, DA was suppressed only during the first approach, where the CV of the short of the long-short action potential (AP) pattern was selectively increased. These results show that negative CV restitution, which is considered characteristic of SNC, per se, is not causal in suppressing DA, rather, the critical factor is a change in the ratio of the velocities of the short and the long APs.

Supernormal conduction revealed by extremely late atrial extrasystole during phase 3 right bundle branch block

Supernormal conduction revealed by extremely late atrial extrasystole during phase 3 right bundle branch block

Supernormal conduction in the left bundle branch block revealed by relatively late atrial extrasystoles

Supernormal conduction in the left bundle branch block revealed by relatively late atrial extrasystoles

To the Editor—Supernormal conduction or masked bundle branch block?

Carbone et al present an interesting case report in which both right bundle branch block (RBBB) and left bundle branch block (LBBB) aberrancy are seen during different initiations of an atrial tachycardia. They postulate that this is caused by phase 3–dependent block in the left bundle branch (LBB; long-short coupling interval) resulting in RBBB aberration with a prolonged PR interval, followed by intermittent supernormal conduction over the right bundle branch (RBB) resulting in LBBB aberration and a nearnormal PR interval. The existence of true supernormal conduction in the intact human heart has not been shown conclusively, however, and before invoking this phenomenon, alternative physiological mechanisms can be considered. In Figure 3, impulse 1 conducts with an LBBB morphology and a PR interval of 220 ms. Carbone et al propose that conduction is entirely blocked in the LBB at this time, when it may simply be significantly delayed by the premature atrial impulse. Impulse 2 (Figure 3) occurs slightly earlier and may block completely in the RBB and unmask the slowly conducting LBB, leading to a longer PR interval (340 ms) and an RBBB morphology. The principle of supernormal conduction does not need to be invoked because there is delayed conduction in the LBB with both impulse 1 and 2; it is simply masked by greater delay in the RBB after

Intermittent bundle branch block: a clinical model for the study of electrophysiological phenomena

Disorders of intraventricular conduction (bundle branch block and hemiblock) are usually stable and remain unchanged irrespective of heart rate. Not infrequently, however, their appearance is related to the duration of the cardiac cycle, so that they appear and disappear with changes in heart rate. This may not even represent a pathological phenomenon, since sudden and consistent changes in cardiac cycle can result, even physiologically, in aberrant conduction. However, when a bundle branch block appears intermittently for simple and progressive increments, or even deceleration, of the sinus rate, this is related to a true bundle branch pathology, i.e. tachycardia-dependent (or phase 3) block or bradycardia-dependent (or phase 4) block, respectively. Phase 3 block is believed to express a pathological increase in the duration of the recovery period of the bundle branch. Phase 4 block was best explained on the basis of enhanced phase 4 depolarization of the bundle branch system, with inability of excitation if the cardiac cycle is particularly prolonged. The two types of block, phase 3 and phase 4, often coexist. An intraventricular conduction disturbance that appears during increasing heart rate for a phase 3 block is maintained, if frequency slows down, even for cycles greater than those that brought about its appearance. This is due to retrograde activation of the bundle branch blocked in the antegrade direction, with delay of its action potential inscription. Sometimes, in the presence of phase 3 bundle branch block, very early atrial ectopic beats are paradoxically conducted in the normal way (supernormal conduction). Perhaps, this phenomenon is related to a possible "climb over" of the injured zone of the bundle branch by the blocked impulses that arise beyond the injured area as subliminal impulses, exciting the healthy tissues if catches them during their phase of supernormal excitability. In the presence of intermittent bundle branch block, it is not uncommon to observe long periods of sinus rhythm with regular PP interval, conducted with alternating (2:1) bundle branch block. Intermittent left bundle branch block is a clinical model of cardiac memory: in these cases, negative T waves in the antero-septal leads during normal conduction are often evident. This negativity is an expression of cardiac memory, and not of ischemia as initially interpreted. Intermittent bundle branch block is an excellent model to study in vivo the effects of antiarrhythmic drugs on the pathological bundle branches. Narrowing of the QRS complex in the presence of bundle branch block is not always an expression of intermittent aberrancy: beware of late ectopic beats originating from the ipsilateral ventricle to the blocked branch, that merging with the antegrade beat conducted with bundle branch block, restrict the QRS, simulating intermittent aberrancy.

症例 副伝導路の過常伝導(Supernormal conduction)が示唆されるWPW症候群の2症例

症例 副伝導路の過常伝導(Supernormal conduction)が示唆されるWPW症候群の2症例

Atrioventricular reentrant tachycardia with a 2:1 right bundle branch block

The phenomenon of a 2:1 bundle branch block is reported during atrioventricular (AV) nodal reentrant tachycardia, sinus tachycardia, atrial fibrillation, and atrial flutter. A 2:1 bundle branch block is attributed to first- and second-degree bundle branch block, linking, electrical alternans, aberrancy, or supernormal conduction. However, the same phenomenon has not been reported in AV reentrant tachycardia. Herein, we report the case of a 52-year-old man presenting with orthodromic atrioventricular reentrant tachycardia with a 2:1 right bundle branch block.