Model of Bipolar Electrogram Fractionation and Conduction Block Associated With Activation Wavefront Direction at Infarct Border Zone Lateral Isthmus Boundaries

Abstract

Background-Improved understanding of the mechanisms underlying infarct border zone electrogram fractionation may be helpful to identify arrhythmogenic regions in the postinfarction heart. We describe the generation of electrogram fractionation from changes in activation wavefront curvature in experimental canine infarction. Methods and Results-A model was developed to estimate the extracellular signal shape that would be generated by wavefront propagation parallel to versus perpendicular to the lateral boundary (LB) of the reentrant ventricular tachycardia (VT) isthmus or diastolic pathway. LBs are defined as locations where functional block forms during VT, and elsewhere they have been shown to coincide with sharp thin-to-thick transitions in infarct border zone thickness. To test the model, bipolar electrograms were acquired from infarct border zone sites in 10 canine heart experiments 3 to 5 days after experimental infarction. Activation maps were constructed during sinus rhythm and during VT. The characteristics of model-generated versus actual electrograms were compared. Quantitatively expressed VT fractionation (7.6±1.2 deflections; 16.3±8.9-ms intervals) was similar to model-generated values with wavefront propagation perpendicular to the LB (9.4±2.4 deflections; 14.4±5.2-ms intervals). Fractionation during sinus rhythm (5.9±1.8 deflections; 9.2±4.4-ms intervals) was similar to model-generated fractionation with wavefront propagation parallel to the LB (6.7±3.1 deflections; 7.1±3.8-ms intervals). VT and sinus rhythm fractionation sites were adjacent to LBs ≈80% of the time. Conclusions-The results suggest that in a subacute canine infarct model, the LBs are a source of activation wavefront discontinuity and electrogram fractionation, with the degree of fractionation being dependent on activation rate and wavefront orientation with respect to the LB. (Circ Arrhythm Electrophysiol. 2014;7:152-163.)

Techniques for automated local activation time annotation and conduction velocity estimation in cardiac mapping

“…Conduction velocity measurements provide an important quantity in identifying potential reentrant circuits and regions of tissue which, for example, might act as an anchor point for rotors [8] . Areas of tissue with slower conduction velocity are widely thought to be in a more diseased state, where either fibrosis or altered cell-to-cell coupling has reduced connectivity [9–22] , or changes in the ionic currents such as the sodium current leads to slower action potential upstroke [23] . Slow conduction is associated with increased risk of wavefront reentry which may initiate an arrhythmia [24,25] .…”

“…The data modalities most frequently encountered in the context of conduction velocity estimation are the extracellular electrogram [9,12,13,38,39] and optical recordings of myocardium [40–42] or cell cultures using voltage-sensitive fluorescent dyes, in which changes in the optical signal are proportional to those in the transmembrane voltage. Calculation of the CV of an activation wavefront requires knowledge of both the speed and the direction of activation – the angle between the normal to the wavefront and the axis joining the measuring points.…”

Mechanistically based mapping of human cardiac fibrillation

“…Transmural rotation of ventricular fibres from the epicardium to the endocardium (rotational anisotropy) (Thomas, 1957) may destabilize scroll waves to produce complex dynamics and wavebreak (Rappel, 2001). In patients at risk for sudden cardiac arrest, an ischaemic border zone may present thick-thin transitions and gap junction remodelling, which may also impact wavefront curvature and re-entry (Macia et al 2011;Ciaccio et al 2014).…”

Reprint of 'Model of unidirectional block formation leading to reentrant ventricular tachycardia in the infarct border zone of postinfarction canine hearts'

“…This compares with the normal condition in which a single activation wavefront is present, the source of the biphasic electrogram shape which is recorded from healthy myocardium. Because the geometric configuration of the conducting medium in postinfarction hearts is intransigent over time intervals of hours or more, electrogram fractionation can often be observed at the same recording location during normal sinus rhythm as well as during reentrant VT, depending on the wavefront direction [8] and the coupling interval for electrical activation.…”