Local Conduction Velocity Research Articles

Determination of refractory periods and conduction velocity during atrial fibrillation using atrial capture in dogs: Direct assessment of the wavelength and its modulation by a sodium channel blocker, pilsicainide

OBJECTIVESThe purposes of this study were to measure the atrial refractory period and the conduction velocity (CV) during atrial fibrillation (AF) and to explore the antiarrhythmic mechanism of a sodium channel blocker, pilsicainide, during AF.BACKGROUNDSodium channel blockers not only decrease the CV, but also prolong the atrial refractory period, particularly during rapid excitation. Because these effects on the wavelength are counteractive and rate dependent, it is critical to measure these parameters during AF.METHODSIn eight dogs, after AF was induced under vagal stimulation, a single extra-stimulus was repeatedly introduced from the left atrium and its capture was statistically determined for each coupling interval. The local CV was also measured during constant capture of the fibrillating atrium by rapid pacing. The same procedure was repeated after pilsicainide administration.RESULTSPilsicainide significantly increased the mode of AF intervals from 81 ± 10 to 107 ± 16 ms (p < 0.01). While the CV was decreased from 0.9 ± 0.1 to 0.7 ± 0.1 m/s (p < 0.02), the effective refractory period during AF was increased from 69 ± 11 ms to 99 ± 17 ms (p < 0.01). As a result, the wavelength was significantly increased by pilsicainide from 6.6 ± 0.9 to 7.6 ± 1.2 cm (p < 0.05).CONCLUSIONSDuring AF, whereas the sodium channel blocker pilsicainide decreases CV, it lengthens the wavelength by increasing the refractory period, an action that is likely to contribute to the drug’s ability to terminate the arrhythmia. The direct measurement of refractoriness and CV during AF may provide new insights into the determinations of the arrhythmia and antiarrhythmic drug action.

High-density mapping of activation through an incomplete isthmus ablation line.

Activation mechanisms through gaps in ablation lines and resulting electrograms are poorly understood. Eight patients (all men; age, 59+/-9 years) were studied during a recurrence of typical atrial flutter (cycle length, 233+/-19 ms) after a previous catheter ablation in the cavotricuspid isthmus. High-density 3-dimensional mapping of the isthmus was performed with the Cordis-Biosense EP Navigation system, and local conduction velocity (CV) was estimated. Maps created with 96+/-19 points revealed 0.8+/-0.3-cm gaps of recovered conduction in the ablation line. A broad wave front entered the lateral isthmus with a CV of 1.8+/-0.7 m/s, halted on the lesion line, and penetrated slowly through the gap with a CV of 0.3+/-0.1 m/s. Activation then curved and returned antidromically to activate the downstream flank of the line with a CV of 1.1+/-0.7 m/s. This front fused downstream of the line with slow transverse activation (CV, 0.4+/-0.3 m/s) parallel to it. The ablation line was demarcated by an incomplete line of convergent double potentials with isoelectric intervals (from 123+/-34 to 62+/-16 ms); each potential corresponded to local activation upstream and downstream of the lesions, while the intervening delay was produced by slow conduction through the gap combined with the progressively longer curved pathway of downstream antidromic activation as a function of distance from the gap. High-density isthmus mapping during recurrent flutter indicates slow conduction through gaps of recovered conduction of varying dimensions in the ablation line followed by a curved front of activation antidromically activating its downstream flank, this detour producing wide double potentials on the line.

Propagation Delays Across Cardiac Gap Junctions and their Reflection in Extracellular Potentials: A Simulation Study

Propagation Delays and Extracellular Potentials. There is increasing evidence that the complex microscopic structure of the myocardium (distribution of cell‐to‐cell connections) plays an important role in determining propagation of excitation in cardiac muscle. To study this phenomenon, extracellular potentials must be measured with microscopic spatial resolution in cardiac tissue. In this article, the relationships between propagation delays across cardiac gap junctions and extracellular potential waveforms are analyzed using a one‐dimensional model of a propagating action potential, for different degrees of cellular coupling. The central question addressed by this study is whether propagation discontinuities at the cellular level can be detected by microscopic resolution extracellular potential measurements, and whether the discrete junctional propagation delay can be measured by extracellular electrodes. Results demonstrate that the discontinuous nature of propagation at the cellular level is reflected as nonuniformities in the local (microscopic) conduction velocity measured by extracellular electrodes with microscopic resolution (interelectrode distance of 50 μm); the degree of nonuniformities in the microscopic velocity is amplified as a result of decreased cellular coupling. These observations are in agreement with recent experimental findings. Propagation time between the middle regions of adjacent cells can be estimated accurately from extracellular potentials at these sites. In contrast, two extracellular electrodes positioned at opposite ends of the gap junction (electrode spacing of 5 μm) cannot detect or measure the propagation delay across the junction. This limitation results from the fact that extracellular potentials do not reflect only the localized underlying electrical sources on such a microscopic scale. As cells become less coupled, irregularities appear in the unipolar extracellular potential waveforms. The simulations relate these irregularities to depolarization of individual cells in the fiber. Under the condition of reduced cellular coupling, the depolarization events of neighboring cells are sufficiently separated in time to appear as separate events in the extracellular waveforms.

Oscillations of conduction, action potential duration, and refractoriness. A mechanism for spontaneous termination of reentrant tachycardias.

The mechanism of cycle length oscillation and its role in spontaneous termination of reentry was studied in an in vitro preparation of canine atrial tissue surrounding the tricuspid orifice. Reentry occurred around a fixed path with incomplete recovery of excitability. Among 18 experiments, there was complete concordance between the occurrence of spontaneous cycle length oscillation and spontaneous terminations; both were observed in 10 experiments and neither in the other eight (p less than 0.001). Local changes in conduction during oscillations resulted from the dependence of both conduction velocity and action potential duration on the preceding local diastolic interval. Interval-dependent changes in action potential duration contributed to the oscillation by altering the next diastolic interval. Because of changes in action potential duration, changes in cycle length were poorly correlated with changes in diastolic interval and, therefore, with local conduction velocity. Complex oscillations resulted from variations in conduction time at multiple sites in the circuit. Oscillations caused most spontaneous terminations. The critical event was an exceptionally long diastolic interval preceding the next-to-last cycle that accelerated local conduction (which tended to shorten the last cycle) and prolonged action potential duration and refractoriness at the site of block. Ninety-two of 99 recordings of spontaneous termination showed evidence of oscillation of conduction and refractoriness causing block.