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Biomedical subjects

A M Pertsov

Publications and source records attributed to A M Pertsov.

At least 37 records · Page 2Linked to original sources
PubMed1995

Effects of pacing on stationary reentrant activity. Theoretical and experimental study.

It is well known that electrical pacing may either terminate or change the rate and/or ECG appearance of reentrant ventricular tachycardia. However, the dynamics of interaction of reentrant waves with waves initiated by external pacing are poorly understood. Prevailing concepts are based on simplistic models in which propagation occurs in one-dimensional rings of cardiac tissue. Since reentrant activation in the ventricles occurs in two or three dimensions, such concepts might be insufficient to explain the mechanisms of pacing-induced effects. We used numerical and biological models of cardiac excitation to explore the phenomena, which may take place as a result of electrical pacing during functionally determined reentry. Computer simulations of a two-dimensional array of electrically coupled FitzHugh-Nagumo cells were used to predict the response patterns expected from thin slices of sheep ventricular epicardial muscle, in which self-sustaining reentrant activity in the form of spiral waves was consistently initiated by premature stimulation and monitored by means of video mapping techniques. The results show that depending on their timing and shape, externally induced waves may collide with the self-sustaining spiral and result in one of three possible outcomes: (1) direct annihilation of the spiral, (2) multiplication of the spiral, or (3) shift of the spiral center (ie, core). Multiplication and shift of the spiral core were attended by changes in rate and morphology of the arrhythmia as seen by "pseudo-ECGs." Furthermore, delayed termination (ie, termination of the activity one to three cycles after the stimulus) occurred after both multiplication and shift of the spiral center. Both numerical predictions and experimental results support the hypothesis that whether a pacing stimulus will terminate a reentrant arrhythmia or modify its ECG appearance depends on whether the interactions between the externally induced wave and the spiral wave result in the de novo formation of one or more "wavebreaks." The final outcome depends on the stimulus parameters (ie, position and size of the electrodes and timing of the stimulus) as well as on the position of the newly formed wavebreak(s) in relation to that of the original wave.

Acceleration↗
PubMed1994

Wave-front curvature as a cause of slow conduction and block in isolated cardiac muscle.

We have investigated the role of wave-front curvature on propagation by following the wave front that was diffracted through a narrow isthmus created in a two-dimensional ionic model (Luo-Rudy) of ventricular muscle and in a thin (0.5-mm) sheet of sheep ventricular epicardial muscle. The electrical activity in the experimental preparations was imaged by using a high-resolution video camera that monitored the changes in fluorescence of the potentiometric dye di-4-ANEPPS on the surface of the tissue. Isthmuses were created both parallel and perpendicular to the fiber orientation. In both numerical and biological experiments, when a planar wave front reached the isthmus, it was diffracted to an elliptical wave front whose pronounced curvature was very similar to that of a wave front initiated by point stimulation. In addition, the velocity of propagation was reduced in relation to that of the original planar wave. Furthermore, as shown by the numerical results, wave-front curvature changed as a function of the distance from the isthmus. Such changes in local curvature were accompanied by corresponding changes in velocity of propagation. In the model, the critical isthmus width was 200 microns for longitudinal propagation and 600 microns for transverse propagation of a single planar wave initiated proximal to the isthmus. In the experiments, propagation depended on the width of the isthmus for a fixed stimulation frequency. Propagation through an isthmus of fixed width was rate dependent both along and across fibers. Thus, the critical isthmus width for propagation was estimated in both directions for different frequencies of stimulation. In the longitudinal direction, for cycle lengths between 200 and 500 milliseconds, the critical width was < 1 mm; for 150 milliseconds, it was estimated to be between 1.3 and 2 mm; and for the maximum frequency of stimulation (117 +/- 15 milliseconds), it was > 2.5 mm. In the transverse direction, critical width was between 1.78 and 2.32 mm for a basic cycle length of 200 milliseconds. It increased to values between 2.46 and 3.53 mm for a basic cycle length of 150 milliseconds. The overall results demonstrate that the curvature of the wave front plays an important role in propagation in two-dimensional cardiac muscle and that changes in curvature may cause slow conduction or block.

Animals↗
PubMed1993

Spiral waves of excitation underlie reentrant activity in isolated cardiac muscle.

The mechanism of reentrant ventricular tachycardia was studied in computer simulations and in thin (approximately 20 x 20 x 0.5-mm) slices of dog and sheep ventricular epicardial muscle. A two-dimensional matrix consisting of 96 x 96 electrically coupled cells modeled by the FitzHugh-Nagumo equations was used to analyze the dynamics of self-sustaining reentrant activity in the form of elliptical spiral waves induced by premature stimulation. In homogeneous anisotropic media, spirals are stationary and may last indefinitely. However, the presence of small parameter gradients may lead to drifting and eventual termination of the spiral at the boundary of the medium. On the other hand, spirals may anchor and rotate around small discontinuities within the matrix. Similar results were obtained experimentally in 10 preparations whose electrical activity was monitored by means of a potentiometric dye and high-resolution optical mapping techniques; premature stimulation triggered reproducible episodes of sustained or nonsustained reentrant tachycardia in the form of spiral waves. As a rule, the spirals were elongated, with the major hemiaxis parallel to the longitudinal axis of the cells. The period of rotation (183 +/- 68 msec [mean +/- SD]) was longer than the refractory period (131 +/- 38 msec) and appeared to be determined by the size of the spiral's core, which was measured using a newly devised "frame-stack" plot. Drifting of spiral waves was also observed experimentally. Drift velocity was 9.8% of the velocity of wave propagation. In some cases, the core became stationary by anchoring to small arteries or other heterogeneities, and the spiral rotated rhythmically for prolonged periods of time. Yet, when drift occurred, spatiotemporal variations in the excitation period were manifested as a result of a Doppler effect, with the excitation period ahead of the core being 20 +/- 6% shorter than the excitation period behind the core. As a result of these coexisting frequencies, a pseudoelectrocardiogram of the activity in the presence of a drifting spiral wave exhibited "QRS complexes" with an undulating axis, which resembled those observed in patients with torsade de pointes. The overall results show that spiral wave activity is a property of cardiac muscle and suggest that such activity may be the common mechanism of a number of monomorphic and polymorphic tachycardias.

Animals↗
PubMed1992

Spatiotemporal irregularities of spiral wave activity in isolated ventricular muscle.

Voltage-sensitive dyes and high resolution optical mapping were used to analyze the characteristics of spiral waves of excitation in isolated ventricular myocardium. In addition, analytical techniques, which have been previously used in the study of the characteristics of spiral waves in chemical reactions, were applied to determine the voltage structure of the center of the rotating activity (ie, the core). During stable spiral wave activity local activation occurs in a periodic fashion (ie, 1:1 stimulus: response activation ratio) throughout the preparation, except at the core, which is a small elongated area where the activity is of low voltage and the activation ratio is 1:0. The voltage amplitude increases gradually from the center of the core to the periphery. In some cases, however, regular activation patterns at the periphery may coexist with irregular local activation patterns near the core. Such a spatiotemporal irregularity is attended by variations in the core size and shape and results from changes in the core position. The authors conclude that functionally determined reentrant activity in the heart may be the result of spiral waves of propagation and that local spatiotemporal irregularities in the activation pattern are the result of changes in the core position.

Animals↗
PubMed1991

Vagally induced depression of impulse propagation as a cause of atrial tachycardia.

It is known that parasympathetic influence favors induction of re-entrant atrial tachycardias (ATs). This effect is usually interpreted as a result of inhomogeneous shortening of atrial refractoriness leading to increased probability of circus movement following a premature impulse. However, early microelectrode studies showed that in spontaneously beating isolated frog atria, intensive vagal stimulation (VS) induced paroxysms of rapid AT in the absence of myocardial extrastimulation. This AT was found to correlate with inexcitability of some of the impaled fibers of the atria. It was supposed that temporary, vagally induced, inexcitable areas of the atria could lead to re-entry, serving as a site of unidirectional conduction. This hypothesis was recently evaluated by direct multielectrode mapping of excitation sequence during vagally induced AT in frog atria. Recording from 32 sites with a spatial resolution of 1-2 mm clearly showed that the AT was due to re-entry. The ATs were always preceded by vagally induced depression of conduction, with some areas of the atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner. The re-entrant AT was initiated when a sinus impulse arrived during a certain phase of the recovery. Unlike the well-known mechanism of re-entry, which is based on inhomogeneous refractoriness and extrabeat(s), the re-entrant AT in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.

Animals↗
PubMed1991

[Isolated right ventricle after coronary perfusion as a model for the study of ischemic and reperfusion-induced arrhythmia in rats].

A catheter through which perfusion was performed with oxygenated saline (2.1 ml/min) was introduced into the right coronary artery ostium of the rat right ventricle that had been isolated during cardioplegia. Super perfusion (12 ml/min) was simultaneously made. Termination of the perfusion caused arrhythmias at minutes 6 to 28 of ischemia. The highest likelihood of occurrence of such arrhythmias was observed on minutes 16-20 (premature beats being seen in 86% of the experiments, extrastimulus-induced tachycardias in 75%, spontaneous tachycardias in 25%). Reperfusion was made at 3, 5, 7, 10, 13, 15, 20, 30 and 60 min following ischemia (n = 7 in each case). The occurrence of reperfusion arrhythmias is likely to be related to the duration of ischemia with the highest likelihood of 20 minutes after ischemia (tachycardia and fibrillation were observed in 100 and 71%, respectively).

Animals↗
PubMed1990

[Effects of lidocaine on intramural circulation in isolated rabbit heart ventricle preparations].

Mapping was used on isolated rabbit ventricular specimens to study effects of lidocaine, 2-8 mg/l, on persistent intramural reentry involving the areas of slow transmural conduction. The agent was shown to produce antiarrhythmic and arrhythmogenic effects at the same time. Lidocaine reduced the duration of an arrhythmia, but provoked its initiation. Both these effects of lidocaine were attributable to its action on the refractory period of a slow transmural conduction area.

Animals↗
PubMed1989

Vagally induced block and delayed conduction as a mechanism for circus movement tachycardia in frog atria.

Episodes of tachycardia induced by strong vagal stimulation in spontaneously beating isolated atria of frog (Rana temporaria) were studied with multielectrode mapping technique. These episodes were inducible in 19 of 39 preparations. The arrhythmia started several seconds after cessation of vagal stimulation strong enough to cause sinus arrest, without electrical stimulation of the myocardium. The arrhythmia consisted of two to 20 beats (6 +/- 4, mean +/- SD, n = 42) with a cycle length of 100-500 msec. Recording from 32 sites with spatial resolution of 1-2 mm showed that the arrhythmia was due to intra-atrial circus movement. The estimated perimeter of the reentrant circuit ranged from 6 to 20 mm. In circuits of the minimal size, the average conduction velocity along the circuit was as low as 2-3 cm/sec. Paroxysms of the tachycardia were always preceded by vagally induced nonuniform depression of conduction, with some areas of atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner, their unblocking being significantly (p less than 0.05) delayed after inhibition of tissue cholinesterase by proserine. The reentrant tachycardia was initiated when a sinus impulse arrived during certain phase of the unblocking. Unlike the well-known mechanism of reentrant excitation, which is based on inhomogeneous refractoriness and critically timed extrabeat(s), the circus movement in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.

Animals↗
PubMed1989

[Study of excitation circulation around an unexcitable myocardial obstacle].

An experimental model of tachy-arrhythmias due to myocardial excitation wave circulation round an unexcitable obstruction was explored. Artificial openings of various sizes and shapes in an isolated rabbit left atrium posed as obstacles. Acetylcholine, having a potent effect on the refractory period of atrial cells, was used to alter refractory characteristics. It has been demonstrated that differences in the sensitivity to the action of pharmacologic agents on both re-entry types can actually be absent. Acetylcholine is shown to shorten the period of circulation round the hole, i.e. act on such circulation in the same fashion as it does on the leading cycle, in a wide range of hole diameters, approaching the ones comparable with the size of the atrium. Sensitivity to acetylcholine only disappears when a labyrinth is set up with artificially prolonged circulation pathway. The action of acetylcholine can be attributed to the absence of tissue with fully recovered excitability between the anterior and posterior fronts of the wave circulating round the obstacle.

Acetylcholine↗
PubMed1989

[Study of spontaneous acetylcholine-dependent tachyarrhythmias using isolated specimens of the right canine atrium by bilateral mapping of the spread of excitation].

The authors examined tachycardias induced by administering acetylcholine (AC), 1-2 micrograms into the artery of sinus node (ASN) of an isolated specimen of the canine right atrium, which had spontaneous automatism. Bilateral multielectrode mapping was employed. The episodes of tachycardia occurred during AC-induced arrest of sinus rhythm. In 81% of the cases, episodes of arrhythmia consisted of 2-3 beats, in 19%, 6-150 beats. The mapping revealed a focal picture of activation during short-term episodes of arrhythmia and transition from a focal type of activation to the re-entry in most cases of "prolonged" episodes. With this, excitation circulation might be detected only on one side of the specimen, in the presence of the focal activation picture, on the other. Focus-re-entry transition is proposed to be caused by a mechanism associated with heterogeneous refractoriness of atrial tissue.

Acetylcholine↗
PubMed1988

[The mechanism of the development of atrial tachyarrhythmia after stimulation of the vagus nerve].

Multielectrode mapping of stimulus propagation was used to investigate arrhythmias, developing in atrial preparations of frogs after vagal stimulation. Vagal stimulation produced attacks of tachycardia (one to several dozens extra-excitations) in 10 of 16 specimens. In such cases, mapping demonstrated re-entry of the excitation wave that appeared where the front of the next excitation wave from the sinus went along the border of temporarily-unexcitable area during the recovery of excitability in vagus-inhibited atrial areas. The emergence of re-entry was possible, because the excitation wave length (lambda), was shortened owing to reduced refraction and speed of conduction under vagal effect. After myocardial tissue got rid of vagal influence, lambda increased, after which re-entry was no longer possible, and arrhythmia discontinued.

Animals↗
PubMed1987

[3-dimensional reentry in paroxysmal ventricular tachycardias: the results of electrophysiological mapping].

The mechanism of sustained ventricular tachycardias with a focal type of activation initiated by an extrastimulus was studied in isolated rabbit heart ventricle preparations by endocardial and epicardial mapping. Sixty-four electrograms were simultaneously recorded using unipolar electrodes (32 on each side of the preparation). The electrodes were spaced 3 mm apart. Data recording and processing were computerized. Sustained (greater than 0.5 min) tachycardias of a focal type were registered in 6 of 17 experiments. In each case, the three-dimensional macro-reentry mechanisms was involved. The closed circuit was around the intramural ischemic zone resulting from impairment of coronary circulation. Endocardial and epicardial points of early activation occurred at the sites where the wave passed from one surface to another.

Animals↗
PubMed1985

[Cold-induced arrhythmias in the isolated rabbit atrium studied by mapping].

Arrhythmias developing in isolated rabbit atria following the cooling of the perfusion solution were studied by multielectrode mapping. In 10 out of the 12 initially invulnerable preparations, the cooling to 27 +/- +/- 0.7'C induced arrhythmias. The effect was reversible, disappearing with the temperature normalization. Mapping showed that in 60% of the cases the arrhythmias were caused by the emergence of the leading cycles (functionally determined re-entry). In 40% of the cases, the re-entry was not demonstrable by mapping. However, arrhythmias in these experiments developed at the same temperature and had the same period as the leading cycles. The appearance of arrhythmias was closely correlated with a decrease in the wave length which strongly suggests the re-entry mechanism of hypothermic arrhythmias.

Animals↗