A. Bardou

Reduction of Energy Required for Defibrillation by Delivering Shocks in Orthogonal Directions in the Dog

Reduction of energy required to defibrillate (ERD) seems to represent a necessary condition for intensive development of implantable defibrillator, so as for minimization of cardiac and pulmonary damages provoked by high energy transthoracic defibrillation electric shocks. The present work describes a defibrillation method using shocks delivered in orthogonal directions and separated by a 100 ms delay. Defibrillation threshold measured with classical unidirectional shocks on 30 dogs has been found to be 286.8 ± 22.2 joules. In the same animals, defibrillation threshold measured by use of orthogonal shocks has been found to be 101.4 ± 14.9 joules. We conclude that this crossed shocks method leads to a substantial reduction of ERD (64%).

EFFECTS OF LOCAL ISCHEMIA AND TRANSIENT CONDUCTION BLOCKS ON THE INDUCTION OF CARDIAC REENTRIES

The present work is aimed at investigating the effects of ischemia and transient blocks on induction of ventricular fibrillation. Electrophysiologic effects of local ischemia induced by minor myocardial infarction (variation of the dispersion of refractory periods as well as conduction velocity) on initiation of reentry mechanisms were studied by means of computer simulations based on a cellular automata model of propagation of activation wave through a ventricular surface element. A local ischemic area was simulated, showing that altered refractoriness can facilitate initiation of reentry phenomena. The probability of reentries is a function of the size of ischemic zone and of the spatial rate of dispersion of refractory periods. Our results show that the dispersion of refractoriness is an important parameter in triggering cardiac reentries. Above a threshold value of dispersion, even very small ischemic zones can induce spiral waves. We also study the effects of transient conduction blocks on reentries....

Effect of myocardial infarction and ischemia on induction of cardiac reentries and ventricular fibrillation

The present work is aimed at investigating the effects of myocardial infarction and ischemia on induction of ventricular fibrillation. Electrophysiologic effects of global and local ischemia (variation of the dispersion of refractory periods as well as conduction velocity) on initiation of reentry mechanisms was studied by means of computer simulations based on a cellular automata model of propagation of activation wave through a ventricular surface element. A local area of ischemia where effects of the dispersion of refractory periods are investigated is then simulated. This is made using a Gaussian distribution characterized by its mean and standard deviation. These simulations show that ischemia is capable of initiating reentry phenomena which propagate through the whole ventricle; they are responsible for ventricular fibrillation which causes sudden cardiac death, even when ischemia only involves limited parts of the myocardium. Statistical study of the probability of reentries as a function of both of the size of ischemic zones and the rate of dispersion of refractory periods shows that the latter parameter is of primary importance in triggering cardiac reentries.

Computer simulation of defibrillating electric shocks: critical mass

Computer simulations of the propagation of depolarizing waves through the ventricular wall based on the Huygens principle are presented. Permanent troubles induced by unidirectional blocks are simulated. A critical size of a unidirectional block required in order to trigger a reentry for normal and ischemic tissues is calculated. The influence of anisotropic conduction on the initialization of reentries is also studied. It is shown that the reentry is favored when the unidirectional block is perpendicular to the direction of heart fibers. Electric shocks applied to the ventricle are simulated. Once a permanent trouble is initialized, an electric shock with a given percentage of depolarized cells is applied. The simulations show that in order to be sure that the reentry has been stopped, one must apply an electric shock with 100% depolarized cells. A very few nondepolarized cells are able to reinitialize several secondary reentries.<<ETX>>

Initiation of ventricular fibrillation caused by cellular coupling modifications a computer simulation study

In this work, the authors investigate a mechanism which can generate multiple reentries. They use computer simulations based on the Van Capelle and Durrer (VCD) model. This model allows to describe the propagation of the depolarizing wave through the ventricle. A 128/spl times/128 matrix is used to simulate muscle layer of the ventricular wall. The authors study the influence or a random increase of the coupling resistance between cells on the patterns of the wave propagation. They consider aggregates of cells which are randomly distributed along the ventricular wall. Computer simulations show that reentries can be initiated by this process. For a given distribution of aggregates, random changes in coupling resistances may lead to major variations of the patterns or the reentries: from ventricular tachycardia to more complex patterns which could correspond to fibrillation.

Role of the dispersion of refractoriness on cardiac reentries.

We used computer simulation to study the possible role of the dispersion of cellular coupling, refractoriness or both, in the mechanisms underlying cardiac arrhythmias. Local ischemia was first assumed to induce cell to cell dispersion of the coupling resistance (case 1), refractory period (case 2), or both (case 3). Our numerical experiments based on the van Capelle and Durrer model showed that vortices could not be induced. On the other hand, with cellular properties dispersed in a patchy way within the ischemic zone, a single activation wave could give rise to abnormal activities. This demonstrates the stability of the wave front under small inhomogeneities. Probabilities of reentry, estimated for the three cases cited above showed that a severe alteration of the coupling resistance may be an important factor in the genesis of reentry. Moreover, use of isochronal maps revealed that vortices were both stable and sustained with an alteration of the coupling alone or along with a reduction of the action potential duration. Conversely, simulations with reduction of the refractoriness alone, inducing only transient patterns, could exhibit functionally determined reentries.

THEORETICAL STUDY BY MEANS OF COMPUTER SIMULATION OF CONDITIONS IN WHICH EXTRASYSTOLES CAN TRIGGER VENTRICULAR FIBRILLATION. VALIDATION BY EPICARDIAL MAPPINGS

A cellular automata model of ventricular activation wave propagation has been developed in order to study the mechanisms of ventricular fibrillation induction. A 256X256 matrix is used to simulate a muscle layer in the ventricular wall. Huyghens’ construction method is used in order to compute the wave front position instant by instant. In this work, this model is specifically applied to the study of relationships between extrasystoles and sudden cardiac death. This theoretical study shows that if a ventricular extrasystole is initiated in contiguity of transitory block zone, it immediately initiates a rotating wave invading the entire myocardium, this rotating wave being self-sustained and not spontaneously reversible. Experimental validation derived from cardiac mapping experiments performed in canine preparations of myocardial infarction showed that an extrasystole induced by electrical stimulation in the neighbourhood of zone of temporary block induced by lidocaine is able to trigger a reentry phenomenon similar to that obtained with the computer model. These results provide evidence that transient fluctuations in refractoriness is a major risk factor when combined with ventricular extrasystole. Furthermore, it appears that this risk factor may be amplified under ischemic conditions and pharmacologic interventions aimed at suppressing ventricular extrasystoles (e.g., lidocaine).

Stimulation threshold of isolated myocytes and cross shock defibrillation

Results of a previous study suggested the possible dependence of heart-fiber stimulation threshold on the stimulus electric axis orientation. The aim of this work has been to demonstrate this phenomenon on isolated cardiomyocytes. The cells were placed in a culture box where they appeared spontaneously arranged along multiple directions. Stimulation pulses were delivered between two parallel electrodes, increasing progressively in intensity until the cells contracted. This contraction was always obtained for the most longitudinally stimulated myocytes first. Progressive recruitment was then observed by increasing the intensity, the most perpendicular myocyte contraction being obtained for a value approximately double that necessary to stimulate the longitudinal ones. This clearly shows that orthogonal shocks depolarize all heart fibers using the lowest energy required.<<ETX>>

Study of relations between arterial oscillation period and heart rate

SummaryThis study was performed to determine the relationship between variations of arterial cross-section and cardiac period. Relative section variations were recorded by impedance rheography. In 176 anesthetized adult mongrel dogs, aortic and femoral rheograms, femoral pressure, and ECG were recorded. The cardiac period (Tc) and the interval between the systolic and the dicrotic wave, i.e., the arterial intrinsic period (Ta), were measured and related to each other (Tc/Ta ratio). In 125 dogs, the dicrotic wave appeared spontaneously. In these cases Tc/Ta 1.98±0.16. In 51 dogs, no dicrotic wave appeared spontaneously. Lenghtening of cardiac period was obtained in 25 of these dogs by vagus stimulation. As related to the cardiac period before vagal stimulation Tc/Ta was then 0.98±0.08. In the remaining 26 dogs, such a lengthening was obtained by inducing a premature ventricular depolarization. In this group, Tc/Ta was 1.00±0.03. The results of the present study suggest that a constant adaptation exists between ventricular ejection and arterial dynamics. The physiologic implications are discussed.

Isopotential and isochronal epicardial mapping during external cardiac pacing in dogs

To investigate cardiac entrainment by external pacing, ventricular epicardial mapping was performed in dogs with atrio-ventricular block. Isopotential maps recorded with 128 unipolar leads during the stimulation artifacts showed that the electrical field was little affected by the electrode type and depended mostly on the electrode position. An antero-posterior electrode pair produced a reproducible and uniform apex-to-base potential gradient which induced activation sequences showing inter-individual differences: the areas of initial activation tended to remain the same in each dog (e.g., apical, apico-lateral, antero-septal) despite changes in the stimulation protocol. Inverting the polarity of the current did not change the site of origin of activation (81% remained the same). Increasing the current intensity from 99 to 120 mA, decreased the total epicardial activation time from 86/spl plusmn/16 to 61/spl plusmn/16 ms (p<0.05). In conclusion, this preliminary study indicates that epicardial mapping may provide useful information about the cardiac response to external pacing.<<ETX>>