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Effect of the left ventricular overload on epicardial repolarization in the rabbit.

ABSTRACT

Objective: We have investigated the local durations and sequence of repolarization in the ventricular epicardium in the rabbit under the increase of the left ventricular (LV) afterload.

Methods: The LV overload was produced by the 1-minute aortic stenosis up to systolic blood pressure of 140 mm Hg. The experiments were carried out on eight anaesthetized rabbits (urethane, 1.5 g/kg, ip). Unipolar electrograms were simultaneously recorded from 64 ventricular epicardial leads at 33[degrees]C.

Results: At baseline state, the shortest activation-recovery intervals (ARIs) were observed in the right ventricular (RV) base, the longest ARIs in the LV apex and lateral wall, and ARIs of intermediate durations in the RV apex and LV base. According to ARI distribution, a significant gradient in repolarization times was observed between the apex and base (p<0.01). Under acute LV overload, the repolarization duration increased significantly (p<0.01) locally at the LV apex and adjacent area of the free wall. Dispersion of repolarization is increased in the apex. A decrease of ARIs (p<0.05) was observed at the RV base, as well.

Conclusion: Under acute increase in the LV afterload, ventricular epicardial activation sequence remained largely unaltered which, along with changes in local repolarization durations, resulted in the repolarization sequence being quite similar to the baseline one. The earliest repolarization occurred in posterobasal region of RV whereas the areas over the LV apex and adjacent area of the free wall were the last to repolarize. (Anadolu Kardiyol Derg 2007: 7 Suppl 1; 93-4)

Key words: heart ventricle, recovery sequence, aortic stenosis, rabbit

Introduction

The conditions of mechanical contraction of the heart influence the myocardial electrical processes by a phenomenon termed mechano-electrical feedback. The experimental studies provide in part contradictory findings suggesting that ventricular overload leads to the changes in action potential duration: Franz et al (1) showed, that the myocardial stretching caused the abbreviation of monophasic action potential duration and the reduction of refractoriness, whereas Kim (2) demonstrated the increase in the duration of monophasic action potentials. The majority of studies has been done on single myocardial areas of the isolated heart preparations. The data on the comparison of the responses of the different left ventricular (LV) and right ventricular (RV) regions to the LV overload in in situ heart are lacking. Such data may provide further insight into the arrhythmogenic mechanisms operating under the ventricular overload.

The objective of the present investigation was to study the local durations and sequence of repolarization in the ventricular epicardium in the rabbit under the increase of the LV afterload in situ.

Methods

The experiments were carried out on eight anaesthetized rabbits (urethane, 1.5 g/kg, ip). The animals were ventilated artificially. The heart was exposed through median sternotomy. For the recording of electric potentials, a sock with 64 electrodes was placed on heart ventricles. Unipolar electrograms were simultaneously recorded from 64 ventricular epicardial leads at spontaneous sinus rhythm at 33[degrees]C. The LV overload was produced by the 1-minute aortic stenosis up to systolic blood pressure of 140 mm Hg. Activation time, repolarization time, and activation-recovery interval (ARI) as a marker of local repolarization duration, were determined in each epicardial lead as the minimum of the potential time derivative during the QRS, maximum of the potential time derivative during ST-T, and the period between the two, respectively. Corrected ARIs were calculated as: ARIc=ARI / RR1/2 The time measurements were made with respect to the QRS onset in the limb I lead. Statistical estimations were done using Student's paired t-test. The difference was considered significant at p<0.05.

Results

In the ventricular epicardium, the earliest activation occurred in the middle anterior-lateral area of RV. In 3 ms after the detection of primary excitation, an additional independent locus of early activation was observed in the LV apex of a free wall. Further, the wave of excitation spread to the RV surface and the middle part of anterior and posterior LV surfaces (4-6 ms). In 7-8 ms, depolarization traveled to the lateral LV surface and the RV base. At last (12-14 ms), the LV base was depolarized. Generally, the spread of the depolarization wave has two directions: from the apex to the base and from the septum to the free wall. In LV overload, there were no significant changes of the ventricular epicardial activation pattern.

At the baseline state, the shortest ARIs were observed in the RV base and the longest ARIs--in the heart apex (p<0.0002). Repolarization durations increased in the following order: 1) RV base 2) LV base, RV lateral surface, 3) LV lateral surface, 4) heart apex. Under acute LV overload, the distribution of local repolarization durations was rather similar to the baseline with the shortest ARIs being also observed in the base, and the longest ones in the apical area (p<0.01). However, the repolarization duration significantly increased locally at the apex and adjacent area of the LV free wall (7%, p<0.05), whereas a decrease in the ARIs (10%, p<0.05) was observed at the RV base. The local ARI dispersion (measured as the longest ARI--the shortest ARI) in the heart apex increased from 30 [+ or -] 10 ms at baseline to 73 [+ or -] 26 ms at the LV overload (p<0.05) indicating the development of potential arrhythmogenic conditions. The overall ventricular epicardial ARI dispersion did not change significantly at LV overload. Since under overload ventricular epicardial activation sequence remained largely unaltered, along with the changes in local repolarization durations, aggravating the preexistent differences in the repolarization durations, the repolarization sequence under the increase of the LV afterload was similar to the baseline one with the earliest repolarization being in the posterobasal region of RV and the latest repolarization in the lateral surface and the apex of the LV. Repolarization times of intermediate magnitude occurred in the LV base and in the RV free wall.

Discussion

The present study demonstrated that the LV overload induced the heterogeneous changes in repolarization durations in the ventricular epicardium: the LV apical ARIs increased whereas the RV basal ARIs decreased. The prolongation of repolarization in the apical area was associated with the local increase in ARI dispersion.

The data concerning ventricular repolarization under various loading conditions obtained by different authors are conflicting. In the isolated rabbit heart preparations, Reiter et al (3) found that the increase of the LV volume resulted in the abbreviation of the LV effective refractory periods which was the most pronounced in the apical area. Similarly, Taggart et al (4) reported the reduction of the duration of monophasic action potentials under the increase of the LV volume and pressure in humans. In contrast, Benditt et al (5) demonstrated prolonged LV epicardial and endocardial effective refractory periods as a result of aortic occlusion in dogs in situ. The data of the present study suggest that the changes of repolarization duration in response to the LV overload in the LV and RV epicardial sites can be of opposite directions.

The overload of heart chambers is strongly associated with arrhythmias (6). The results of the present investigation provide evidences for two related potential arrhythmogenic mechanisms. On the one hand, prolonged repolarization durations found at the LV apex and adjacent areas under LV overload may provoke early afterdepolarizations. On the other hand, the local prolongation of ARIs at the apex produced sharp repolarization heterogeneities in the apical area of the LV, resulted in the increased dispersion of repolarization exacerbating by the shortening of ARIs in the RV base that predisposes reentrant arrhythmias. Although we did not observe an increase in the overall dispersion of repolarization, this may be the case for the larger hearts, such as human one, due to the lower electrotonic cancellation of repolarization inhomogeneities in large myocardial volumes (7).

References

(1.) Franz MR, Burkhoff D, Yue DT, Sagawa K. Mechanically induced action potential changes and arrhythmia in isolated and in situ canine hearts. Cardiovasc Res 1989; 23: 213-23.

(2.) Kim D. Novel cation-selective mechanosensitive ion channel in the atrial cell membrane. Circ Res 1993; 72: 225-31

(3.) Reiter MJ, Synhorst DP, Mann DE. Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart. Circ Res 1988; 62: 554-62.

(4.) Taggart P, Sutton P. Cardiac mechano-electric feedback in man: clinical relevance. Progr Biophys & Mol Biol 1999; 71: 139-54.

(5.) Benditt DG, Kriett JM, Tobler HG, Gornick CC, Detloff BL, Anderson RW. Electrophysiological effects of transient aortic occlusion in intact canine heart. Am J Physiol 1985; 249: H1017-23.

(6.) Hansen DE, Craig CS, Hondeghem LM. Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. Circulation 1990; 81: 1094-105.

(7.) Sampson KJ, Henriquez CS. Electrotonic influences on action potential duration dispersion in small hearts: a simulation study. Am J Physiol Heart Circ Physiol 2005; 289: H350-60.

Ksenia Sedova, Vladimir Vityazev, Jan Azarov, Dmitry Shmakov

Institute of Physiology, Komi Science Center, Ural Division, Russian Academy of Sciences, Syktyvkar, Komi, Russia

Address for Correspondence: Ksenia Sedovia, Institute of Physiology, Komi Science Center, Ural Division, Russian Academy of Sciences, 50 Pervomayskaya st, Syktyvkar, 167000 Komi Republic, Russia E-mail: ksenya_nastya@mail.ru
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Article Details
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Title Annotation:Original Investigation
Author:Sedova, Ksenia; Vityazev, Vladimir; Azarov, Jan; Shmakov, Dmitry
Publication:The Anatolian Journal of Cardiology (Anadolu Kardiyoloji Dergisi)
Article Type:Clinical report
Geographic Code:4EXRU
Date:Jul 1, 2007
Words:1520
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