Effect of atrial artificial electrical stimulation on depolarization and repolarization and hemodynamics of the heart ventricle in rainbow trout Oncorhynchus mykiss.

The spatial-temporal organization of the activation, repolarization and hemodynamics of the heart ventricle in rainbow trout, Oncorhynchus mykiss, adapted to a temperature of 5-7 °C, were studied from the normal sinus rhythm (21.6 ± 4.9 bpm) to the highest possible heart rhythm (HR) (60 bpm), during which deterioration of the contractile activity of the myocardium occurred. Regardless of the HR, the main pattern of excitation of the heart ventricle was the movement of the depolarization wave from the dorsal areas of the base in the base-apical and ventral directions with the capture of the entire thickness of the walls, with a slight difference in the time of activation of the subendocardium compared to the subepicardium. The increase in HR above the sinus rhythm caused significant shortening of local repolarization durations in all areas and layers (endocardial, intramural and subepicardial) of the heart ventricle. Changes in local durations of repolarization led to an increase in the heterogeneity of repolarization of the ventricular myocardium; as a result, a deterioration of its contractility was observed. In relation to the sinus rhythm, the maximal systolic pressure in the heart ventricle decreased, the diastolic and end-diastolic pressure increased, and the maximum rates of pressure rise and fall decreased. In rainbow trout adapted to a temperature of 5-7 °C at sinus rhythm, the pumping function of the heart was probably within the upper limit of the physiological norm, and a further increase in the heart rate led to a decline in myocardial contractility.

Repolarization in perfused myocardium predicts reperfusion ventricular tachyarrhythmias.

BACKGROUND: Aim of the study was to find out which myocardial repolarization parameters predict reperfusion ventricular tachycardia and fibrillation (VT/VF) and determine how these parameters express in ECG. METHODS: Coronary occlusion and reperfusion (30/30min) was induced in 24 cats. Local activation and end of repolarization times (RT) were measured in 88 intramyocardial leads. Computer simulations of precordial electrograms were performed. RESULTS: Reperfusion VT/VF developed in 10 animals. Arrhythmia-susceptible animals had longer RTs in perfused areas [183(177;202) vs 154(140;170) ms in susceptible and resistant animals, respectively, P<0.05]. In logistic regression analysis, VT/VFs were associated with prolonged RTs in the perfused area (OR 1.068; 95% CI 1.012-1.128; P=0.017). Simulations demonstrated that prolonged repolarization in the perfused/border zone caused precordial terminal T-wave inversion. CONCLUSIONS: The reperfusion VT/VFs were independently predicted by the longer RT in the perfused zone, which was reflected in the terminal negative phase of the electrocardiographic T-wave.

Action potential duration gradients in the heart ventricles and the cardiac electric field during ventricular repolarization (a model study).

BACKGROUND: We simulated contributions of transmural, apicobasal, anteroposterior and interventricular action potential duration (APD) gradients to the body surface potential distribution (BSPD) with constant or varied magnitudes of the transmural and apicobasal gradients. METHODS: Simulations were done in the framework of the discrete computer model of the rabbit heart ventricles on the basis of realistic activation sequence and APDs. The APD gradients were set constant at 20 ms or varied in the range of ±80 ms. RESULTS: The apicobasal, transmural and interventricular APD gradients of 20 ms produced similar BSPDs, whereas the BSPD inversion was caused by the inverted apicobasal or transmural 80 ms gradients. The transmural APD gradient produced transversal and mainly apicobasal T-wave vectors due to wall curvature and cancellation effects. The "normal" transversal and apicobasal repolarization gradients were decreased and increased by activation sequence, respectively. CONCLUSION: The different APD gradients contributed consistently to the development of BSPD.

Doxorubicin-induced changes of ventricular repolarization heterogeneity: results of a chronic rat study.

Anthracycline chemotherapy produces cardiac repolarization abnormalities and arrhythmias because of cardiac toxicity of drugs. Ventricular arrhythmogenesis is attributable to increase in repolarization heterogeneity that is characterized by spatial dispersion of repolarization. The purpose of this work was to study the delayed effects of doxorubicin, the most frequently used anthracycline, on repolarization heterogeneity of the ventricular epicardium. Doxorubicin was administered to rats in a cumulative dose of 15 mg/kg (six equal intraperitoneal injections over a period of 2 weeks). Six weeks after the last injection, electrophysiological mapping of the ventricular epicardium was performed by sequential superimposition of a 64-electrode array on the left ventricular base, left ventricular apex, right ventricular base, and right ventricular apex. Activation-recovery intervals (ARIs) were measured. In doxorubicin-treated rats, ARIs were inhomogeneously prolonged, the overall ARI dispersion and local ARI dispersions were increased, and the interregional differences in ARI dispersion were decreased. These data demonstrate that doxorubicin-induced inhomogeneous prolongation of repolarization of the ventricular epicardium results in increasing heterogeneity of ventricular repolarization because of increasing intraregional heterogeneity while interregional differences are lost. Repolarization of the right ventricle is more sensitive to doxorubicin than that of the left one.

Acute effects of pacing site on repolarization and haemodynamics of the canine ventricles.

AIMS: To determine the repolarization duration gradients in different ventricular regions at atrial and ventricular pacing and to test the hypothesis that acute haemodynamic response to ventricular pacing is related to the lead position with respect to repolarization gradients. METHODS AND RESULTS: Repolarization durations estimated as activation-recovery intervals (ARIs) were measured from unipolar electrograms recorded in the subepicardial (Epi), mid-myocardial (Mid), and subendocardial (Endo) layers of the apical and basal parts of the right ventricle (RV) and left ventricle (LV) of 15 healthy dogs under atrial and ventricular pacing. Cardiac haemodynamic variables were measured as well. At atrial pacing, ARIs were shorter in Epi than in the innermost layers (P< 0.05) in the RV apex and LV base, but not in the LV apex and RV base. Activation-recovery intervals increased from apex to base and from base to apex in RV and LV, respectively (P ≤ 0.05). At apical or basal pacing of RV and LV, repolarization gradients decayed. The dispersion of repolarization increased at LV apical pacing and preserved at RV apical pacing. The pump function of a ventricle was altered dramatically at pacing of the area with the shorter ARIs and to a lesser degree at pacing of the area with the longer ARIs (P ≤ 0.051). CONCLUSION: The transmural and apicobasal differences in repolarization durations were heterogeneously distributed at atrial pacing. The acute haemodynamic response of the individual ventricle was better with pacing of the region with the longest repolarization suggesting a promising criterion for the lead position selection on the basis of ARIs measurements.

The contribution of ventricular apicobasal and transmural repolarization patterns to the development of the T wave body surface potentials in frogs (Rana temporaria) and pike (Esox lucius).

The study aimed at the simultaneous determination of the transmural and apicobasal differences in the repolarization timing and the comparison of the contributions of these two repolarization gradients to the development of the body surface T wave potentials in animals with the single heart ventricle (fishes and amphibians). Unipolar potentials were measured on the body surface, epicardium and in the intramural (subepicardial, Epi; midmyocardial; and subendocardial, Endo) ventricular layers of 9 pike and 8 frogs. Activation times, repolarization times and activation-recovery intervals were determined. A transmural gradient in repolarization durations in frogs (Endo>Epi, P<0.024) corresponds to the gradient in repolarization times. No significant transmural difference in repolarization duration is observed in pike that produces a repolarization sequence from Endo to Epi (Endo

The effects of renovascular hypertension on repolarization of ventricular epicardium.

BACKGROUND AND OBJECTIVE: Alterations in the recovery sequence of hypertrophied myocardium favour the development of cardiac arrhythmias. The aim of the present study was to investigate apex-to-base and interventricular heterogeneities in the duration of epicardial ventricular repolarization in rats with renovascular hypertension. METHOD: Renovascular hypertension was induced in six Wistar rats by constricting the left renal artery for one month. Six sham-operated Wistar rats served as normotensive controls. Epicardial mapping was performed using 32 unipolar leads distributed over the apex and base of the heart ventricles under sinus rhythm. Activation-recovery intervals (ARIs) were calculated from electrograms. RESULTS: The ratio of left ventricular weight to body weight was increased in hypertensive rats compared with controls. In control rats, ARIs at the base of both ventricles were shorter than those at the apex. In hypertrophied hearts, ARIs were prolonged on both the left and right ventricular epicardium. Heterogeneous prolongation was observed via reduced apex-to-base differences in ARIs and increased interventricular differences, with a trend toward increasing dispersion of ARIs. In rats with renovascular hypertension, nonuniform prolongation of epicardial ARIs on both ventricles and the changes in the ARI distribution resulted in a reduction of the repolarization time gradient between the ventricles. CONCLUSION: Nonuniformly prolonged ARIs across the ventricular epicardium and the interventricular electrical inhomogeneity in rats with renovascular hypertension should be considered when interpreting the T wave alterations together with the reduction of the transmural and apex-to-base repolarization gradients.

Characterization of systolic intervals in healthy, conscious sheep.

OBJECTIVE: To characterize systolic intervals of the left ventricle and their relationship with heart rate in conscious sheep. Animals-11 healthy Romanov sheep (age range, 3 months to 10 years). PROCEDURES: Systolic intervals and indices of myocardial contractility of the left ventricle were measured in conscious sheep by use of polycardiography. RESULTS: The mean +/- SD pre-ejection period was 59 +/- 12 milliseconds, and the mean left ventricular ejection time was 194 +/- 34 milliseconds. The mean myocardial tension index was 0.22 +/- 0.05, and the mean ratio of the pre-ejection period to ejection time was 0.30 +/- 0.09. Total electromechanical systole, mechanical systole, and ejection time varied inversely with heart rate. The electromechanical delay and pre-ejection period were not correlated with heart rate, nor were the myocardial tension index and the ratio of the pre-ejection period to ejection time. The isovolumetric contraction index and isovolumetric contraction time were not significantly correlated with heart rate, although the values for the correlation coefficient were moderate (r = -0.561 and r = -0.482, respectively). CONCLUSIONS AND CLINICAL RELEVANCE: Although a larger study would be needed to provide reference intervals for healthy sheep, the results of the study reported here provided useful information for the cardiac evaluation of sheep.

Activation and repolarization patterns in the ventricular epicardium under sinus rhythm in frog and rabbit hearts.

Our study compared the contributions of activation sequence and local repolarization durations distribution in the organization of epicardial repolarization in animals with fast (rabbit) and slow (frog) myocardial activation under sinus rhythm. Activation times, repolarization times and activation-recovery intervals (ARI) were obtained from ventricular epicardial unipolar electrograms recorded in 13 Chinchilla rabbits (Oryctolagus cuniculus) and 10 frogs (Rana temporaria). In frogs, depolarization travels from the atrioventricular ring radially. ARIs increased progressively from the apex to the middle portion and finally to the base (502+/-75, 557+/-73, 606+/-79 ms, respectively; P<0.01). In rabbits, depolarization spread from two epicardial breakthroughs with the duration of epicardial activation being lower than that in frogs (17+/-3 vs. 44+/-18 ms; P<0.001). ARI durations were 120+/-37, 143+/-45, and 163+/-40 ms in the left ventricular apex, left, and right ventricular bases, respectively (P<0.05). In both species, repolarization sequence was directed from apex to base according to the ARI distribution with dispersion of repolarization being higher than that of activation (P<0.001). Thus, excitation spread sequence and velocity per se do not play a crucial role in the formation of ventricular epicardial repolarization pattern, but the chief factor governing repolarization sequences is the distribution of local repolarization durations.

P-wave body surface potential distribution in rats.

The aim of this study was to investigate body surface potential distribution during the P wave in Wistar rats. We performed body surface potential mapping by means of a 64-channel synchronous electrocardiotopography. The positive area covered the caudal part of the thorax, and the negative one covered the cranial part of the thorax. During the P wave, we observed 1 maximum and 1 minimum on the body surface. The dynamics of the P-wave body surface potential distribution in rats was characterized by minor movement of the positive and negative areas, and a counterclockwise shift of the extrema on the ventral body surface. The obtained results are discussed in comparison with those in dogs and humans.

Myocardial contractility in chickens (Gallus gallus): analysis of systolic time intervals.

The avian cardiovascular system is of special interest because avian hearts are relatively larger than mammalian hearts, and activation of ventricular myocardium in birds has a "flash" pattern. Systolic time intervals and indices of myocardial contractility were examined in anaesthetized open-chest chickens by polycardiography, including synchronous recordings of electrocardiogram, phonocardiogram, and apex cardiogram. The asynchronous contraction time, isometric contraction time, pre-ejection period and ejection time were 26 +/- 3 (Mean +/- SD), 21 +/- 9, 47 +/- 12, and 83 +/- 23 ms, respectively, for heart rates of 260 +/- 57 bpm. The myocardial tension index, isometric contraction index and the pre-ejection period/ejection time ratio were 0.39 +/- 0.11, 0.42 +/- 0.10, and 0.54 +/- 0.14, respectively. A "flash" pattern of ventricular myocardial depolarization causes more rapid excitation and as a consequence shorter asynchronous contraction time of relatively larger chicken hearts compared with rabbit hearts. Inverse relation (P < 0.05) of the asynchronous contraction time to the heart rate in chickens is probably associated with the specific activation pattern of avian ventricles. Establishment of the values of systolic time intervals will facilitate a better understanding of cardiac function in birds. The obtained results are discussed in comparison with the rabbit. The indices calculated from the systolic time intervals show disadvantageous contractile function of chicken heart compared to rabbit heart.

Depolarization pattern of ventricular epicardium in two-kidney one-clip hypertensive rats.

The present study is the first attempt to examine the effect of left ventricular hypertrophy (LVH) on the excitation pattern of the ventricular epicardium in experimental hypertensive rats. The left renal artery was clipped in Wistar rats (n = 8; 6-8 months old; weight, 174-295 g) to produce two-kidney one-clip (2K1C) hypertension. After 4 weeks, blood pressure was measured, and epicardial potential mapping was performed under sinus rhythm from 64 unipolar electrodes regularly distributed over the ventricular epicardium. Systolic blood pressure was approximately 40% higher in the rats with a clipped renal artery (162 +/- 14 mmHg, mean +/- s.d.) than in the normotensive rats (115 +/- 3 mmHg). LVH (approximately 23% increase in the ratio of the left ventricular weight to the body weight, P < 0.05) was observed in the 2K1C hypertensive rats. The depolarization pattern of the ventricular epicardium in the normotensive rats was similar to that in the rats with 2K1C hypertensive LVH. The duration of ventricular epicardial activation was shown to increase (approximately 35%, P < 0.05) in the hypertensive rats as compared to the normotensive animals. This study provides an explanation for alterations of the body surface potential distribution in hypertensive patients with LVH.