Remodeling of ventricular repolarization in experimental right ventricular hypertrophy.

BACKGROUND: To understand electrophysiological mechanisms that underlie the progression of compensated right ventricular hypertrophy (RVH) to heart failure, the purpose of the study was to evaluate remodeling of ventricular repolarization in connection with hemodynamic abnormalities and vulnerability of the heart ventricles to arrhythmias in RVH rats with pulmonary arterial hypertension (PAH) and heart failure. METHODS: PAH followed by heart failure was induced by monocrotaline in adult female Wistar rats. Unipolar epicardial electrograms and cardiac hemodynamic parameters were recorded in situ. Vulnerability to ventricular arrhythmias was measured as the threshold dose of aconitine required to produce sustained ventricular tachycardia. Histological examination of the heart ventricles was performed. Activation-recovery intervals (ARIs) and ARI dispersions were used as indices of durations and heterogeneity of repolarization respectively to assess ventricular repolarization. RESULTS AND CONCLUSIONS: The development of compensated RVH was characterized by the dramatic prolongation of repolarization against the less expressed increase in repolarization heterogeneity, whereas the dramatic increase in repolarization heterogeneity against the less expressed but inhomogeneous prolongation of repolarization occurred in the progression of compensated RVH to heart failure. These changes increased vulnerability of the failing heart but not the compensated heart to aconitine-induced ventricular arrhythmias.

[Effect of the heart electric stimulation on repolarization of fish and amphibian ventricular myocardium].

By the method of synchronous multielectrode cartography (24-unipolar leads), distribution of durations and time of end of repolarization were studied on ventricular epicardium of pikes (Esox lucius) and frogs (Rana esculenta) and in ventricular intramural layers of toads (Bufo bufo) at the ectopic heart excitation. The time of arrival of the excitation wave and of the end of repolarization in each lead was determined from the minimum of time derivative of potential at the period of the QRS complex and by minimum of the T wave, respectively. It has been established that at the ventricle electrostimulation, alongside with deceleration and a change of sequence of the myocardium activation, there occurs redistribution of local repolarization durations: in areas of late activation the repolarization being longer than in zones of early activation (p < 0.05). At stimulation, the apicobasal gradient of repolarization is predominantly changed due to electrophysiological processes in the apical areas. In all studied species. at ectopical excitation of the heart ventricle the sequence of its repolarization repeats the depolarization sequence due to delay of activation (in fish) and redistribution of repolarization durations (in amphibians).

[Repolarization pattern of the ventricular myocardium in pikes].

The study aimed at investigation into the repolarization pattern in the myocardium of fish. Activation times, activation-recovery intervals and repolarization times were determined in the intramural layers of the heart ventricle in eight pikes with multiple plunge electrodes. In the heart ventricle of the pike, the earliest end of repolarization was found in the subendocardium of the base and the subepicardium of the apex, the areas corresponding to the earliest and latest depolarization, respectively. The latest repolarization was observation on the anterior epicardial surface of the base. Endocardialto-epicardial repolarization sequence at the base corresponded to the activation sequence in this area with the transmural gradient of the end of repolarization times being 54 +/- 23 ms (p < 0.001). The transmural difference in activation-recovery interval durations and end of repolarization times decreased as one moved from the base to apex with the maximal apex-to-base end of repolarization gradient being 133 +/- 98 ms (p < 0.10).

[Effect of ectopic excitation on pump function of the hen and dog right heart ventricle].

The pump function of the right heart ventricle has been studied in anesthetized dogs and hens at sinus rhythm, supraventricular rhythm, and subepicardial ectopic excitation of base and apex of the right and left ventricles. Dynamics of the ventricle intracavital pressure was recorded by transmural catheterization. The pump function of the right ventricle in hen (as compared with sinus rhythm) retained to the greater degree at stimulation of the left ventricle apex and deteriorated significantly at stimulation of the right ventricle, whereas in dog (as compared with supraventricular rhythm) it retained to the greater degree at stimulation of the left ventricle base and deteriorated at stimulation of the right ventricle apex. Changes of the pump function of the right heart ventricle at ectopic ventricle stimulation are similar in birds and mammals. Differences in changes of dog and hen pump functions under effect of location of the ectopic excitation seem to be due to morphofunctional peculiarities of heart ventricles.

[Repolarization of canine ventricular myocardium under the supraventricular rhythm].

The ventricular myocardium is characterized by heterogeneity of activation-recovery interval durations. The transmural ARI gradients are present in the right ventricular apex (ARIs monotonically decreased as one moved from the endocardium to the epicardium), and in the left ventricular base (repolarization in the subepicardial layers was significantly shorter than that in the midmyo cardial layers whereas subendocardial ARIs did not differ from the others). The repolarization pattern of these myocardial regions is governed by the distribution of ARIs. In the apical left ventricular and basal right ventricular areas, no significant transmural differences in the repolarization durations were found. The repolarization pattern of these myocardial regions is governed by the activation sequence. In the right ventricle, ARIs were significantly longer at the base and shorter at the apex. In contrast, in the left ventricle, the apical ARIs were prolonged whereas the basal ARIs were abbreviated. The apex-to-base sequence of myocardial repolarization seems to depend on apex-to-base gradient of activation-recovery intervals durations.

Repolarization of ventricular myocardium in atrioventricular electrical stimulation of the heart in dogs.

The duration of ventricular myocardium excitation increases during atrioventricular stimulation of dog heart and the sequence of depolarization of the right and left ventricles is desynchronized. Significant shortening of the activation-recovery interval in the intramural and subendocardial layers of the left ventricular base leads to modification of the repolarization sequence in this area and to an increase of total dispersion of activation-recovery intervals in the cardiac ventricles, as a result of which repolarization sequence starts partially repeating the depolarization sequence.