Antiarrhythmic effects of melatonin have been demonstrated ex vivo and in rodent models, but its action in a clinically relevant large mammalian model remains largely unknown. Objectives of the present study were to evaluate electrophysiological and antiarrhythmic effects of melatonin in a porcine model of acute myocardial infarction. Myocardial ischemia was induced by 40-min coronary occlusion in 25 anesthetized pigs. After ischemia onset, 12 animals received melatonin (4 mg/kg). 48 intramyocardial electrograms were recorded from left ventricular wall and interventricular septum (IVS). In each lead, activation time (AT) and repolarization time (RT) were determined. During ischemia, ATs and dispersion of repolarization (DOR = RTmax − RTmin) increased reaching maximal values by 3–5 and 20–25 min, respectively. Ventricular fibrillation (VF) incidence demonstrated no relations to redox state markers and was associated with increased DOR and delayed ATs (specifically, in an IVS base, an area adjacent to the ischemic zone) (p = 0.031). Melatonin prevented AT increase in the IVS base, (p < 0.001) precluding development of early VF (1–5 min, p = 0.016). VF occurrence in the delayed phase (17–40 min) where DOR was maximal was not modified by melatonin. Thus, melatonin-related enhancement of activation prevented development of early VF in the myocardial infarction model.

In myocardial ischemia, melatonin confers antiarrhythmic action, but its electrocardiographic expression is unclear. We aimed to evaluate the effects of melatonin treatment on electrocardiogram (ECG) parameters reflecting major arrhythmogenic factors and to test the association of these parameters with ventricular fibrillation (VF) incidence. Myocardial ischemia was induced by 40 min coronary artery occlusion in 25 anesthetized pigs. After induction of ischemia, 12 and 13 animals were given melatonin or placebo, respectively. Twelve-lead ECGs were recorded and durations of QRS, QT, Tpeak-Tend intervals and extrasystolic burden were measured at baseline and during occlusion. During ischemia, VF episodes clustered into early and delayed phases (20 min, respectively), and QRS duration was associated with VF incidence. QT interval and extrasystolic burden did not differ between the groups. The Tpeak-Tend interval was progressively prolonged, and the prolongation was less pronounced in the treated animals. QRS duration increased, demonstrating two maxima (5–10 and 25 min, respectively). In the melatonin group, the earlier maximum was blunted, and VF development in this period was prevented. Thus, acute melatonin treatment prevented excessive prolongation of the QRS and Tpeak-Tend intervals in the porcine myocardial infarction model, and QRS duration can be used for the assessment of antiarrhythmic action of melatonin.

E intense movement of the heart and the presence of blood on surface, the application of the necessary small markers is rather difficult, and the use of luminous chemicals would harm physiological functioning. Moreover, these videos contain motion artifacts that complicate further analysis with Particle Image Velocimetry. In this paper, an image preprocessing algorithm was proposed. It is based on approximate tracking individual fragments using the Mean Squared Error for the matrix. The result is binary images where small points are built instead of each fragment. In this study, the proposed algorithm showed better results in comparison with the most suitable filtering methods for specific frames, namely, the Sobel filter and the Canny edge detector. This can be partially explained by the higher density of vector fields due to the absence of unreliable vectors. Thus, the proposed method, unlike others, allows to get vector fields with visible vortex-like mechanical movements.

The aim of the study was to evaluate electrophysiological remodeling of the right ventricle in rats in experimental heart failure of different etiologies. Materials and methods. Isadrin-, doxorubicin- and monocrotaline-induced heart failure models were developed. Unipolar epicardial electrograms of the ventricles (256 recording sites) were recorded using a 144-channel system. The cardiac output and pressure in both ventricles of the heart were measured. Activation-recovery intervals were used as an index of duration of local repolarization, and the general and local dispersions of activation-recovery intervals were used as an index of heterogeneity of ventricular repolarization. Results. In all models of heart failure, the following were identified: 1) non-uniform prolongation of repolarization with the greatest elongation at the apex of the right ventricle; 2) an increase in apicobasal differences of repolarization with the greatest change in the right ventricle; 3) an increase in the heterogeneity of the repolarization of the epicardial layer of the ventricles with heterogeneous changes in the local heterogeneity of repolarization and a decrease in the interregional differences in the heterogeneity of the electrophysiological properties of the myocardium; 4) more pronounced changes in the repolarization of the right ventricle than in the repolarization of the left ventricle. Conclusion. Thus, irrespective of the cause of the heart failure, the following changes occur: 1) prolongation of the right ventricular repolarization occurs non-uniformly (mostly due to the apical area), which results in an increase in the right ventricular repolarization heterogeneity; 2) an increase in the heterogeneity of right ventricular repolarization is observed, which causes an increase in the overall heterogeneity of the ventricular epicardial surface.

Life-threatening cardiac arrhythmias such as ventricular tachycardia and/or fibrillation often complicate myocardial ischemia and constitute a cause for sudden cardiac death. Development of strategies for the prevention of such arrhythmias present an important research problem. The use of classical antiarrhythmic drugs is related to significant risk due to their aggressive action and probable proarrhythmic side-effects. Such risks are generally affordable in urgent situations, but unacceptable for preventive use in large patient populations. It poses the necessity to develop a safe and effective medication to be applied for arrhythmia prophylaxis and treatment. Melatonin has been proved to be safe for use in humans even in relatively high doses. It has been reported to confer versatile cardioprotective effects, which include antiarrhythmic action. Traditionally, the antiarrhythmic effect is considered as a manifestation of the general protective action of melatonin, based largely on its antioxidative properties. In this review, we strive to provide evidence of specific electrophysiological mechanisms brought about by melatonin application. Here, we discuss the pathways by which melatonin targets ion channels and causes changes in the cellular and tissue properties relevant to arrhythmogenesis.The obtained data suggest that melatonin can modify a number of electrophysiological characteristics of a cardiomyocyte and myocardium. However, the changes in conduction velocity appear to be the major effect functionally relevant for arrhythmogenesis. The most probable mechanisms of the melatonin-related conduction enhancement are discussed. These mechanisms differ in acute and chronic applications of melatonin and related to the increase of inward rectifier potassium current maintaining the resting membrane potential and the upregulation of sodium channel protein expression, respectively.The novel melatonin-related mechanism regulating myocardial conduction velocity might be considered for potential use in different contexts that include arrhythmia risks from myocardial ischemia to inherited channelopathies. The functional relevance of this effect warrants its further exploration concerning cellular mechanisms, efficiency and limitations.Key words: melatonin, arrhythmias, ischemia, reperfusion, conduction velocity, dispersion of repolarization, ionic currents, oxidative stress