Characterization of repetitive ventricular responses and tachyarrhythmias induced by single ventricular premature stimulation during sinus rhythm. An epicardial mapping study in normal adult rats

Abstract

Abstract. Introduction. The mode of onset of life-threatening ventricular tachycardia and fibrillation (VF) has been well described in patients with organic heart disease and long QT syndromes. However, less is known about the mode of onset of VF initiated by premature ventricular complexes (PVCs) with very short coupling intervals in rare patients who have no evidence of organic heart disease or identifiable etiology. Hence, the aim of this work was to identify the reentry circuits induced by critical PVCs that initiate VF in normal ventricular myocardium. Methods. Unipolar potentials were measured by means of a high resolution epicardial electrode array in seventeen normal rats. Single premature stimulation was performed during normal sinus rhythm at test sites of the epicardial array or single endocardial electrodes. Strength was gradually increased from near diastolic threshold (100 μA) to 10 mA. For each strength, coupling interval was gradually decreased until absence of ventricular response. All premature stimulations and induced arrhythmias through a test site were summarily represented in a characteristic strength-interval plane. Electrical data were processed off line as electrogram, isopotential and isochrone maps. Results. Critical premature stimuli triggered repetitive ventricular responses (RVRs) and tachyarrhythmias. RVRs are defined as one or more (but less than five) non-stimulated ventricular beats after a paced ventricular premature beat. RVRs include two types of reentry: bundle branch reentries (BBRs), characterized by reentry circuit through the conducting system and the myocardium of both ventricles, and intraventricular reentries (IVRs) characterized by reentry circuits within the same stimulated ventricle either through terminal Purkinje fibers and myocardium (IVR-P) or through myocardium alone (IVR-M, figure 8 reentry). Tachyarrhythmias occurred when very short coupled IVRs induced VF. Discussion. Our findings show that VF induced by low strength premature stimuli (less than 1 mA) was characterized by the initial occurrence of very short coupled IVR-Ps with focal pattern followed by sustained arrhythmia. Moreover, focal IVR-Ps could be followed by multiple IVR-Ms with figure 8 reentry pattern before degenerating into sustained arrhythmia. Hence, our findings suggest that, in some instances, the initial reentry beats act like "premature stimulus equivalents" (i.e. S2, S3, S4) aiding the emergence of sustained ventricular tachyarrhythmias. Alternatively, VF induced by high strength premature stimuli (more than 5 mA) was often characterized by the initial occurrence of IVR-Ms with figure 8 reentry pattern that eventually became sustained.