Clinical and prognostic significance of left ventricular dysfunction predictors in patients with ventricular ectopy and without structural heart disease

Abstract

Aim . To determine the predictors of left ventricular dysfunction in patients with ventricular ectopic beats without structural heart disease. Material and Methods . We modeled ventricular ectopy in rats through early afterdepolarization (aconitine-induced arrhythmia) and delayed afterdepolarization (adrenaline arrhythmia). In addition, we modeled ventricular ectopy in rabbits and cats by delayed afterdepolarization (barium chloride-induced and strophanthin arrhythmias, respectively) and also modeled ventricular ectopy in dogs by re-entry hydrogen peroxide-induced arrhythmia. In addition to conventional electrocardiography parameters, we analyzed pre-ectopic interval, its variability, and the internal deviation index. Further, the study included 514 patients aged 16 to 34 years (mean 21.2 ± 0.2 years), and the number of premature ventricular contractions (PVCs) per day of observation ranged from 6,157 to 37,254 (mean 19,706 ± 656 PVCs). We registered the same parameters as in experimental arrhythmias but calculated them separately for mono- and polymorphic, left and right ventricular out-flow tract arrhythmias. The duration of follow-up of patients was up to 10 years. The endpoint was the detection or absence of cardiovascular and/or extracardiac pathology. Results . We recorded polymorphic PVCs and early monomorphic PVCs when modeling ventricular arrhythmias by the mechanism of delayed post-depolarization and early post-depolarization, respectively. Both early and late monomorphic PVCs were documented when inducing ventricular arrhythmias by re-entry. When modeling hydrogen peroxide-induced and strophanthin arrhythmias, we observed significantly higher values of PVC-QRS complex and ventricular arrhythmia internal deviation index in comparison with aconitine-induced arrhythmia. Favourable outcome was registered in 50.97% of patients, whilst coronary artery disease, arterial hypertension, and mitral valve prolapse were documented in 7.98%, 16.73% and 2.92% patients. The rest of the patients had gastrointestinal diseases. In patients with favourable outcome, the signs of monomorphic PVCs correlated with those revealed during the modeling of ventricular ectopy by early afterdepolarization (r = 0.92), whereas those signs of polymorphic PVCs correlated with those observed at barium chloride-induced delayed afterdepolarization (r = 0.94). In patients with CAD, signs of PVCs correlated with those registered during re-entry hydrogen peroxide-induced arrhythmia (r = 0.93), Finally, in patients with arterial hypertension and mitral valve prolapse signs of PVCs correlated with those documented at strophanthin-(r = 0.92) and adrenaline-induced delayed afterdepolarization (r = 0.89). In these patients, the values for both monomorphic and polymorphic PVCs, ventricular arrhythmia internal deviation index, duration of PVC-QRS complex and PVC-QRS/QRS average did not exceed 0.42 units, 149 ms and 1,44 units, respectively. The development of coronary artery disease and arterial hypertension well correlated with an increase in ventricular arrhythmia internal deviation index ≥ 0.56 units and QRS complex duration ≥ 157 ms. Mitral valve prolapse was associated with the duration of the QRS complex ≥ 159 ms of polymorphic PVCs. Conclusion . In patients with ventricular ectopy but without structural heart disease, an increase in the values of ventricular arrhythmia internal deviation index and the duration of PVC-QRS complex was ≥ 0.48 units and 149 ms, respectively, associated with the development of cardiovascular pathology. Development of coronary artery disease and hypertension correlated with ventricular arrhythmia internal deviation index ≥ 0.56 units, and QRS complex duration ≥ 157 ms in monomorphic and polymorphic PVCs, whereas development of mitral valve prolapse correlated QRS complex duration ≥ 159 ms in polymorphic PVCs.