Why the study?
The study aimed to determine individualized therapy for monomorphic PVCs in patients without structural cardiac changes by assessing predictors of arrhythmogenic cardiomyopathy and its clinical and prognostic course.
Does the type of monomorphic PVC and presence of arrhythmogenic cardiomyopathy predictors determine the optimal antiarrhythmic drug class and long-term cardiovascular prognosis in patients without structural cardiac changes?
Does the type of monomorphic PVC and presence of arrhythmogenic cardiomyopathy predictors determine the optimal antiarrhythmic drug class and long-term cardiovascular prognosis in patients without structural cardiac changes?
In young patients with PVCs but no structural heart disease, PVC morphology and mechanism correlate with long-term risk of coronary artery disease and dictate the optimal choice between class I and class III antiarrhythmic drugs.
Experimental PVC models may identify ACM predictors; leaves open individualized therapy selection in patients without structural changes.
Aim. To determine the individualized choice of therapy for monomorphic premature ventricular contractions (PVCs) in patients without structural cardiac changes by assessing the predictors of arrhythmogenic cardiomyopathy (ACM) and the clinical and prognostic significance of its course. Material and methods. Experimental study . Animals were used to model PVCs by the mechanism of early post-depolarization (EPD) (aconitine), re-entry (peroxide or H 2 O 2 arrhythmia). In addition to the generally accepted parameters, the following ACMs were analyzed during electrocardiography (ECG): pre-ectopic interval, its variability, maximum index of internal deviation of PVCs, the QRS complex of PVC (QRSpvc), QRS of sinus rhythm (QRSsr), their ratio (QRSpvc/QRSsr), etc. Clinical study . A total of 343 patients with class IV-V PVCs aged 16 to 34 years were observed (B. Rayn, 1984). The same parameters were determined by ECG as in experimental arrhythmias. The follow-up duration was up to 10 years. The end point was the detection or absence of cardiovascular pathology. Results. Experimental study . When modeling ventricular arrhythmias using the EPD mechanism, early (R/T) monotopic PVCs were recorded, and re-entry — early and late monomorphic PVCs. ACM predictors were recorded only when modeling arrhythmia by the re-entry mechanism. Clinical study . In patients without structural cardiac changes, early (R/T) monotopic PVC highly correlated with ventricular ectopy induced by the EPD mechanism (aconitine) (r=0,92). These patients did not have cardiovascular diseases, and the most effective antiarrhythmic drugs for eliminating ventricular ectopy were class I drugs. In patients without structural cardiac changes, early and late monomorphic PVCs highly correlated with experimental ventricular ectopy caused by the re-entry mechanism (H 2 O 2 arrhythmia). In these patients, on average, 7,2±0,5 years after inclusion in the study, various clinical forms of coronary artery disease were detected, and the positive clinical effect of PVC treatment was achieved mainly with the use of class III antiarrhythmic drugs. Conclusion. In patients with early monotopic ventricular ectopia, without detection of ACM predictors, the most effective were class I antiarrhythmic drugs. In other patients with early and late monomorphic ventricular ectopia and detected ACM predictors, class III agents were found to be effective.
No takes yet. Share an insight, caveat, or question.
Olesin et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: