Why the study?
Premature ventricular contractions (PVCs) in ARVD may occur before morphological changes appear, requiring SCD risk assessment based on the electrophysiological mechanisms of PVC development.
Treadmill stress testing in ARVD patients reveals that ventricular ectopy is predominantly driven by triggered activity (stress-induced), though automaticity (stress-inhibited) also occurs, which may aid in risk stratification.
May support mechanism-based SCD risk assessment in early ARVD; leaves open need for prospective validation.
Relevance of the problem. Arrhythmogenic right ventricular dysplasia (ARVD) is one of the significant causes of sudden cardiac death (SCD) among young people. ARVD is characterized by premature ventricular ectopic contractions (PVCs) from the right ventricular outflow tract (RVOT), which may occur before morphological changes appear and, in these cases, it is necessary to assess the risk of developing SCD based on an analysis of the electrophysiological mechanism of the development of PVCs. Purpose of the study. To evaluate the electrophysiological mechanisms of PVCs in patients with ARVD according to stress tests. Material and methods. We examined 13 patients with confirmed ARVD on MRI, including 9 men and 4 women, aged from 26 to 63 years (42.9±11.0). All patients underwent the following studies: standard electrocardiography (ECG), 24-hour ECG monitoring, echocardiography, cardiac MRI, treadmill stress test. During the stress test, at each load level, ventricular ectopy was analyzed (morphology, number of ventricular ectopic complexes), and the dependence of corrected QTc on heart rate was assessed. Results. According to the data obtained, the patients were divided into two groups depending on the response of PVCs to physical activity. The first group – patients in whom the number of PVCs increased during physical activity – stress-induced ventricular ectopy – 10 people (77%). The second group – patients in whom the number of PVCs decreased, or they disappeared at the peak of the load – stress-inhibited ventricular ectopy – 3 people (23%). All patients had a normal reaction of the QT interval to physical activity – its shortening in response to an increase in heart rate. Conclusions. ARVD is characterized by ventricular ectopia from the right ventricle outflow tract or bifocal ectopia from the right ventricle outflow tract and the right ventricle apex. The electrophysiological mechanisms of ventricular ectopia in ARVD are different: the mechanism of trigger activity and increased automaticity.
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L. F. Salyamova (2024) studied this question.
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