Abstract
Background and AimsThe wavefront propagation velocity in the myocardium with fibrosis is characterized by the presence of deceleration zones and late activated zones, that are absent in the normal myocardium. Our aim was to study the right ventricular outflow tract (RVOT) endocardial activation duration in sinus rhythm, and assess the presence of deceleration zones, in patients with premature ventricular contractions (PVCs) and in controls.MethodsWe studied 29 patients with idiopathic PVCs from the outflow tract, subjected to catheter ablation that had an activation and voltage map of the RVOT in sinus rhythm. A control group of 15 patients without PVCs that underwent ablation of supraventricular arrhythmias was also studied. RVOT endocardial activation duration and number of 10 ms isochrones across the RVOT were assessed. Propagation speed was calculated at the zone with the higher number of isochrones per cm radius. Deceleration zones were defined as zones with >3 isochrones within 1 cm radius. Low voltage areas were defined as areas with local electrogram with amplitude <1.5 mV.ResultsThe two groups did not differ in relation to age, gender or number of points in the map. RVOT endocardial activation duration and number of 10 ms isochrones were higher in the PVC group; 56 (41–66) ms vs. 39 (35–41) ms, p = 0.001 and 5 (4–8) vs. 4 (4–5), p = 0.001. Presence of deceleration zones and low voltage areas were more frequent in the PVC group; 20 (69%) vs. 0 (0%), p < 0.0001 and 21 (72%) vs. 0 (0%), p < 0.0001. The wavefront propagation speed was significantly lower in patients with PVCs than in the control group, 0.35 (0.27–0.40) vs. 0.63 (0.56–0.66) m/s, p < 0.0001. Patients with low voltage areas had longer activation duration 60 (52–67) vs. 36 (32–40) ms, p < 0.0001, more deceleration zones, 20 (95%) vs. 0 (0%), p < 0.0001, and lower wavefront propagation speed, 0.30 (0.26–0.36) vs. 0.54 (0.36–0.66) m/s, p = 0.002, than patients without low voltage areas.ConclusionRight ventricular outflow tract endocardial activation duration was longer, propagation speed was lower and deceleration zones were more frequent in patients with PVCs than in controls and were associated with the presence of low voltage areas.
Highlights
It is usually accepted that premature ventricular contractions (PVCs) from the outflow tracts result from triggered activity and occur in structurally normal hearts (Lerman, 2015)
From July 2019 to December 2020, we prospectively studied consecutive patients with symptomatic idiopathic frequent PVCs (>10,000/24 h) with a LBBB or RBBB, vertical axis, negative polarity in lead aVL, that were referred for catheter ablation by the same operator
PVCs originated in the right ventricular outflow tract (RVOT) in 23 patients and in the left ventricular outflow tract (LVOT) in six
Summary
It is usually accepted that PVCs from the outflow tracts result from triggered activity and occur in structurally normal hearts (Lerman, 2015). It has been previously observed that the velocity of the wavefront propagation of the PVC across the RVOT is slower in patients with PVCs from the RVOT than from the left ventricular outflow tract (LVOT), but the authors attributed this finding to the presence of differences in myocardial fiber orientation (Herczku et al, 2012; Masuda et al, 2018) This finding might be due to subtle disease of the RVOT manifested by the presence of LVAs. Based on previous studies it has become clear that activation delay is a hallmark of arrhythmogenic right ventricular cardiomyopathy (ARVC) (Tandri et al, 2009). Our aim was to study the right ventricular outflow tract (RVOT) endocardial activation duration in sinus rhythm, and assess the presence of deceleration zones, in patients with premature ventricular contractions (PVCs) and in controls
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