Key result
Biventricular pacing cuts TdP inducibility ~69% vs idioventricular rhythm in dogs with chronic AV block.
Why the study?
Altered ventricular activation promotes pro-arrhythmic electrical remodelling in chronic AV block dogs, but the arrhythmogenic and electromechanical outcomes of different degrees of altered activation remained to be studied.
Does the severity of altered ventricular activation affect pro-arrhythmic electrical remodelling and Torsade de Pointes inducibility in a chronic AV block dog model?
Does the severity of altered ventricular activation affect pro-arrhythmic electrical remodelling and Torsade de Pointes inducibility in a chronic AV block dog model?
Absolute Event Rate: 20% vs 65.5%
p-value: p=<0.05
In a chronic AV block dog model, the severity of intraventricular mechanical dyssynchrony correlates with the extent of pro-arrhythmic electrical remodelling and Torsade de Pointes inducibility.
Pacing may attenuate TdP inducibility in dyssynchronous models; leaves open translation to human chronic AV block.
AIMS: Altered ventricular activation (AVA) causes intraventricular mechanical dyssynchrony (MD) and impedes contraction, promoting pro-arrhythmic electrical remodelling in the chronic atrioventricular block (CAVB) dog. We aimed to study arrhythmogenic and electromechanical outcomes of different degrees of AVA. METHODS AND RESULTS: Following atrioventricular block, AVA was established through idioventricular rhythm (IVR; n = 29), right ventricular apex (RVA; n = 12) pacing or biventricular pacing [cardiac resynchronization therapy (CRT); n = 10]. After ≥3 weeks of bradycardic remodelling, Torsade de Pointes arrhythmia (TdP) inducibility, defined as ≥3 TdP/10 min, was tested with specific IKr-blocker dofetilide (25 μg/kg/5 min). Mechanical dyssynchrony was assessed by echocardiography as time-to-peak (TTP) of left ventricular (LV) free-wall minus septum (ΔTTP). Electrical intraventricular dyssynchrony was assessed as slope of regression line correlating intraventricular LV activation time (AT) and activation recovery interval (ARI). Under sinus rhythm, contraction occurred synchronous (ΔTTP: -8.6 ± 28.9 ms), and latest activated regions seemingly had slightly longer repolarization (AT-ARI slope: -0.4). Acute AV block increased MD in all groups, but following ≥3 weeks of remodelling IVR animals became significantly more TdP inducible (19/29 IVR vs. 5/12 RVA and 2/10 CRT, both P < 0.05 vs. IVR). After chronic AVA, intraventricular MD was lowest in CRT animals (ΔTTP: -8.5 ± 31.2 vs. 55.80 ± 20.0 and 82.7 ± 106.2 ms in CRT, IVR, and RVA, respectively, P < 0.05 RVA vs. CRT). Although dofetilide steepened negative AT-ARI slope in all groups, this heterogeneity in dofetilide-induced ARI prolongation seemed least pronounced in CRT animals (slope to -0.8, -3.2 and -4.5 in CRT, IVR and RVA, respectively). CONCLUSION: Severity of intraventricular MD affects the extent of electrical remodelling and pro-arrhythmic outcome in the CAVB dog model.
No takes yet. Share an insight, caveat, or question.
Weperen et al. (2022) studied Chronic atrioventricular block (n=51). Biventricular pacing (CRT) or right ventricular apex (RVA) pacing vs. Idioventricular rhythm (IVR) was evaluated on Torsade de Pointes arrhythmia (TdP) inducibility (≥3 TdP/10 min) with dofetilide (p=<0.05). Biventricular pacing (20%) and right ventricular apex pacing (41.7%) significantly reduced Torsade de Pointes inducibility compared to idioventricular rhythm (65.5%) in chronic AV block dogs (P<0.05).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: