Active Heart, Stroke & Blood

Arrhythmia Risk in Conduction System Pacing

In plain English

AI plain-English summary

A standard pacemaker for heart failure creates an electrical pattern that can itself trigger dangerous heart rhythms. This fellowship directly compares a newer pacing method—conduction system pacing (CSP)—with the current standard, biventricular pacing (BVP), to see which is safer over the long term. The problem is that BVP, while improving the heart’s pumping ability, produces an unnatural electrical recovery pattern that can set the stage for ventricular arrhythmias—potentially fatal fast heartbeats. CSP mimics the heart’s natural electrical activation more closely, but its long-term effects on arrhythmia risk are unknown. This study will use high-resolution electrical mapping to measure repolarisation heterogeneity—a key marker of arrhythmia risk—in patients receiving each type of pacing. It will also test how the heart responds to simulated arrhythmia triggers and analyse 24-hour ECG recordings to capture real-world heart-rate variability. If CSP proves to reduce arrhythmia risk, it could lower the need for implantable defibrillators and their associated complications—infections, lead fractures, inappropriate shocks. This would directly improve quality of life for thousands of heart failure patients and reduce long-term healthcare costs. The findings will also guide future clinical trial design for cardiac resynchronisation therapy.

View original technical description
Biventricular pacing (BVP) improves pump failure outcomes but produces non-physiological repolarisation patterns which can trigger ventricular arrhythmias. Conduction system pacing (CSP) is an emerging alternative for delivering cardiac resynchronisation therapy (CRT). Acute CSP repolarisation patterns are much more physiological than BVP but there are several important unanswered questions: Acute CSP repolarisation changes often attenuate; longer-term effects are unknown. CSP leads are combined with conventional coronary sinus leads in a hybrid approach when CSP resynchronisation is incomplete. This may negate repolarisation benefits. Arrhythmogenesis requires repolarisation substrate and triggering heart-rate changes; resting heart-rate assessments do not fully realise pro-arrhythmic potential. In this fellowship I will conduct a randomised head-to-head study comparing CSP with BVP, measuring long-term repolarisation heterogeneity using validated, non-invasive, high-resolution electrical mapping (ECGi). Incomplete CSP resynchronisation will necessitate coronary sinus leads, allowing assessment of the trade-off between activation synchrony and repolarisation heterogeneity. I will perform programmed pacing manoeuvres to replicate arrhythmogenic coupling intervals, and analyse 24-hour 12-lead ECGs to assess spontaneous heart-rate variability effects. This fellowship will provide mechanistic insights into the arrhythmogenicity of BVP and CSP, informing future trial design. Physiological repolarisation with CSP could reduce fatal arrhythmias and defibrillator lead requirement, along with their associated complications.

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Researchers

Zachary Whinnett (EPMC Awardee)

Related Research

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Original classification

None

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