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Understand who is likely to benefit from cardiac resynchronisation therapy (CRT).
Provide an overview of CRT trial data.
Appreciate approaches to maximise patient selection and maximise patient benefit from CRT.
Consider the potential for conduction system pacing to deliver CRT and to possibly expand the indications to additional patient groups.
The aim of cardiac resynchronisation therapy (CRT) is to improve cardiac function by delivering more physiological cardiac activation to patients with conduction system disease. The most widely investigated method for delivering CRT is biventricular pacing (BiV-CRT).
Multiple randomised control trials (RCTs) have found BiV-CRT improves outcomes when it is delivered to patients with heart failure, reduced ejection fraction (EF) and prolonged QRS duration.1–3 The majority of patients included in RCTs assessing BiV-CRT had left bundle branch block (LBBB), were in sinus rhythm, New York Heart Assocation (NYHA) class II or greater and had an EF ≤35%.
BiV-CRT is also used as an alternative to right ventricular (RV) pacing in patients who have ventricular impairment and require a high percentage of ventricular pacing.4
Understanding the mechanism through which BiV-CRT delivers its beneficial effects is useful when considering patient selection.
BiV-CRT: treatment targets
Improving ventricular electrical dyssynchrony
When a patient develops LBBB, this prolongs left ventricular (LV) activation time and produces a non-physiological LV activation pattern. These changes result in less efficient contraction and reduced cardiac output.5
BiV pacing aims to deliver more effective ventricular activation by pacing the left and right ventricles. Ventricular activation occurs via cell-to-cell conduction with activation wavefronts originating from the two pacing sites. The activation time during BiV pacing is typically longer than occurs during activation via the intact conduction system and is relatively constant regardless of intrinsic activation.6
The potential for BiV pacing to deliver improvements in ventricular activation time is dependent on the presenting (intrinsic) conduction delay. A …
Contributors Both authors contributed equally to this article.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Provenance and peer review Commissioned; internally peer reviewed.
Author note References which include a * are considered to be key references.
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