Device therapy for non-ischaemic cardiomyopathy with LBBB and paroxysmal atrial fibrillation
A 58-year-old woman with non-ischaemic dilated cardiomyopathy is reviewed 4 months after optimisation. She is NYHA class II with no hospital admissions in that period, but becomes breathless when climbing one flight of stairs. Current therapy is sacubitril/valsartan 97/103 mg twice daily, bisoprolol 10 mg, eplerenone 50 mg and dapagliflozin 10 mg. Echocardiography shows LVEF 28%, LVEDD 62 mm, moderate functional mitral regurgitation and no significant valvular stenosis. ECG shows sinus rhythm at 72/min with left bundle branch block, QRS 158 ms. Ambulatory monitoring documents paroxysmal atrial fibrillation with a burden of 18%, with ventricular rates up to 130/min. Bloods: eGFR 42 mL/min/1.73 m², potassium 4.8 mmol/L, ferritin 85 µg/L, transferrin saturation 14%, haemoglobin 11.6 g/dL. She is 168 cm tall and weighs 74 kg, has no diabetes, and has no frailty. Coronary angiography two years ago was normal.
1. Which device, if any, should she receive, and what does she need before implantation?
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She meets criteria for cardiac resynchronisation therapy: symptomatic HFrEF with EF ≤35%, sinus rhythm, LBBB with QRS ≥150 ms, on optimal medical therapy for at least 3 months. In this setting CRT reduces mortality and HF hospitalisation, and the benefit is greatest with LBBB and wide QRS.
CRT-D rather than CRT-P: she has a primary-prevention ICD indication (EF ≤35%, NYHA II, on optimal therapy, expected survival >1 year), so CRT-D is appropriate unless comorbidity favours CRT-P. At 58 with no frailty, CRT-D is reasonable.
Before implantation:
- Iron deficiency: ferritin 85 µg/L (<100) qualifies. Give intravenous ferric carboxymaltose, which improves symptoms and reduces HF hospitalisation. Recheck haemoglobin; investigate the anaemia.
- Rate control of AF: her AF burden (18%) will undermine biventricular capture if conducted AF is rapid and irregular. Ensure adequate beta-blockade; assess AF burden after device implantation, and if biventricular pacing falls below about 95%, consider AV nodal ablation or rhythm control (catheter ablation) to protect CRT benefit.
- Renal function and potassium are acceptable for MRA continuation; monitor after implant.
- Consent and counselling: discuss infection, pneumothorax, lead displacement, and the possibility of an upgrade to a leadless or His-bundle/LBBAP system if coronary sinus anatomy is unfavourable.
- Optimisation: document NYHA class and confirm no further titration is possible, and treat the anaemia before an elective implant.
2. Six weeks after CRT-D implantation, a device check shows biventricular pacing at only 71% of the time, with atrial fibrillation in 60% of the recording. What is your approach?
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Suboptimal biventricular pacing defeats CRT and predicts non-response. First, determine the cause from the device diagnostics:
- Conducted rapid AF: the commonest cause. Ventricular rates are irregular and intrinsic conduction competes with biventricular pacing. Optimise beta-blocker or digoxin; consider rhythm control with AF ablation, which is reasonable in HFrEF to restore sinus rhythm and improve CRT delivery.
- Frequent premature ventricular complexes or PVCs: atrioventricular timing is disturbed; optimise AV/PV delays and consider PVC ablation.
- Loss of biventricular capture (phrenic stimulation, high thresholds, lead displacement): check pacing thresholds, lead position and program the vectors; a chest radiograph/echo confirms position.
- Patient-triggered mode switching: ensure the device is appropriately programmed.
If AF cannot be controlled medically and pacing remains <95%, AV node ablation is a well-established option that guarantees near-100% biventricular capture and improves symptoms in selected patients, at the cost of lifelong pacing dependency. Discuss this explicitly with the patient.
Also reassess clinical response: repeat echocardiography, review HF therapy, and check for ongoing causes of decompensation. Do not simply accept the device check as "normal" - pacing percentage is a modifiable determinant of outcome.