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Cardiac Resynchronisation Therapy (CRT)

📋 Key Information Summary

📋
  • Cardiac Resynchronisation Therapy (CRT) uses biventricular pacing to restore mechanical synchrony in heart failure patients with electrical dyssynchrony (prolonged QRS).
  • Class I indication (ESC/NHFA/CSANZ): NYHA II–IVa symptoms, LVEF ≤ 35%, LBBB with QRS ≥ 150 ms on optimal medical therapy for ≥ 3 months.
  • LBBB morphology is the strongest ECG predictor of CRT response; non-LBBB patterns have lower benefit.
  • CRT-P (pacing only) is first-line for patients without a primary ICD indication; CRT-D (defibrillator) adds sudden cardiac death protection.
  • Approximately 60–70 % of patients are clinical responders; one-third are non-responders, defined as failure to improve NYHA class or reduce LVESV by ≥ 15 %.
  • Optimisation of guideline-directed medical therapy (ACEi/ARNI, beta-blocker, MRA, SGLT2i) must precede and continue after CRT implantation.
  • Post-implantation AV and VV optimisation can improve haemodynamics but evidence for hard outcomes is mixed; echo-guided optimisation is common practice.
  • CRT reduces heart failure hospitalisations by ~25–35 % and all-cause mortality by ~25 % in landmark RCTs (COMPANION, CARE-HF, MADIT-CRT, RAFT).
  • In Australia, CRT implantation is performed in ≈ 40 centres nationally; procedural MBS item numbers 38300 (CRT-P) and 38303 (CRT-D) apply.
  • Remote device monitoring (Medtronic CareLink, Abbott Merlin) is MBS-rebatable and recommended at 3–6 monthly intervals post-implantation.
  • Contraindications include active infection, severe peripheral venous access issues, and lack of patient compliance with follow-up.
  • First Nations Australians experience higher HF prevalence and worse outcomes — CRT access and referral equity must be actively addressed.
  • Special populations (pregnancy, paediatric/congenital heart disease, dialysis patients) require individualised multi-disciplinary assessment.

Introduction & Australian Epidemiology

Cardiac Resynchronisation Therapy (CRT), also termed biventricular pacing, is an established device-based therapy for selected patients with heart failure and reduced ejection fraction (HFrEF) who demonstrate electrical dyssynchrony on the surface ECG. CRT simultaneously stimulates the left and right ventricles (or, in some systems, the left ventricle alone) to restore mechanical synchrony, improve myocardial efficiency, reverse adverse ventricular remodelling, and thereby reduce symptoms, heart failure hospitalisations, and mortality.

Heart failure affects an estimated 500,000 Australians, with a prevalence of approximately 2 % in adults and rising steeply with age. Around half of patients have HFrEF (LVEF ≤ 40 %), the population most likely to be considered for CRT. Despite advances in pharmacotherapy — including angiotensin receptor–neprilysin inhibitors (ARNIs), mineralocorticoid receptor antagonists (MRAs), and sodium-glucose cotransporter-2 inhibitors (SGLT2is) — morbidity and mortality remain substantial. CRT has been evaluated in multiple landmark randomised controlled trials involving > 4,000 patients (COMPANION, CARE-HF, MADIT-CRT, RAFT, and others) and consistently demonstrates a 20–36 % relative risk reduction in all-cause mortality and a 25–35 % reduction in heart failure hospitalisation.

In Australia, approximately 4,000–5,000 CRT devices are implanted annually. Implantation is performed in public and private tertiary cardiac electrophysiology centres across all states and territories. MBS reimbursement is available under item 38300 (CRT-pacemaker) and 38303 (CRT-defibrillator). The Cardiac Society of Australia and New Zealand (CSANZ) and the National Heart Foundation of Australia (NHFA) endorse current European and American guideline criteria adapted for the Australian context. This guideline provides a comprehensive overview of CRT mechanism, patient selection, device choice, response optimisation, and special population considerations for Australian clinicians.

Cardiac Resynchronisation Therapy (CRT) clinical infographic — pathophysiology, clinical clues, diagnosis, imaging, and management
Tap or click image to enlarge — Cardiac Resynchronisation Therapy (CRT): pathophysiology, clinical clues, diagnosis, imaging, and management.
Cardiac Resynchronisation Therapy (CRT) infographic, full size

Mechanism & Rationale

Electrical Dyssynchrony

In patients with HFrEF and LBBB (or other forms of intraventricular conduction delay), electrical activation of the left ventricle is markedly delayed relative to the right ventricle. The interventricular septum contracts earlier than the lateral and posterior LV free walls. This regional dyssynchrony results in wasted myocardial work, reduced diastolic filling time, functional mitral regurgitation (due to papillary muscle dyssynchrony), and diminished stroke volume.

Biventricular Pacing — How It Works

CRT delivers near-simultaneous electrical stimulation to the RV apex (or septum) and a posterolateral tributary of the coronary sinus (accessing the LV epicardium). This synchronises contraction of the septum and lateral wall, restoring coordinated ventricular shortening. Haemodynamic benefits include:

  • Improved LV ejection fraction (+5–10 % absolute in responders).
  • Reduced LV end-systolic volume (reverse remodelling — hallmark of response).
  • Decreased mitral regurgitation via improved papillary muscle alignment.
  • Enhanced diastolic filling through optimised AV timing.
  • Neurohormonal modulation with reduced sympathetic drive.

Electrical vs Mechanical Dyssynchrony

While the QRS duration is a surrogate for electrical dyssynchrony, echocardiographic measures (septal-to-posterior wall motion delay, tissue Doppler longitudinal strain, speckle tracking) can detect mechanical dyssynchrony independently of QRS width. However, large-scale randomised trials (EchoCRT) demonstrated that CRT does not benefit — and may harm — patients with narrow QRS (< 120 ms) even in the presence of echo-detected mechanical dyssynchrony. Thus, the QRS criterion remains the primary selection tool in current guidelines.

ℹ️
Australian context: The LBBB pattern on ECG is the strongest predictor of CRT response. CSANZ recommends that CRT be considered only when the QRS is genuinely prolonged and the morphology is consistent with LBBB (Sgarbossa criteria, Strauss criteria), rather than non-specific intraventricular conduction delay.

Indications (NYHA, LVEF, QRS Criteria)

Class I — Strong Evidence

NYHA II
Mild–Moderate Symptoms
Symptoms with ordinary activity; comfortable at rest.
LVEF ≤ 35 %, LBBB, QRS ≥ 150 ms, OMT ≥ 3 months
NYHA II–III
Moderate–Moderately Severe
Symptoms with less-than-ordinary activity; comfortable at rest or with minimal limitation.
LVEF ≤ 35 %, LBBB, QRS ≥ 150 ms, OMT ≥ 3 months
NYHA III–IVa
Severe (Ambulatory)
Symptoms at rest or with minimal exertion; IVa = ambulatory, not inotrope-dependent.
LVEF ≤ 35 %, LBBB, QRS ≥ 120 ms, OMT ≥ 3 months
⚠️
Optimised medical therapy (OMT) is a prerequisite. Before referral for CRT, patients must be on maximally tolerated doses of guideline-directed HFrEF therapy — ACEi/ARB/ARNI, beta-blocker, MRA, SGLT2i, and diuretics — for at least 3 months. CRT does not replace pharmacotherapy.

Class IIa — Reasonable

  • LVEF ≤ 35 %, LBBB, QRS 120–149 ms, NYHA II–IVa (lower QRS threshold, less robust evidence).
  • LVEF ≤ 35 %, non-LBBB pattern, QRS ≥ 150 ms, NYHA II–IVa (reduced benefit but still considered).
  • Patients with HFrEF who have a conventional pacemaker indication and are expected to require > 40 % ventricular pacing (to avoid pacing-induced cardiomyopathy).

Class IIb — May Be Considered

  • LVEF ≤ 35 %, non-LBBB, QRS 120–149 ms (weakest evidence).
  • LVEF 36–50 % with significant dyssynchrony on imaging and QRS ≥ 150 ms (limited data; consider in expert centre).

Contraindications

  • Active systemic infection or bacteraemia.
  • Inadequate coronary sinus venous anatomy (unable to place LV lead).
  • Life expectancy < 1 year due to non-cardiac comorbidities.
  • NYHA IVb/IVc (inotrope-dependent, VAD/transplant-expected — CRT role unclear).
  • Patient refusal or inability to attend device follow-up.

ECG Morphology Criteria — LBBB vs Non-LBBB

Parameter LBBB (Strauss Criteria) Non-LBBB / RBBB / IVCD
QRS duration for benefit ≥ 120 ms (men), ≥ 130 ms (women) — Class I if ≥ 150 ms ≥ 150 ms (Class IIa); ≥ 120 ms (Class IIb)
Expected response rate 70–80 % 40–50 %
Mortality benefit Robust (CARE-HF, MADIT-CRT) Inconsistent; subgroup analyses variable
Recommendation Strong Individualised, discuss with HF/EP team

CRT-P vs CRT-D

The choice between a CRT-Pacemaker (CRT-P) and a CRT-Defibrillator (CRT-D) is one of the most common clinical decisions in CRT referral. CRT-P provides biventricular pacing alone; CRT-D adds an integrated implantable cardioverter-defibrillator (ICD) capable of anti-tachycardia pacing (ATP) and high-voltage defibrillation for ventricular tachyarrhythmias.

CRT-P (Pacemaker)
Biventricular pacemaker — no defibrillator function
Best suited for Primary indication is dyssynchrony, no independent ICD indication; older patients (≥ 75–80 yrs); significant non-cardiac comorbidities limiting expected survival benefit from SCD prevention
MBS Item 38300 — CRT pacemaker implantation
PBS status ✔ PBS General Benefit
Advantages Smaller device, longer battery life (7–10 yrs), fewer inappropriate shocks, lower cost
CRT-D (Defibrillator)
Biventricular pacemaker + ICD
Best suited for Younger patients (< 75 yrs); prior VT/VF arrest; inducible VT on EPS; ischaemic cardiomyopathy with viable myocardium; patients willing to accept shock risk
MBS Item 38303 — CRT defibrillator implantation
PBS status ✔ PBS General Benefit
Disadvantages Larger device, shorter battery life (5–7 yrs), inappropriate shocks (2–5 %/yr), higher cost
⚠️
Shared decision-making is essential. COMPANION showed CRT-P reduced combined death/HF hospitalisation by 34 %; CRT-D by 40 %. However, CRT-D did not significantly reduce all-cause mortality over CRT-P in meta-analyses. Australian practice increasingly favours CRT-P for patients aged > 75 with non-ischaemic aetiology, given the diminishing absolute SCD risk with age and comorbidity.

Decision Framework

1
Assess SCD Risk
Prior VT/VF → CRT-D strongly favoured. Ischaemic aetiology with viable myocardium → CRT-D preferred.
2
Assess Comorbidities & Life Expectancy
Age > 80, eGFR < 30, severe COPD, frailty score > 5 → CRT-P may be more appropriate.
3
Discuss Patient Preferences
Some patients decline ICD shocks; quality-of-life preference may favour CRT-P.
4
Multidisciplinary HF Team Review
CSANZ recommends HF cardiologist, electrophysiologist, and allied health input before final device selection.

Response & Non-Response

Defining CRT Response

There is no single universally accepted definition of CRT response. Commonly used criteria include:

  • Clinical response: Improvement of ≥ 1 NYHA functional class, or patient-reported improvement on Kansas City Cardiomyopathy Questionnaire (KCCQ) ≥ 5 points.
  • Echocardiographic response: Reduction in LV end-systolic volume (LVESV) ≥ 15 % at 6 months — considered the most objective and prognostically meaningful marker.
  • Super-response: Normalisation of LVEF to ≥ 50 % — occurs in approximately 10–15 % of CRT recipients and is associated with excellent long-term prognosis.
Responder
Clinical + Echo Response
NYHA class improved, LVESV reduced ≥ 15 %, LVEF improved. ~60–70 % of CRT recipients.
Continue OMT; routine device follow-up 3–6 monthly
Partial Responder
Clinical but No Echo Response
Symptoms improve but LV volumes unchanged. Consider suboptimal biventricular pacing (< 95 %), AF burden, or inadequate medical therapy.
Optimise % biv pacing, AV/VV timing, intensify OMT
Non-Responder
No Clinical Improvement
No NYHA class improvement, no echo reverse remodelling. ~30 % of patients. Systematic evaluation required.
Assess lead position, pacing %, AF, ischaemia, correctable factors

Predictors of Response

Predictor Favours Response Predicts Non-Response
ECG morphology True LBBB (Strauss criteria) Non-LBBB, RBBB, narrow QRS
QRS duration ≥ 150 ms 120–130 ms
Aetiology Non-ischaemic cardiomyopathy Extensive scar (ischaemic, large transmural infarction)
LV scar location No scar at LV lead site Scar at posterolateral wall (lead tip)
Rhythm Sinus rhythm Permanent atrial fibrillation (inadequate biv pacing %)
Gender Female (smaller heart, higher scar-free myocardium) Male (larger LV, more ischaemic scar)
Biv pacing percentage ≥ 95 % < 95 % (frequent PVCs, AF, inappropriate programming)

Managing Non-Response

When a patient is identified as a non-responder at the 3–6 month follow-up, a systematic approach should be undertaken:

1
Verify Biventricular Pacing Percentage
Must be ≥ 95 %. If not, identify cause — frequent PVCs (consider catheter ablation), AF (consider rate control, AV node ablation), premature ventricular beats from sensing issues (adjust sensitivity settings).
2
Assess Lead Position on CXR / CT
Optimal LV lead position is mid-lateral or posterolateral wall, avoiding scar and apex. Suboptimal positioning (anterior, apical) correlates with non-response.
3
AV & VV Optimisation
Echocardiographic AV delay optimisation (iterative method or Ritter formula). VV timing — LV pre-excitation of 20–40 ms may benefit some patients. Some modern devices offer adaptive algorithms (SyncAV™, AdaptivCRT™).
4
Assess Myocardial Ischaemia & Viability
If ischaemic — consider revascularisation (CABG/PCI) to improve viability at lead site. Late gadolinium enhancement CMR can quantify scar burden.
5
Consider LV Lead Revision or Conduction System Pacing
His-bundle pacing or left bundle branch area pacing (LBBAP) are emerging alternatives in CRT non-responders with suboptimal LV lead positions. Referral to an experienced EP centre is recommended.
6
Intensify Heart Failure Therapy
Ensure ARNI, beta-blocker (target dose), MRA, SGLT2i, diuretics are at optimal doses. Consider ivabradine if HR ≥ 70 bpm in sinus rhythm. Refer for advanced therapies (VAD/transplant) if NYHA IIIb–IV and declining.
Super-response: Patients who normalise LVEF (≥ 50 %) after CRT have an excellent prognosis. Consider deactivation of the ICD function in CRT-D super-responders after ≥ 2 years of sustained normalisation — this decision should be made in a multidisciplinary HF/EP clinic with informed patient consent.

Investigations

Pre-implantation assessment for CRT requires a structured diagnostic workup to confirm eligibility, exclude reversible causes, and plan the procedure.

ESSENTIAL
12-lead ECG
QRS duration, morphology (LBBB vs non-LBBB), rhythm (sinus vs AF). Strauss criteria for LBBB recommended. MBS item 11707.
ESSENTIAL
Transthoracic Echocardiogram
LVEF (Simpson biplane), LV dimensions, LVESV, mitral regurgitation severity, diastolic function, RV function. MBS item 55122.
AVAILABLE
Cardiac MRI (CMR)
Late gadolinium enhancement for scar quantification and localisation — valuable for predicting response and guiding LV lead placement. Limited availability in some regional centres; MBS item 63501.
AVAILABLE
Coronary Angiography / CT Coronary
If ischaemic aetiology suspected; may guide revascularisation decisions before CRT. MBS item 38218 (CTCA).
AVAILABLE
BNP / NT-proBNP
Baseline marker of HF severity; useful for serial monitoring and response assessment. MBS item 66831.
AVAILABLE
Coronary Sinus Venography
Performed during implantation to identify suitable LV lead target veins. Not a pre-implantation outpatient test.
REFERRAL
EPS (Electrophysiology Study)
Consider if non-ischaemic cardiomyopathy with unexplained syncope or to assess VT inducibility for CRT-D vs CRT-P decision. Specialist only.
REFERRAL
Cardiopulmonary Exercise Test (CPET)
Peak VO₂ assessment for advanced HF therapy candidacy (transplant/VAD) if NYHA IIIb–IV despite maximal therapy.

Monitoring

Post-Implantation Device Follow-Up

CSANZ and the Heart Rhythm Society (HRS) recommend the following surveillance schedule:

1–2 weeks
Wound check, device interrogation, verify biventricular pacing % ≥ 95 %, assess lead thresholds and sensing.
1–3 months
First formal device clinic review. AV/VV optimisation (echo-guided if available). Confirm biv pacing %, review therapies (if CRT-D).
6 months
Repeat echocardiogram — assess LVEF improvement and LV reverse remodelling (LVESV reduction ≥ 15 % = echo-response). Clinical response assessment (NYHA class, KCCQ). Titrate OMT.
Every 3–6 months
Routine device interrogation (in-clinic or remote monitoring via CareLink/Merlin). Review pacing %, battery status, arrhythmia logs, lead impedances.
Annually
Comprehensive HF review — echo, BNP, medication optimisation, functional status, discuss advanced therapies if deteriorating.
At ERI*
*Elective Replacement Indicator — plan generator change. CRT-P ≈ 7–10 yrs; CRT-D ≈ 5–7 yrs. Discuss CRT-P vs CRT-D re-assessment at replacement.
ℹ️
Remote monitoring: MBS item 12322 rebates remote device monitoring in Australia. Telemetry-transmitted alerts for high VT/VF episodes, lead malfunction, or battery depletion enable timely intervention between clinic visits. Patients should be educated to report symptoms between uploads.

Special Populations

🤰 Pregnancy
CRT implantation is generally contraindicated during pregnancy
Radiation exposure from fluoroscopy during lead implantation poses risk to the foetus. If a pregnant patient has severe HFrEF with dyssynchrony, optimise medical therapy (avoiding ACEi/ARB/ARNI — use hydralazine + nitrate) and consider early delivery if feasible. If CRT is already in situ, device programming can be safely managed through pregnancy; battery changes avoid fluoroscopy.
👶 Paediatric / Congenital Heart Disease
CRT in paediatric patients
Off-label but increasingly used in children with congenital heart disease (post-surgical RV pacing cardiomyopathy, systemic RV failure, dilated cardiomyopathy). Coronary sinus anatomy is often challenging. Epicardial LV lead placement via thoracotomy is common. Outcomes data are limited to case series. Referral to a tertiary paediatric cardiac centre is essential (e.g., Royal Children's Hospital Melbourne, Children's Hospital Westmead Sydney).
👴 Elderly (≥ 80 years)
CRT-P preferred over CRT-D
Competing non-cardiac mortality reduces the absolute benefit of ICD component. CRT-P has been shown to improve quality of life, reduce HF hospitalisations, and improve survival in octogenarians in observational studies. Consider frailty assessment (Clinical Frailty Scale) and comorbidity burden. CRT is not excluded by age alone but requires careful individual risk–benefit discussion.
🫘 Renal Impairment
eGFR < 30 mL/min
CRT is still indicated if other criteria met. Patients on haemodialysis have higher procedural infection risk — consider epicardial lead approach or enhanced antibiotic prophylaxis (vancomycin + cefazolin). CKD does not preclude CRT benefit but is a negative prognostic marker. MRA use requires careful potassium monitoring in CKD.
🫁 Hepatic Impairment
Significant liver disease
Coagulopathy increases procedural bleeding risk — check INR, platelets pre-implantation. Cirrhotic cardiomyopathy may mimic HFrEF; ensure diagnostic certainty. Pharmacotherapy adjustments: amiodarone hepatotoxic risk; digoxin dose reduction; loop diuretics may worsen encephalopathy. CRT may still benefit selected patients with cardiomyopathy secondary to liver disease.
🛡️ Immunocompromised
Device infection risk is significantly elevated
Patients on immunosuppressants (post-transplant, chemotherapy, biologics) have 2–5× higher pocket infection rates. Consider subcutaneous ICD (S-ICD) + separate CRT-P approach to reduce transvenous infection risk. Antibiotic-eluting envelopes (TYRX™) may be considered. Infectious diseases consultation pre-implantation is recommended.

Aboriginal and Torres Strait Islander Health Considerations

Aboriginal and Torres Strait Islander Health
HF Burden
Aboriginal and Torres Strait Islander peoples experience heart failure at 1.5–2× the age-standardised rate of non-Indigenous Australians, with onset at younger ages and more advanced disease at presentation (AIHW 2023). Rheumatic heart disease, ischaemic cardiomyopathy, and chronic kidney disease contribute substantially.
CRT Access
Equity gaps exist in CRT referral and implantation. Remote and very remote communities face geographic barriers to tertiary electrophysiology centres. Telehealth pre-assessment, culturally safe referral pathways, and RFDS-supported transport are essential enablers. CSANZ supports outreach EP clinics in northern Australia.
Device Follow-Up
Remote monitoring (MBS 12322) is particularly valuable for First Nations patients in remote areas, reducing the need for long-distance travel. Device companies (Medtronic, Abbott) provide free remote monitoring platforms. Local Aboriginal Health Workers can be trained to facilitate device uploads.
Cultural Safety
Shared decision-making must incorporate cultural values, family involvement, and connection to Country. Implantable device concerns (body image, 'foreign body' beliefs) should be discussed openly and respectfully. Aboriginal Liaison Officers should be involved at all stages of device therapy.
RHD Considerations
Rheumatic heart disease — prevalent in remote NT, QLD, WA communities — can lead to LV dysfunction and dyssynchrony suitable for CRT. Secondary prophylaxis (benzathine penicillin) adherence and echocardiographic screening (RHD Australia guidelines) are critical co-interventions.
Data & Research
Indigenous-specific CRT outcome data are limited. Participation in registries such as the Australian and New Zealand Cardiac Device Registry (ANZCDR) with Indigenous identifiers is encouraged to address this evidence gap. NHMRC guidelines for ethical conduct of research in Aboriginal and Torres Strait Islander populations must be followed.

📚 References

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  9. 9. Australian Institute of Health and Welfare (AIHW). Heart, stroke and vascular disease — Australian facts. AIHW, Canberra. 2023.
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  11. 11. Strauss DG, Selvester RH, Wagner GS. Defining left bundle branch block in the context of cardiac resynchronisation therapy. Heart Rhythm. 2011;8(6):885–889.
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