Bradycardia and pacing indications

Overview and definitions

The working definition of bradycardia depends on whose document you are reading. ANZCOR gives the conventional definition of bradyarrhythmia as a heart rate below 60/min.^[7] It notes that for some people or some situations a rate below 60/min is not harmful and may be entirely physiological.^[7] The 2018 ACC/AHA/HRS guideline quotes the National Institutes of Health definition: a heart rate below 60 bpm in adults other than well-trained athletes.^[4] Population studies frequently use a lower cut-off of 50 bpm.^[4]

In SND, the number matters less than the patient.^[4] ACC/AHA/HRS 2018 chose a sinus rate below 50 bpm and/or a sinus pause over 3 seconds as potential components of the definition of SND.^[4] Sinus bradycardia or a pause over 3 seconds alone should not be used to diagnose SND.^[4] With rare exceptions, the sole reason for considering any treatment for SND is the presence of symptoms.^[4]

ESC 2021 describes SND, also known as sick sinus syndrome, as a wide spectrum of sinoatrial dysfunctions, ranging from sinus bradycardia, sinoatrial block and sinus arrest to bradycardia–tachycardia syndrome.^[1] An inadequate chronotropic response to exercise, chronotropic incompetence, is an additional manifestation.^[1]

Not every slow heart is diseased.^[1] ESC 2021 gives an example: sinus bradycardia of 40–50 b.p.m. at rest, or as slow as 30 b.p.m. while sleeping, particularly in trained athletes.^[1] This could be accepted as a physiological finding that does not require cardiac pacing.^[1] In healthy subjects, pauses over 2.5 s are uncommon, but this per se does not necessarily constitute a clinical disorder, and asymptomatic bradyarrhythmias are common in athletes.^[1] In its section on SND, ESC 2021 says that in the absence of published trials, no recommendations can be made for bradycardia detected in asymptomatic patients.^[1] However, in patients investigated for syncope in whom asymptomatic pause(s) over 6 s due to sinus arrest are documented, pacing may be indicated.^[1] Its Class I row for permanent or paroxysmal third-degree, second-degree type 2, infranodal 2:1 or high-degree AVB in sinus rhythm, covered below, applies irrespective of symptoms (Class I, Level C).^[1] In asymptomatic narrow-QRS 2:1 AVB, pacing may be avoided if supra-Hisian block is clinically suspected (concomitant Wenckebach is observed and block disappears with exercise) or demonstrated at EPS.^[1]

Classification

Start by asking where the problem sits and whether it is reversible. ESC 2021 broadly categorises pathological bradyarrhythmias into intrinsic and extrinsic aetiologies, and stresses that it is essential to differentiate reversible from non-reversible causes.^[1] In general, patients considered for pacing can be broadly classified into two groups: persistent bradycardia, and intermittent bradycardia (with or without ECG documentation).^[1] Persistent bradycardia usually indicates intrinsic disease in the sinus node tissue or the AV conduction system, whereas intermittent bradycardia can result from a wide variety of intrinsic and extrinsic pathological processes.^[1]

AV block on the ECG

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Where is the block? Nodal versus infranodal

^[4]

ACC/AHA/HRS 2018 notes that AV block may be classified anatomically by the site of block, usually divided into AV nodal, intra-Hisian (within the His bundle) and infra-Hisian (below the His bundle).^[4] The site of block may be clinically important and can be determined by invasive EPS when it is not apparent from the ECG and clinical circumstances.^[4] High-degree AV block is generally considered to be intra- or infra-Hisian and treated with pacing.^[4] In unusual circumstances (at night, with accompanying sinus slowing) a vagal aetiology may be considered, especially when the QRS is narrow.^[4]

^{[4] [1]}

Conduction disorders without AV block

ESC 2021 groups patients with 1:1 AV conduction and QRS abnormalities from delayed or blocked His–Purkinje conduction.^[1] The group covers bundle branch block (BBB), fascicular block alone or with BBB, and non-specific intraventricular delay.^[1] Bifascicular block is defined as left bundle branch block (LBBB), or right bundle branch block (RBBB) combined with left anterior or posterior fascicular block.^[1] Alternating BBB is a rare condition with clear ECG evidence of block in all three fascicles on successive ECGs.^[1] Examples are LBBB and RBBB morphologies on successive ECGs, or RBBB with left anterior fascicular block on one ECG and left posterior fascicular block on another.^[1]

Epidemiology and natural history

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High-degree AVB and SND are the most common indications for permanent pacing (ESC 2021).^[1] Their natural histories differ.^[1] Non-paced patients with high-degree AVB have poorer survival than paced patients.^[1] SND follows an unpredictable course, and there is no evidence that pacing improves its prognosis.^[1] Studies have been unanimous in finding improved quality of life with pacing.^[1]

Reversible causes matter in acute presentations.^[1] ESC 2021 cites a study of 277 patients referred to the emergency department with bradycardia.^[1] The underlying cause was electrolyte disorders in 4%, intoxication in 6%, acute myocardial infarction (MI) in 14% and adverse drug effects in 21%.^[1]

Sex differs in indication and in risk.^[1] In male patients, primary pacemaker implantation is more often indicated for AVB and less so for SND and AF with bradycardia.^[1] In female patients the rate of procedure-related adverse events is significantly higher, corrected for age and type of device, driven mostly by pneumothorax, pericardial effusion and pocket haematomas (ESC 2021).^[1]

Pathophysiology

Most bradycardias requiring cardiac pacing are observed in the elderly (ESC 2021).^[1] ACC/AHA/HRS 2018: SND, historically referred to as sick sinus syndrome, is most often related to age-dependent, progressive, degenerative fibrosis of the sinus nodal tissue and surrounding atrial myocardium.^[4] The same milieu of degenerative fibrosis is also responsible for atrial arrhythmias, which can coexist with sinus node disease; the combination is often called “tachy-brady syndrome”.^[4]

ESC 2021 calls the bradycardia–tachycardia variant the most common form of SND, characterised by progressive, age-related, degenerative fibrosis of the sinus node tissue and atrial myocardium.^[1] The bradyarrhythmias may be atrial pauses due to sinoatrial blocks, or overdrive suppression after an atrial tachyarrhythmia.^[1] In patients presenting with high ventricular rates, control of atrial tachyarrhythmias may be difficult before implant, as drugs prescribed for rate control may worsen bradyarrhythmias.^[1]

AV block has congenital and acquired causes.^[4] ACC/AHA/HRS 2018 lists congenital and acquired forms; acquired forms are much more common and include infectious, inflammatory, degenerative, ischaemic and iatrogenic causes.^[4] Degenerative causes are the most commonly seen in clinical practice and are associated with increased age, chronic hypertension and diabetes mellitus.^[4] Infectious causes, particularly Lyme carditis, are important to consider in the appropriate patient, as the block may be reversible with appropriate medical treatment.^[4] Block from inferior wall ischaemia or MI may be reversible.^[4] Vagotonic block is usually transient and generally does not require pacing.^[4]

Vagal influences can also produce AV block.^[4] Patients with vagally mediated AV block can be asymptomatic if the block occurs at night during sleep, when parasympathetic tone is increased.^[4] Vagally mediated AV block during sleep can be recognised by concomitant sinus node slowing (P-P prolongation).^[4] Nocturnal bradyarrhythmias are common in the general population and in most circumstances are physiological, vagally mediated, asymptomatic events that do not require intervention (ESC 2021).^[1] In sleep apnoea syndrome, hypoxaemia is a key mechanism leading to increased vagal tone and bradycardic rhythm disorders.^[1]

Why does untreated AV block kill?^[1] ESC 2021: death is due not only to heart failure from low cardiac output.^[1] It is also due to sudden cardiac death from prolonged asystole or bradycardia-triggered ventricular tachyarrhythmia.^[1] Although randomised controlled trials (RCTs) of pacing in AVB have not been performed, several observational studies show that pacing prevents recurrence of syncope and improves survival.^[1]

Coronary supply and infarction

The right coronary artery supplies the sinus node in 60% and the AV node and His bundle in 90% of patients (ESC 2021).^[1] AVB is located above the His bundle in most patients with inferior infarction, but is usually infra-Hisian and preceded by intraventricular conduction disturbances in anterior infarction.^[1]

When the pacemaker itself causes harm

ESC 2021: there is strong evidence that chronic conventional RV pacing may be deleterious in some patients.^[1] It may lead to left ventricular (LV) dysfunction and heart failure, even when AV synchrony is maintained.^[1] The effect is only partly explained by the abnormal activation sequence and may involve myocardial perfusion and humoral, cellular and molecular changes.^[1] Pacing-induced cardiomyopathy occurs in 10–20% of patients after 2–4 years of RV pacing.^[1] It is associated with a RV pacing burden over 20%.^[1] Yet no data support any percentage as a true limit below which RV pacing is safe and beyond which it is harmful.^[1]

The 2023 HRS/APHRS/LAHRS guideline adds that RV pacing and LBBB produce similar electromechanical dyssynchrony.^[5] Factors such as the degree of dyssynchrony, percentage of RV pacing, functional mitral regurgitation and pre-existing LV dysfunction contribute to cardiomyopathy.^[5] It cites a systematic review of 26 studies (6 prospective) in nearly 58,000 patients with a pooled prevalence of pacing-induced cardiomyopathy of 12%, using 15 unique definitions.^[5] Reported incidence has ranged from 5.9% to 39% over follow-up of 0.7 to 16 years.^[5]

Clinical presentation

ESC 2021: patients with SND may have symptoms from the bradyarrhythmia and/or from accompanying atrial tachyarrhythmias in the bradycardia–tachycardia form.^[1] Symptoms may be present at rest, at the end of a tachyarrhythmic episode (the conversion or pre-automaticity pause) or during exercise.^[1] They may range from mild fatigue to light-headedness, dizzy spells, near-syncope and syncope.^[1] Dyspnoea on exertion may be related to chronotropic incompetence.^[1]

In AVB, first-degree block is usually asymptomatic, and syncope and dizziness are mainly seen in high-degree and complete AVB, especially paroxysmal forms (ESC 2021).^[1] Heart failure symptoms are more common in chronic AVB with permanent bradycardia, but can occur in first-degree AVB with a very prolonged PR interval.^[1] Given the commonly advanced age at onset of AVB, fatigue, exertional intolerance and heart failure are sometimes underestimated.^[1] Deterioration of cognitive function is often only speculative, so improvement after implantation is unpredictable and unlikely.^[1]

Profound first-degree AV block can cause fatigue or exertional intolerance when the PR interval is long enough to lose AV synchrony (ACC/AHA/HRS 2018).^[4] This is often called “pseudo pacemaker syndrome”, and may occur with a PR interval over 300 ms.^[4] Wenckebach block is often asymptomatic and seen in active, healthy patients with no history of heart disease, but if frequent or occurring during exercise it can cause exertional intolerance or dizziness.^[4]

A normal ECG does not exclude paroxysmal AV block in syncope.^[4] One study cited by ACC/AHA/HRS 2018 found paroxysmal idiopathic AV block with no identifiable underlying cause in 8% of syncope patients with a normal ECG and echocardiogram.^[4] Other studies of patients with syncope and bundle branch or bifascicular block found clinically relevant His–Purkinje conduction abnormalities at EPS in 61%.^[4]

Isolated fascicular block and BBB are rarely associated with symptoms, but may mark underlying structural heart disease (ESC 2021).^[1] Between 15% and 20% of unexplained falls may be syncopal, possibly bradyarrhythmic, and retrograde amnesia, frequent in the falling elderly, is responsible for misinterpretation of the event.^[1]

Differential diagnosis and reversible causes

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Two ECG traps from ACC/AHA/HRS 2018. A 1:1 P–QRS relationship may be missing if the atrial and ventricular rates are similar (isorhythmic dissociation).^[4] It may also be missing when sinus bradycardia coexists with an accelerated junctional rhythm without consistent retrograde ventriculoatrial conduction.^[4] In atrial bigeminy, a repetitive premature atrial contraction may conduct normally, with delay, or be blocked, and any of these can lead to an erroneous diagnosis of AV block.^[4]

A drug does not always explain the block.^[4] Overdoses of antiarrhythmic drugs, beta blockers and calcium channel blockers may cause reversible AV block (ACC/AHA/HRS 2018).^[4] But several studies have shown that therapeutic doses are not commonly responsible for new AV block.^[4] Most patients in this scenario ultimately require permanent pacing.^[4]

Clinical and bedside assessment

ESC 2021: a complete history should include family history, comprehensive cardiovascular risk assessment and recent or past diagnoses that may cause bradycardia.^[1] The history should focus on the frequency, severity and duration of symptoms that might suggest bradycardia or conduction system disease.^[1] Explore the relation of symptoms to physical activity, emotional distress, positional changes, medical treatment and typical triggers (e.g. urination, defecation, cough, prolonged standing and shaving), as well as the pulse rate if measured during an episode.^[1] Family history may be especially important in young patients with progressive cardiac conduction disease, isolated or with cardiomyopathies and/or myopathies.^[1]

Examination looks for manifestations of bradycardia and for structural heart disease or systemic disorders.^[1] A symptomatic slow peripheral pulse should be confirmed with cardiac auscultation or an ECG, so that other rhythms, such as premature ventricular contractions, are not misread as bradycardia.^[1] Orthostatic changes in heart rate and blood pressure may help, because autonomic regulation disorders are important in the differential diagnosis of syncope.^[1]

Investigations

A 12-lead ECG or rhythm strip during the symptomatic episode provides the definitive diagnosis (ESC 2021).^[1] The ECG may also show signs of structural heart or systemic illness, such as LV hypertrophy, Q waves, a prolonged QT interval or low voltage.^[1] These predict adverse outcomes in symptomatic patients.^[1] ACC/AHA/HRS 2018 recommends a 12-lead ECG in suspected bradycardia or conduction disorder to document rhythm, rate and conduction, and to screen for structural heart disease or systemic illness (COR I, LOE B-NR).^[4] Its purpose is to document rhythm, rate and conduction, and to screen for structural heart disease or systemic illness.^[4]

ESC 2021 diagnostic recommendations

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Choosing and reading the tests

• Monitoring: the intermittent nature of most symptomatic bradycardia secondary to conduction system disease often requires prolonged ambulatory monitoring to correlate rhythm with symptoms, and the device is chosen by the frequency and nature of symptoms (ESC 2021).^[1]
• Implantable loop recorder: symptoms less than once a month need longer monitoring; the implantable loop recorder can monitor for up to 3 years without active patient participation.^[1]
• Exercise: symptoms during exercise are likely to be due to cardiac causes, whereas symptoms after exercise are usually reflex. Tachycardia-related exercise-induced second-degree and complete AVB are located distal to the AV node and predict progression to permanent AVB.^[1]
• Exercise without symptoms: there are no data supporting exercise testing in patients without exercise-related symptoms.^[1]
• Chronotropic incompetence: the most commonly used definition is failure to reach 80% of the expected heart rate reserve, the difference between the age-predicted maximal heart rate (220 – age) and the resting heart rate. Some medical treatments and comorbidities cause exercise intolerance and make the diagnosis of chronotropic incompetence by exercise testing more difficult.^[1]
• Imaging: echocardiography is the most commonly available technique and can be used in haemodynamic instability. Late gadolinium enhancement (LGE) and T2 cardiac magnetic resonance (CMR) can diagnose specific causes of conduction disturbances (sarcoidosis and myocarditis), and T2 sequences detect inflammation as a potential cause of transitory conduction abnormalities that may not need a permanent pacemaker.^[1]
• Genetics: progressive cardiac conduction disease may be diagnosed with unexplained progressive conduction abnormalities in young (under 50 years) individuals with structurally normal hearts, without skeletal myopathy, especially if there is a family history of progressive cardiac conduction disease; common genes are SCN5A and TRPM4 (isolated forms) and LMNA (with heart failure).^[1]
• Sleep apnoea: appropriate treatment reduces bradycardia episodes by 72–89%. Patients with asymptomatic nocturnal bradyarrhythmias or conduction disease should be evaluated for sleep apnoea; if confirmed, treatment with continuous positive airway pressure (CPAP) and weight loss can improve sleep-related bradyarrhythmias and permanent pacing should be avoided.^[1]
• Tilt: a positive cardioinhibitory response predicts, with high probability, asystolic spontaneous syncope; a vasodepressor, mixed or negative response does not exclude asystole during spontaneous syncope.^[1]

Electrophysiology study

Non-invasive monitoring has reduced the need for EPS, which is generally an adjunct in syncope when bradycardia is suspected but undocumented after non-invasive evaluation (ESC 2021).^[1] In syncope with bifascicular block, three findings identify a group at higher risk of developing AVB.^[1] They are a His–ventricular (HV) interval of 70 ms or more; an HV of 100 ms or more after pharmacological stress (ajmaline, procainamide, flecainide or disopyramide); or induction of second- or third-degree AVB by atrial pacing or pharmacological stress.^[1] In the Scheinman data, which ESC 2021 quotes in its section on bundle branch block, unexplained syncope and abnormal EPS, progression to AVB at 4 years was 4% with HV under 70 ms.^[1] It was 12% with HV 70–100 ms and 24% with HV over 100 ms.^[1]

EPS is preferred over an implantable loop recorder (ILR) in syncope with a high pre-test probability of significant conduction disease (e.g. abnormal ECG, BBB, ischaemic heart disease or scar-related cardiomyopathy).^[1] With a low pre-test probability (no structural heart disease, normal ECG), the ILR is preferred.^[1] A negative EPS does not exclude arrhythmic syncope: about one-third of patients with a negative EPS in whom an ILR is implanted develop AVB at follow-up.^[1]

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Management — the unstable slow heart

The first decision is not which drug, but whether this patient needs treatment now.^[7] ANZCOR: patients with a slow heart beat who do not experience symptoms usually do not require emergency therapy.^[7] Common symptoms of bradycardia include syncope, shortness of breath, dizziness or chest pain.^[7] A pulseless patient with a bradyarrhythmia is managed with the cardiac arrest algorithm (ANZCOR Guideline 11.2).^[7]

While assessing, ANZCOR advises giving oxygen and obtaining IV access if not already done (particularly if adverse signs are present), and recording a 12-lead ECG without delaying treatment.^[7] ANZCOR stresses recognising patients who are stable and have no adverse signs from an arrhythmia.^[7] If there is no immediate urgency for treatment, and especially if there is any uncertainty about the best choice of treatment, it advises seeking expert help (e.g. cardiology).^[7]

ANZCOR sequence

1. Atropine first: 500–600 mcg IV, repeated as necessary every 3–5 min up to a total dose of 3 mg (ANZCOR level of evidence III-2).^[7]
2. If atropine fails: low-dose adrenaline is the second-line agent, as a bolus or as an infusion, usually 2–10 mcg/min to maintain a satisfactory heart rate (a stable heart rate with a mean arterial pressure of 70 mmHg).^[7]
3. Other drugs ANZCOR lists: isoprenaline 2–5 mcg/minute, dopamine 2–5 mcg/kg/minute, theophylline and glycopyrrolate.^[7]
4. Pacing: patients who fail to respond to pharmacotherapy, or who are at high risk of asystole, may require electrical pacing by an internal or external route.^[7]

Transcutaneous pacing in practice (ANZCOR): many defibrillators can pace externally through the defibrillation paddles or adhesive pads; external pacing stimulates skeletal as well as cardiac muscle and may be uncomfortable.^[7] Pacing is usually set to demand at 70–80 beats per minute, starting low (for example 30 mA) and increasing until electrical capture with established output occurs.^[7] In some settings (such as pre-hospital) where there is a concern that electrical artefact may inhibit pacing in the demand mode, it is reasonable to use a fixed (asynchronous) mode.^[7]

^{[7] [1] [4]}

Temporary pacing (ESC 2021)

^[1]

Temporary pacing carries real costs.^[1] ESC 2021 says chronotropic medication should be considered before starting temporary pacing, taking side effects, contraindications and interactions into account.^[1] Transvenous temporary pacing carries a high risk of procedure-related complications, for example cardiac perforation, bleeding, malfunction, arrhythmias and accidental electrode displacement.^[1] It also risks complications of immobilisation, for example infection, delirium and thrombotic events.^[1] Previous temporary pacing is associated with an increased risk of permanent pacemaker infection.^[1] The ESC Task Force concludes that temporary transvenous pacing should be avoided if possible, and when required the lead should remain in situ for as short a time as possible.^[1]

• Balloon-tipped floating catheters are easier to insert, more stable and safer than semi-rigid catheters.^[1]
• No good data support either jugular or axillary/subclavian access, but intrathoracic subclavian puncture should be avoided to reduce pneumothorax risk, and a jugular access should be preferred if a permanent ipsilateral device is planned.^[1]
• A femoral access may be used in selected cases where fast and efficient pacing is needed; because passive femoral leads are unstable and the patient is immobilised, its duration should be as short as possible, until the bradycardia has resolved or a more permanent solution has been established.^[1]
• Transcutaneous pacing is fast, effective and non-invasive but less stable than transvenous pacing and limited by the need for continuous sedation; use it only in emergencies or when no other option is available, under close haemodynamic monitoring.^[1]
• If a patient meets the criteria for permanent pacemaker implantation, it should be performed promptly.^[1]

ACC/AHA/HRS 2018 acute recommendations (selected rows)

^[4]

On atropine dose, ACC/AHA/HRS 2018 notes that in sinus bradycardia, atropine 0.5 to 2 mg usually enhances automaticity.^[4] In rare cases it can be associated with intra-atrial re-entry or sinus pauses.^[4] The sinus node response is bimodal: lower doses (usually under 0.5 mg) are associated with slower rates, and higher doses with acceleration.^[4]

For SND with symptoms or haemodynamic compromise in the setting of acute spinal cord injury, ACC/AHA/HRS 2018 says aminophylline or theophylline is reasonable to increase heart rate and improve symptoms (COR IIa, LOE C-LD).^[4]

Toxic and drug-induced bradycardia (ACC/AHA/HRS 2018, selected rows)

• Calcium channel blocker overdose with bradycardia and symptoms or haemodynamic compromise: intravenous calcium is reasonable to increase heart rate and improve symptoms (COR IIa, LOE C-LD).^[4]
• Beta-blocker or calcium channel blocker overdose with bradycardia and symptoms or haemodynamic compromise: glucagon is reasonable, and high-dose insulin therapy is reasonable, to increase heart rate and improve symptoms (each COR IIa, LOE C-LD).^[4]
• Digoxin toxicity with bradycardia and symptoms or haemodynamic compromise: digoxin Fab antibody fragment is reasonable to increase heart rate and improve symptoms (COR IIa, LOE C-LD).^[4]
• Antidote doses: per local formulary and specialist guidance.

Management — permanent pacing indications

Once a reversible cause has been ruled out, two questions decide a permanent pacemaker. Are the symptoms caused by the bradycardia? And does the conduction abnormality carry a risk that justifies pacing even without symptoms?^[1] ESC 2021 frames the contrast directly: in general, pacing for asymptomatic SND has never been shown to affect prognosis, as opposed to pacing for AVB.^[1] SND can therefore be considered an appropriate indication for permanent pacing only when bradycardia due to SND is symptomatic.^[1] Treatment of AVB aims at ameliorating symptoms and preventing syncope and sudden cardiac death.^[1]

^{[1] [4]}

Sinus node dysfunction (ESC 2021)

^[1]

Correlation is the crux.^[1] ESC 2021 calls establishing a correlation between symptoms and bradyarrhythmia a crucial step in decision-making.^[1] Age, concomitant heart disease and other comorbidities may make a clear cause–effect relationship difficult to establish.^[1] When exercise intolerance comes with identified chronotropic incompetence, the usefulness of pacing is uncertain and the decision should be made case by case.^[1] In some cases, symptomatic bradyarrhythmias may be related to transient, potentially reversible or treatable conditions; correction of these factors is then required, whereas permanent pacing is not indicated.^[1]

Atrioventricular block (ESC 2021)

^[1]

Why are Mobitz II and complete block paced without symptoms?^[1] ESC 2021: in the absence of a reversible cause, the risk of severe symptoms and/or possible progression to more severe or complete AVB means these patients should receive a pacemaker even without symptoms.^[1] For an incidental asymptomatic 2:1 AVB, the decision is made case by case, distinguishing nodal from infranodal block.^[1] The distinction may be based on observations such as PR or PP interval prolongation before the block, the effect of exercise on AV conduction, and an EPS.^[1]

In Mobitz I, the course depends on the level of block.^[1] ESC 2021: supranodal block has a benign course, and the risk of progression to type II or a higher degree of AV block is low.^[1] Small, retrospective studies have suggested that, over the long term, second-degree type I AVB carries a higher risk of death in patients aged 45 years or older in the absence of pacemaker implantation.^[1] Infranodal block, rare in this form, carries a high risk of progression to complete heart block, syncope and sudden death, and warrants pacing even without symptoms.^[1] First-degree AVB usually has a good prognosis in the absence of structural heart disease, and without a clear symptom correlation a pacemaker is generally not indicated.^[1]

Paroxysmal AVB is paced on the same indications as permanent AVB, because of the risk of syncope, sudden death and progression (ESC 2021).^[1] It is crucial to rule out a reversible cause and to recognise reflex forms of AVB, which may not need pacing.^[1] Infranodal block documented by EPS supports intrinsic infranodal AVB.^[1] So does block initiated by atrial or ventricular premature beats, by an increased heart rate (tachy-dependent) or by a decreased heart rate (brady-dependent).^[1]

AF changes the picture. With AF and no permanent AVB or symptoms, ESC 2021 says there is no identifiable minimum pause duration as an indication for pacing.^[1] In the absence of a potentially reversible cause, bradycardia or inappropriate chronotropic response (from intermittent or complete AVB) associated or reasonably correlated with symptoms is an indication.^[1] Any high-degree or infranodal block is also an indication, even without symptoms.^[1] Without symptoms due to bradycardia and without high-degree or infranodal block, pacing is unlikely to be beneficial and is not indicated.^[1]

Bundle branch block and unexplained syncope (ESC 2021)

^[1]

A positive EPS yielded a positive predictive value as high as 80% for identifying patients who develop AVB.^[1] A negative EPS cannot rule out intermittent or paroxysmal AVB as the cause of syncope.^[1] In patients with a negative EPS, intermittent or stable AVB was documented by implantable loop recorder in about 50%.^[1] Elderly patients with bifascicular block and unexplained syncope might therefore benefit from an empirical pacemaker.^[1] This applies especially to unpredictable recurrent syncope with a high risk of traumatic recurrence, and the decision should rest on individual risk–benefit evaluation.^[1] Permanent pacemaker implantation is not indicated for BBB without symptoms, except alternating BBB, because only a minority (1–2% per year) develop AVB.^[1]

Reflex syncope (ESC 2021)

^[1]

In reflex syncope, ESC 2021 calls pacing the last resort, to be considered only in highly selected patients.^[1] These are patients over 40 years of age (mostly over 60) with severe forms of reflex syncope and frequent recurrences associated with a high risk of injury, often without a prodrome.^[1] Pacing may be effective if asystole is a dominant feature, but the fact that pacing is effective does not mean it is always necessary.^[1] Know the ESC 2021 definitions.

• Cardioinhibitory carotid sinus syndrome: the spontaneous syncope is reproduced by carotid sinus massage in the presence of an asystolic pause over 3 s.^[1]
• Asystolic tilt-positive test: the spontaneous syncope is reproduced in the presence of an asystolic pause over 3 s.^[1]
• Asystole on an implantable loop recorder: a symptomatic asystolic pause over 3 s, or an asymptomatic pause over 6 s, due to sinus arrest, AV block or the combination of the two.^[1]

ESC 2021 upgraded from IIb to I the indication for pacing in patients aged over 40 years with an asystolic tilt response over 3 s.^[1] The upgrade rested on studies including the SPAIN and BioSync CLS trials.^[1] For patients aged 40 years or under with the same severity criteria, the Task Force could make no recommendation for lack of trial evidence.^[1] Patients with hypotensive susceptibility need measures against it in addition to pacing, such as physical counterpressure manoeuvres, stopping or reducing hypotensive drugs, and fludrocortisone or midodrine.^[1]

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Suspected (undocumented) bradycardia: unexplained syncope and falls (ESC 2021)

^[1]

For recurrent unexplained syncope or falls at the end of the conventional work-up, ESC 2021 says ILR monitoring should be considered in an attempt to document a spontaneous relapse instead of embarking on empiric cardiac pacing.^[1] In a randomised double-blind trial, pacing did not prevent recurrences in patients with an unexplained fall in whom carotid sinus hypersensitivity could not induce syncope.^[1]

ACC/AHA/HRS 2018: selected rows on the same decisions

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ACC/AHA/HRS 2018 also recommends a pre-implant assessment of the risk of future ventricular arrhythmias and the need for an ICD in patients who require permanent pacing (COR I, LOE B-NR).^[4] Its supporting text on AF notes that diagnosing AV block in AF can be less straightforward than in sinus rhythm.^[4] In that text, it states that in the asymptomatic patient there is no specific pause duration that warrants permanent pacing.^[4]

Management — choosing the pacing mode

Once pacing is indicated, the next decision is the mode. ESC 2021: in SND, controlled studies found DDD superior to single-chamber ventricular pacing in reducing AF, with some effect on stroke.^[1] Dual-chamber pacing reduces the risk of pacemaker syndrome, which may occur in more than a quarter of patients with SND.^[1] DDD(R) is the pacing mode of first choice in SND.^[1] In SND, unnecessary RV pacing should be systematically avoided, because it may cause AF and deterioration of heart failure, particularly if systolic function is impaired or borderline.^[1]

ESC 2021 names potential exceptions in SND: very elderly and/or frail patients with infrequent pauses who have limited functional capacity and/or a short expected survival.^[1] In them, the benefit of DDD(R) over VVIR is expected to have limited or no clinical impact, and the complication risk of the second atrial lead should also be considered.^[1] In SND with prolonged AV conduction, programming an excessively long AV interval to avoid RV pacing may be haemodynamically disadvantageous, causing diastolic mitral regurgitation that may lead to symptoms and/or AF.^[1] A meta-analysis of algorithms for minimising RV pacing failed to show a significant effect compared with conventional DDD in patients with normal ventricular function, with regard to endpoints such as persistent/permanent AF, all-cause hospitalisation and all-cause mortality.^[1] In its SND section, ESC 2021 still calls the rationale for reducing unnecessary RV pacing strong, coupled with the benefit of extending device longevity.^[1]

In AVB, large parallel trials (AVB alone, or AVB and/or SND) failed to show superiority of DDD over ventricular pacing for mortality (ESC 2021).^[1] They have not consistently shown superiority for quality of life or morbidity, including stroke or transient ischaemic attack and AF.^[1] DDD is beneficial through avoidance of pacemaker syndrome, which occurred in up to a quarter of patients with AVB in these trials.^[1] DDD is preferred when reasonable: in patients without significant frailty, very advanced age, significant comorbidities limiting life expectancy, or very limited mobility.^[1] On a case-by-case basis, in frail elderly patients and/or when AVB is paroxysmal and pacing is anticipated to be infrequent, VVIR may be considered, as it carries a lower complication rate.^[1] VDD may be an alternative for advanced AV conduction abnormalities with spared sinus node function.^[1] Compared with DDD, VDD has fewer complications and shorter procedure and fluoroscopy times, but a high incidence of atrial undersensing.^[1]

The ESC 2021 section on AV block in permanent AF compares rate-responsive with fixed-rate pacing in patients with AF.^[1] Rate-responsive pacing is associated with better exercise performance, improved daily activities, fewer symptoms of shortness of breath, chest pain and palpitations, and improved quality of life.^[1] ESC 2021 therefore calls rate-adaptive pacing the mode of first choice in that setting (permanent AF), in line with its Class I row for ventricular pacing with rate response in permanent AF needing a pacemaker (Class I, Level C).^[1] Fixed-rate VVI should be reserved for older sedentary patients with very limited activity.^[1] The minimum rate is commonly programmed higher (e.g. 70 b.p.m.) than in sinus rhythm, to compensate for loss of active atrial filling.^[1] Rate-responsive systems sense surrogates such as body motion, minute ventilation or intracardiac impedance, and are indicated in chronotropic incompetence.^[1] ESC 2021 Figure 5 defines AV management as AV delay programming (avoiding values over 230 ms) or specific algorithms to avoid or reduce unnecessary ventricular pacing.^[1] It also notes that a leadless pacemaker may be considered in patients who would otherwise receive a VVI/VDD pacemaker.^[1]

^{[1] [4] [2]}

The mode trials

^{[9] [8] [10]}

Management — avoiding pacing-induced heart failure

The question has moved from “which chamber?” to “how do we keep the ventricles synchronous?”. The 2023 HRS/APHRS/LAHRS guideline defines cardiac physiologic pacing (CPP) as pacing intended to restore or preserve ventricular synchrony.^[5] CPP includes CRT with LV stimulation, His bundle pacing (HBP) and left bundle branch area pacing (LBBAP).^[5] ESC 2021: compared with RV pacing, HBP gives more physiological simultaneous ventricular activation via the His–Purkinje system.^[1] HBP can restore conduction in a subset of high-degree AVB, and can shorten QRS duration in some patients with LBBB or RBBB.^[1]

CRT and heart failure (ESC 2026 heart failure guideline)

^[2]

Where a row says HFrEF, the 2026 ESC HF guideline defines it as LVEF below 50% with symptoms and/or signs of HF; an LVEF or QRS threshold written in a row is that row’s own criterion.^[2]

The 2026 ESC HF guideline notes that RV pacing leads to HFrEF in some patients.^[2] The incidence of pacemaker- or RV pacing-induced HF varies between 5.9% and 39%, depending on the definition.^[2] In the BUDAPEST-CRT Upgrade trial, upgrading to CRT-D significantly reduced death and HF hospitalisation in patients with at least 20% RV pacing burden and QRS 150 ms or more (HR 0.27).^[2] It was the first RCT and included only 360 patients; the guideline concludes that CRT-D upgrade should be considered in such patients.^[2]

^[11]

LVEF over 35%: choosing the lead (HRS/APHRS/LAHRS 2023)

^[5]

In this guideline CPP is an umbrella term encompassing CRT with biventricular pacing and conduction system pacing (CSP), including HBP and LBBAP.^[5] In its supporting text, a high RV pacing burden (over 40%) has been associated with an increased risk of HF hospitalisation, as observed in the Mode Selection Trial (MOST).^[5]

Detecting and treating pacing-induced cardiomyopathy (HRS/APHRS/LAHRS 2023)

The same guideline addresses patients with reduced LV function (below 35%) or pacing-induced cardiomyopathy in a separate section.^[5] It gives its detection rows in a separate table on electrical dyssynchrony-induced cardiomyopathy, and its treatment rows in a table on pacing-induced cardiomyopathy with high-burden RV pacing.^[5]

^[5]

ACC/AHA/HRS 2018: physiologic pacing in AV block

Compare ACC/AHA/HRS 2018, for AV block with an indication for permanent pacing and LVEF between 36% and 50%.^[4] When ventricular pacing is expected more than 40% of the time, it is reasonable to choose pacing that maintains physiologic ventricular activation (e.g. CRT or HBP) over RV pacing (COR IIa, LOE B-R, SR: systematic review).^[4] When it is expected less than 40% of the time, it is reasonable to choose RV pacing over those methods (COR IIa, LOE B-R).^[4] A separate row has no LVEF condition: in AV block at the level of the AV node with an indication for permanent pacing, His bundle pacing may be considered to maintain physiologic ventricular activation (COR IIb, LOE B-R, SR: systematic review).^[4]

Conduction system pacing

^[1]

ESC 2021: in patients considered for CRT in whom coronary sinus lead implantation is unsuccessful, HBP should be considered as a treatment option along with other techniques such as surgical epicardial lead (Class IIa, Level B).^[1] For CRT in HFrEF, the 2026 ESC HF guideline notes that LBBAP may prove a feasible alternative to CRT when implantation is challenging.^[2] However, no RCT with patient-centred outcomes has evaluated the efficacy or long-term safety of CSP in HFrEF, so no recommendations can currently be made.^[2]

ESC 2021 lists drawbacks of HBP.^[1] Capture thresholds are on average higher and sensing amplitudes lower than with RV pacing.^[1] At 5 years there were 9% generator changes with HBP vs 1% with RV pacing.^[1] Mid-term lead revision runs at about 7%, higher than the 2–3% with RV pacing.^[1] Observational data indicate that patients with HBP fare better than those with RV pacing in terms of HF hospitalisations if the percentage of ventricular pacing is over 20% (HR 0.54).^[1] Implant success was 76% in infranodal AVB and 93% in nodal block in one series of experienced operators.^[1]

For LBBAP, the lead is implanted slightly distal to the His bundle and screwed deep into the LV septum, ideally to capture the left bundle branch (ESC 2021).^[1] Electrical parameters are usually excellent, it may succeed in blocks too distal for HBP, and it facilitates AV junction ablation.^[1] Because data were still scarce, with concern about long-term lead performance and extraction, ESC 2021 could not formulate recommendations for LBBAP.^[1]

Practice has moved on since 2021.^[6] The 2025 ESC clinical consensus statement on conduction system pacing is a consensus document rather than a guideline.^[6] It states that since the 2021 guidelines the use of CSP has greatly evolved, mainly with LBBAP.^[6] Its advice for AV block is listed below; the strength-of-evidence ratings in its tables are graphics that are not reproduced here.^[6]

^[6]

Leadless pacing

Leadless pacemakers are miniaturised intracardiac devices inserted percutaneously through the femoral vein and implanted directly in the RV wall (ESC 2021).^[1] Potential difficulty with retrieval at the end of service is a limitation.^[1]

^[1]

• Real-world results of one system in 1817 patients reported serious adverse events in 2.7%; during initial operator experience, peri-operative major complications (including perforation and tamponade, vascular complications, ventricular arrhythmias and death) were higher, at 6.5%.^[1]
• Implant in an adequate setting with high-resolution multiplane fluoroscopy and cardiac surgery on site, because tamponade may be more difficult to manage than with standard pacing.^[1]
• VVI(R)-only devices restrict indications to AF or very infrequent pacing (e.g. paroxysmal AVB); VDD leadless pacing, detecting atrial contraction by accelerometer, extends indications to AVB with preserved sinus node function, with AV synchrony maintained 70–90% of the time, depending on position and activity, in two studies of 73 patients in sinus rhythm with high-degree AV block.^[1]
• There are no RCT data on the long-term safety and efficacy of leadless versus standard transvenous pacemakers, so the indication should be carefully considered case by case.^[1]
• The absence of long-term performance data and the limited data on retrievability and end-of-life strategy also require careful consideration before choosing a leadless pacemaker, especially in younger patients (e.g. life expectancy over 20 years).^[1]

Specific scenarios

Acute myocardial infarction

ESC 2021: the incidence of high-degree AVB in ST-elevation MI has declined to 3–4% in the primary PCI era, and it is most frequent in inferior or inferolateral infarctions.^[1] Patients with high-degree AVB have higher clinical risk and larger infarctions, especially when the block complicates an anterior infarction.^[1] Sinus bradycardia and AVB at presentation can be vagally mediated and may respond to atropine.^[1] AVB may need temporary pacing for refractory symptoms or haemodynamic compromise, but most often resolves spontaneously within a few days, and only a minority need permanent pacing.^[1]

The 2023 ESC acute coronary syndrome (ACS) guideline sets out its recommendations for ACS complications in Recommendation Table 14.^[3] Three of them sit under one condition: sinus bradycardia with haemodynamic intolerance, or high-degree AV block without a stable escape rhythm.^[3]

^[3]

On timing, the 2021 pacing guideline adds that the waiting period has to be decided individually.^[1] It may last up to 10 days but can be shortened to 5 days, depending on the occluded vessel, time delay and success of revascularisation.^[1] Conditions favouring consideration of earlier pacemaker implantation include unsuccessful or late revascularisation, anterior MI, bifascicular block or AV block before MI, and progression of AV block within the first days after MI.^[1] Sick sinus syndrome after right coronary artery occlusion resolves in most cases; even if revascularisation is incomplete, implantation can usually still be postponed and performed only if symptoms due to sinus bradycardia persist.^[1] In patients with persistent intraventricular conduction abnormalities and transient AVB in whom permanent pacing was recommended in the past, there is no evidence that permanent pacing improves outcome.^[1] These patients frequently have HF and poor LV function.^[1] If early device implantation is considered, they should be evaluated for ICD, CRT-P or CRT-D rather than conventional pacing.^[1]

The 2025 ACC/AHA/ACEP/NAEMSP/SCAI guideline for acute coronary syndromes covers AV block in its section on electrical complications and prevention of sudden cardiac death after ACS.^[13] Its supportive text notes that patients with STEMI with second- or third-degree AV block have higher in-hospital mortality than those without high-degree AV block.^[13] Temporary pacemaker insertion in ACS in patients with high-degree AV block and other pacer indications has been found to improve postdischarge survival.^[13] Permanent pacemaker insertion is recommended with unresolved high-degree AV block that persists over 72 hours; this is supportive-text wording, so no class is given here.^[13] The 2018 ACC/AHA/HRS bradycardia guideline, which predates it, has these acute-MI rows.^[13][4]

^[4]

After cardiac surgery and heart transplantation

ESC 2021 pacing guideline: AVB may occur in 1–4% of cases after cardiac surgery and in about 8% after repeat valve surgery.^[1] The ideal timing of implantation after cardiac surgery is controversial because 60–70% of patients implanted for SND and up to 25% of those implanted for AVB are not pacemaker dependent at follow-up.^[1] With complete AVB in the first 24 h after valvular surgery that persists for 48 h, resolution within the next 1–2 weeks is unlikely and earlier implantation may be considered.^[1]

^[1]

For surgery in infective endocarditis, the 2023 ESC endocarditis guideline has a table of recommendations for pacemaker implantation in patients with complete AV block and infective endocarditis.^[14] Immediate epicardial pacemaker implantation should be considered in patients undergoing surgery for valvular IE and complete AVB if one of the following predictors of persistent AVB is present (Class IIa, Level C).^[14] The predictors are pre-operative conduction abnormality, Staphylococcus aureus infection, aortic root abscess, tricuspid valve involvement, or previous valvular surgery.^[14]

Chronotropic incompetence is always present after standard orthotopic heart transplantation, as a result of loss of autonomic control (ESC 2021).^[1] SND leads to permanent pacemaker implantation after heart transplantation in 8% of patients.^[1] ACC/AHA/HRS 2018, in its recommendations for theophylline/aminophylline for bradycardia attributable to SND: in post-heart transplant patients, aminophylline or theophylline is reasonable to increase heart rate if clinically indicated (COR IIa, LOE C-LD).^[4]

After transcatheter aortic valve implantation (TAVI)

ESC 2021 reports permanent pacemaker rates after TAVI of 3.4% to 25.9% in randomised trials and large registries.^[1] Because RV pacing may lead to deterioration in LV function, efforts to minimise unnecessary permanent pacing are warranted.^[1] Predictors for permanent pacing, especially RBBB, which has been identified as the most consistent and powerful predictor, should be incorporated into procedural planning, including transcatheter valve selection, implantation height and balloon inflations.^[1] Patients without new conduction disturbances after TAVI are at very low risk of developing high-degree AVB.^[1]

^[1]

New-onset LBBB is the most frequent conduction abnormality after TAVI, given the close anatomical proximity of the aortic valve and the left bundle branch (ESC 2021).^[1] Only a small minority of these patients require pacemaker implantation.^[1] ESC 2021 identifies several high-risk subgroups of patients with new LBBB. In such patients with dynamic progression after TAVI (new BBB with dynamic prolongation of QRS and/or PR), an extended in-hospital monitoring period of up to 5 days should be considered.^[1] New-onset LBBB with QRS below 150 ms may not require further evaluation during hospitalisation.^[1] Separately, ESC 2021 Figure 12 has a box for persistent new LBBB with QRS over 150 ms or PR over 240 ms with no further prolongation during more than 48 h after the procedure.^[1] A footnote to that box lists high-risk parameters for high-degree AV block in new-onset LBBB: AF, a prolonged PR interval and LVEF below 40%.^[1] Given low long-term pacing dependency after TAVI, algorithms promoting spontaneous AV conduction should be used.^[1]

Procedural predictors in ESC 2021 Table 10 include a self-expandable valve and deeper valve implantation.^[1] They also include a larger prosthesis-to-annulus or LV outflow tract diameter ratio, and TAVI in a native valve rather than a valve-in-valve procedure.^[1] Patients with pre-existing advanced conduction system disease who may have an indication for permanent pacing irrespective of the TAVI procedure need consultation with an electrophysiologist before the procedure.^[1]

ACC/AHA/HRS 2018 recommends permanent pacing before discharge for new AV block after transcatheter aortic valve replacement associated with symptoms or haemodynamic instability that does not resolve (COR I, LOE B-NR).^[4] In new persistent BBB after the procedure, careful surveillance for bradycardia is reasonable (COR IIa, LOE B-NR).^[4] In new persistent LBBB after the procedure, a permanent pacemaker may be considered (COR IIb, LOE B-NR).^[4] The 2023 HRS/APHRS/LAHRS guideline found insufficient data to recommend a device type after TAVI beyond those for AV block or LBBB in other settings.^[5]

Congenital AV block and congenital heart disease (ESC 2021)

^[1]

Maternal or fetal factors can cause congenital heart block, particularly autoimmune diseases such as systemic lupus erythematosus and Sjögren syndrome.^[1] Patients with congenital AVB may be asymptomatic or present with reduced exercise capacity, syncope, congestive HF, ventricular dysfunction and dilatation.^[1] Sudden death may occur through an increased propensity to bradycardia-related ventricular arrhythmias such as torsades de pointes.^[1] With an intracardiac shunt between the systemic and pulmonary circulations, endovascular lead placement is relatively contraindicated because of the risk of arterial embolism.^[1] Post-operative high-degree AVB is estimated to occur in 1–3% of patients undergoing surgery for CHD, and in children transient early post-operative AVB usually resolves within 7–10 days.^[1]

Pregnancy (ESC 2025 pregnancy guideline; ESC 2021 pacing guideline)

• ESC 2025 pregnancy guideline: there are no data on progression of congenital AV conduction block during pregnancy, and vaginal delivery does not cause extra risk for mothers who are asymptomatic, haemodynamically stable and have a normal cardiac anatomy and function.^[15]
• ESC 2025: prophylactic placement of temporary pacemaker wires is not usually indicated but is an individualised decision; in pregnant women with asymptomatic congenital AV block, normal cardiac anatomy and function, a narrow QRS complex and ventricular rate of 50 b.p.m. or more, a prophylactic temporary pacemaker during delivery is not recommended (Class III, Level C).^[15]
• ESC 2025: pacing indications (temporary and permanent) do not differ between pregnant and non-pregnant women; if an ICD, pacemaker or resynchronisation therapy device is indicated during pregnancy, implantation is recommended with optimal radiation protection (Class I, Level C).^[15]
• ESC 2021 pacing guideline: with a stable, narrow-complex junctional escape rhythm and none of the risk factors (syncope, pauses over 3 times the cycle length of the ventricular escape rhythm, wide QRS escape rhythm, prolonged QT interval, complex ventricular ectopy, mean daytime heart rate below 50 b.p.m.), implantation may not be necessary or can be deferred until after delivery.^[1]
• ESC 2021: women with complete heart block and a slow, wide-QRS escape rhythm should undergo pacemaker implantation during pregnancy.^[1]
• ESC 2021: implantation risks are generally low, especially beyond 8 weeks of gestation, and a pacemaker for symptomatic bradycardia can be implanted at any stage of pregnancy using echo guidance or electroanatomic navigation to minimise fluoroscopy; ESC 2025 adds that pacemakers can be implanted safely during pregnancy using standard methods with minimal fluoroscopy or non-fluoroscopic methods.^[1][15]

Complications and pitfalls

^[1]

Complications after dual-chamber implantation in MOST were 4.8% at 30 days, 5.5% at 90 days and 7.5% at 3 years (ESC 2021).^[1] Risk generally rises with device complexity, and with upgrades or lead revisions compared with de novo implantation.^[1] Complications were 60% higher with inexperienced operators who had performed fewer than 25 implantations.^[1] Leads are a frequent source of complications through dislodgement, insulation defects, fractures and sensing or threshold problems.^[1] Pocket haematoma (2.1–9.5%) can usually be managed conservatively, but evacuation is associated with an approximately 15-fold increase in infection risk.^[1] Lifetime system infection risk was 1.19% with a pacemaker, 1.91% with an ICD, 2.18% with CRT-P and 3.35% with CRT-D.^[1] Risk was higher with reoperations, previous device-related infection, male sex and younger age.^[1] Increased complication risks have been observed in women (mainly pneumothorax and cardiac perforation) and in those with a low body mass index.^[1]

Prognosis, follow-up and disposition

AVB and SND carry different prognoses.^[1] Non-paced patients with high-degree AVB have poorer survival than paced patients (ESC 2021).^[1] In SND there is no evidence that pacing improves prognosis.^[1]

^[1]

Because of their higher lead revision rate, ESC 2021 advises follow-up of HBP patients at least once every 6 months or placing them on remote monitoring.^[1] With remote monitoring, it advises ensuring that automatic threshold measurements correspond to those measured manually, as this may not be the case and depends on device configuration.^[1] When pacing is no longer indicated, ESC 2021 recommends basing the management strategy on an individual risk–benefit analysis in a shared decision-making process together with the patient (Class I, Level C).^[1] One option is to leave the generator and leads in situ.^[1] Its feasibility depends on the end-of-life behaviour of the implanted generator, which is manufacturer dependent and may be erratic and lead to complications in rare cases.^[1] This option is the preferred approach for selected frail and elderly patients.^[1] ACC/AHA/HRS 2018: in patients with indications for permanent pacing but significant comorbidities, such that pacing is unlikely to provide meaningful clinical benefit, implantation or replacement should not be performed (COR III: No Benefit, LOE C-LD).^[4] The same applies if patient goals of care strongly preclude pacemaker therapy.^[4]

Special populations

• Older and frail patients: over 80% of pacemakers go to patients over 65; in AV block, on a case-by-case basis, in frail elderly patients and/or when AVB is paroxysmal and pacing is anticipated to be infrequent, VVIR may be considered for its lower complication rate (ESC 2021).^[1]
• Women: a higher, age- and device-adjusted rate of procedure-related adverse events (ESC 2021).^[1]
• Athletes: sinus bradycardia, even of 40–50 b.p.m. at rest or as slow as 30 b.p.m. asleep, particularly in trained athletes, could be accepted as a physiological finding that does not require cardiac pacing (ESC 2021).^[1]
• Young patients considering leadless pacing: the absence of long-term performance data and the limited data on retrievability and end-of-life strategy require careful consideration before choosing a leadless pacemaker, especially in younger patients (e.g. life expectancy over 20 years) (ESC 2021).^[1]
• Pregnancy and congenital heart disease: see Specific scenarios.

Evidence, guidelines and regional differences

After MI, the acute coronary syndrome guidelines are the newer documents: the 2023 ESC ACS guideline, with its Recommendation Table 14 rows on bradyarrhythmias, and the 2025 ACC/AHA ACS guideline.^[3][13] The US supportive text recommends permanent pacemaker insertion with unresolved high-degree AV block that persists over 72 hours (see Acute myocardial infarction).^[13]

^{[1] [4] [5]}

In Australia and New Zealand

This section summarises Guideline 11.9, Managing Acute Dysrhythmias, from the Australian and New Zealand Committee on Resuscitation (ANZCOR). ANZCOR notes that slow rhythms may be treated with drugs that increase heart rate, such as atropine or adrenergic agents, or with electrical pacing, internally by pacing wires or externally by pads.^[7] Patients with a slow heart beat who do not experience symptoms usually do not require emergency therapy; adverse signs (systolic BP below 90 mmHg, heart rate below 40/min, ventricular arrhythmia, heart failure) suggest a need for immediate treatment.^[7] When treatment is needed, atropine is the initial treatment, 500–600 mcg IV, repeated as necessary every 3–5 min up to a total of 3 mg.^[7] If this fails, low-dose adrenaline (as a bolus or as an infusion) is the second-line agent, usually 2–10 mcg/min to maintain a satisfactory heart rate (stable heart rate with a mean arterial pressure of 70 mmHg).^[7] Pacing may be required for failure to respond to drugs or a high risk of asystole.^[7] The potential risk of asystole is indicated by any of: recent asystole, Mobitz II AV block, complete AV block (especially with broad QRS or an initial rate below 40/min), or ventricular standstill over 3 s.^[7] ANZCOR also warns that every anti-arrhythmic treatment, including pacing, can make the rhythm worse rather than better.^[7]

High-yield summary

• Definitions: bradyarrhythmia is conventionally a rate below 60/min, although for some people or some situations a rate below 60/min is not harmful and may be entirely physiological (ANZCOR); ACC/AHA/HRS 2018 uses a sinus rate below 50 bpm and/or a sinus pause over 3 s as potential components of the definition of SND, but either alone should not be used to diagnose SND.^[7][4]
• Site of block: in general, nodal block has a faster, more reliable escape and greater responsiveness to autonomic manipulation such as atropine; block within or below the His bundle may progress rapidly and will not respond to atropine but will sometimes improve with catecholamines.^[4]
• SND (ESC 2021): pacing indicated when symptoms can clearly be attributed to bradyarrhythmias (I, B); not recommended for SND bradyarrhythmias that are asymptomatic or due to transient causes that can be corrected and prevented (III, C).^[1]
• AVB (ESC 2021): pacing indicated for permanent or paroxysmal third-degree, Mobitz II, infranodal 2:1 or high-degree AVB in sinus rhythm, irrespective of symptoms (I, C).^[1]
• Bifascicular block with unexplained syncope (ESC 2021): pacemaker indicated if baseline HV is 70 ms or more, second- or third-degree intra- or infra-Hisian block appears with incremental atrial pacing, or pharmacological challenge is abnormal (I, B).^[1]
• Acute (ANZCOR): when bradycardia needs treatment, atropine 500–600 mcg IV, repeated as necessary every 3–5 min up to a total of 3 mg; if this fails, low-dose adrenaline (as a bolus or as an infusion), usually 2–10 mcg/min to maintain a satisfactory heart rate (stable heart rate with a mean arterial pressure of 70 mmHg); failure to respond or high asystole risk may require pacing. No atropine after heart transplant.^[7]
• After MI: ESC 2023 ACS: permanent pacemaker recommended when high-degree AV block does not resolve within a waiting period of at least 5 days (I, C); pacing not recommended if it resolves after revascularisation or spontaneously (III, B). ACC/AHA 2025 ACS supportive text: permanent pacemaker insertion is recommended with unresolved high-degree AV block that persists over 72 hours (no class given).^[3][13]
• After TAVI (ESC 2021): permanent pacing recommended for complete or high-degree AVB persisting for 24–48 h (I, B) and for new-onset alternating BBB (I, C).^[1]
• Mode (ESC 2021): DDD(R) first in SND, with rate response (R) preferred only in chronotropic incompetence; in AVB, DDD should be preferred over single-chamber ventricular pacing to avoid pacemaker syndrome and improve quality of life (IIa, A); in its AV block table, in permanent AF needing a pacemaker, ventricular pacing with rate response function is recommended (I, C).^[1]
• Pacing-induced cardiomyopathy: 10–20% after 2–4 years of RV pacing, associated with a burden over 20% (ESC 2021); HFrEF, regardless of NYHA class or QRS width, with an indication for ventricular pacing for high-degree AV block: CRT rather than RV pacing should be considered to reduce the risk of HF hospitalisation and death (ESC 2026 HF, IIa, B1).^[1][2]

References15ShowHide

1. [1]Glikson M, Nielsen JC, Kronborg MB, et al. 2021 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Eur Heart J, 2021.PMID 34455430
2. [2]Køber L, Adamo M, Ruwald AC, et al. 2026 ESC Guidelines for the management of heart failure. Eur Heart J, 2026.PMID 42661420
3. [3]Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC Guidelines for the management of acute coronary syndromes. Eur Heart J, 2023.PMID 37622654
4. [4]Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol, 2019.PMID 30412709
5. [5]Chung MK, Patton KK, Lau CP, et al. 2023 HRS/APHRS/LAHRS guideline on cardiac physiologic pacing for the avoidance and mitigation of heart failure. Heart Rhythm, 2023.PMID 37283271
6. [6]Glikson M, Burri H, Abdin A, et al. European Society of Cardiology (ESC) clinical consensus statement on indications for conduction system pacing, with special contribution of the European Heart Rhythm Association of the ESC and endorsed by the Asia Pacific Heart Rhythm Society, the Canadian Heart Rhythm Society, the Heart Rhythm Society, and the Latin American Heart Rhythm Society. Europace, 2025.PMID 40159278
7. [7]Australian and New Zealand Committee on Resuscitation Guideline 11.9 – Managing Acute Dysrhythmias ANZCOR, 2026.Source
8. [8]Nielsen JC, Thomsen PE, Højberg S, et al. A comparison of single-lead atrial pacing with dual-chamber pacing in sick sinus syndrome. Eur Heart J, 2011.PMID 21300730
9. [9]Lamas GA, Lee KL, Sweeney MO, et al. Ventricular pacing or dual-chamber pacing for sinus-node dysfunction. N Engl J Med, 2002.PMID 12063369
10. [10]Toff WD, Camm AJ, Skehan JD, et al. Single-chamber versus dual-chamber pacing for high-grade atrioventricular block. N Engl J Med, 2005.PMID 16014884
11. [11]Curtis AB, Worley SJ, Adamson PB, et al. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J Med, 2013.PMID 23614585
12. [12]Brignole M, Russo V, Arabia F, et al. Cardiac pacing in severe recurrent reflex syncope and tilt-induced asystole. Eur Heart J, 2021.PMID 33279955
13. [13]Rao SV, O'Donoghue ML, Ruel M, et al. 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation, 2025.PMID 40014670
14. [14]Delgado V, Ajmone Marsan N, de Waha S, et al. 2023 ESC Guidelines for the management of endocarditis. Eur Heart J, 2023.PMID 37622656
15. [15]De Backer J, Haugaa KH, Hasselberg NE, et al. 2025 ESC Guidelines for the management of cardiovascular disease and pregnancy. Eur Heart J, 2025.PMID 40878294