Atrioventricular (AV) Block

Classification

• First-degree AV block – prolonged PR interval >200 ms with maintained 1:1 conduction.
• Second-degree AV block – intermittent failure of conduction, subdivided into:
  • Mobitz I (Wenckebach) – progressive PR prolongation until a beat is dropped.
  • Mobitz II – fixed PR intervals with sudden failure of conduction.
  • 2:1 or high-grade block – every second or multiple consecutive P waves not conducted.
• Third-degree (complete) AV block – complete absence of conduction between atria and ventricles, with independent atrial and ventricular activity.

Congenital Causes

• Congenital AV block may occur with or without structural heart disease.
• With congenital heart disease: commonly associated with atrioventricular canal defects, transposition of the great arteries, heterotaxy syndrome, left atrial isomerism, and tetralogy of Fallot.
• Without structural heart disease: more frequently seen than structural associations.
• Immune-mediated injury is a key mechanism, often due to maternal autoimmune disease (particularly systemic lupus erythematosus).
• Maternal viral infection has also been implicated as a cause of congenital AV block.
• Congenital AV block may also develop in the context of atrioventricular cushion defects, atrial septal defects, or cyanotic congenital lesions.
• Inherited progressive conduction disease in otherwise structurally normal hearts is recognised in younger patients; however, in a Danish study, the cause was unidentified in over half of patients younger than 50 years.

Acquired Causes

Degenerative

• The most common cause of acquired AV block is age-related degeneration of the conduction system.
• Progressive fibrosis and sclerosis lead to chronic idiopathic block.
• Lenègre disease: idiopathic fibrosis of the conduction system.
• Lev disease: calcific or fibrotic changes extending from surrounding valvular and fibrous structures.

Ischaemic

• Myocardial ischaemia or infarction (acute or chronic) can impair conduction.
• Anterior myocardial infarction is more likely to cause irreversible conduction damage, while inferior infarctions are often transient.
• Coronary artery disease, both chronic stable and acute syndromes, is strongly associated with AV block.

Medication-related

• Drugs that depress AV nodal conduction are important causes:
• Beta-blockers, calcium-channel blockers (non-dihydropyridine), digitalis, and adenosine.
• Anti-arrhythmic agents such as sodium-channel blockers and class III drugs (e.g., sotalol, amiodarone).

Functional / Vagal

• Increased vagal tone may lead to nodal block, particularly in young individuals or athletes.
• Vagal-induced AV block is usually benign and seldom requires pacing.

Cardiomyopathies and Infiltrative Disorders

• Hypertrophic cardiomyopathy, sarcoidosis, amyloidosis, and haemochromatosis can all disrupt conduction pathways.
• Muscular dystrophies (myotonic dystrophy, Kearns–Sayre syndrome, Erb dystrophy, peroneal muscular atrophy) may cause progressive conduction impairment.

Inflammatory and Infective

• Myocarditis, rheumatic fever, and infective endocarditis (especially with aortic root abscess) are recognised causes.
• Lyme disease is a well-established reversible cause of AV block.
• Cardiac tuberculosis has been reported in endemic regions.

Iatrogenic / Procedural

• AV block may occur after:
• Cardiac surgery (particularly valve replacement/repair, myectomy, septal surgery).
• Catheter ablation for arrhythmias.
• Transcatheter aortic valve replacement (TAVI) – risk higher in men and in those with pre-existing conduction abnormalities.
• Alcohol septal ablation.

Electrolyte and Metabolic

• Severe electrolyte disturbances (hyperkalaemia, hypokalaemia, hypercalcaemia), acidosis, and hypoxaemia may impair AV conduction.
• Endocrine disorders such as myxoedema may also contribute.

Trauma and Toxic

• Blunt cardiac injury is a rare cause of complete AV block.
• Toxins, including certain indigenous medicines (e.g., “mad honey”), have been implicated.

Congenital Mechanisms

• Immune-mediated congenital AV block arises from transplacental passage of maternal autoantibodies (anti-Ro and anti-La).
• These antibodies bind to fetal cardiomyocytes, disrupting calcium metabolism, which triggers apoptosis of conduction tissue cells.
• The apoptotic process leads to fibrosis of both the conduction pathways and surrounding myocardium.
• Congenital AV block associated with structural cardiac malformations results from abnormal development of the central fibrous body or disruption of atrioventricular conduction tissue.

Acquired Mechanisms

Ischaemia and Reflex-mediated Block

• Myocardial ischaemia or infarction can impair conduction through direct injury to nodal or His–Purkinje tissue.
• Inferior myocardial infarction may activate the Bezold–Jarisch reflex, producing transient high vagal tone and subsequent Mobitz I or even complete AV block.
• Anterior infarction more often causes structural injury and irreversible conduction block.

Degenerative Disease

• Age-related fibrotic or sclerotic changes progressively impair conduction pathways.
• These changes are most prominent in the His–Purkinje system, leading to irreversible advanced block such as Mobitz II or third-degree AV block.
• On ECG, infranodal disease often manifests as wide QRS complexes or bundle-branch block.

Vagal Influence

• Increased vagal tone may cause transient AV nodal block, most often in first-degree or Mobitz I second-degree AV block.
• Triggers include sleep, nausea, vomiting, gagging, micturition, bowel movements, coughing, suctioning, or Valsalva manoeuvres.
• Neurocardiogenic syncope represents another clinical context of vagally mediated AV block.
• Such block is usually benign and reversible.

Pharmacological Effects

• Drugs that impair AV nodal conduction include beta-blockers, non-dihydropyridine calcium-channel blockers, digitalis, and adenosine.
• Additional anti-arrhythmic drugs such as procainamide, flecainide, sotalol, and amiodarone can impair His–Purkinje conduction or prolong AV nodal refractoriness.
• Combination therapy with nodal blocking agents significantly increases risk of AV block.

Infective and Infiltrative Causes

• Myocarditis may directly damage conduction tissue, producing conduction delays or complete block.
• Infiltrative processes such as sarcoidosis, amyloidosis, haemochromatosis, and Lyme disease compromise conduction through fibrotic or granulomatous infiltration.

Nodal versus Infranodal Block

• AV nodal block typically presents as first-degree or Mobitz I second-degree AV block.
• Infranodal block in the His–Purkinje system manifests as Mobitz II or third-degree AV block, usually irreversible and structurally based.
• The His–Purkinje fibres conduct impulses in an “all-or-none” fashion; hence, once impaired, conduction either fails completely (dropped beat) or does not occur at all (complete heart block).

General Trends

• The true prevalence of AV block is not precisely established, as large population-based studies dedicated solely to its incidence are limited.
• Congenital AV block mediated by maternal autoantibodies (anti-Ro/SSA, anti-La/SSB) occurs in approximately 1 in 15,000–20,000 live births. The incidence is likely underestimated because some cases result in intrauterine death.
• Advanced AV block (Mobitz II or complete block) is rare in younger people but becomes increasingly common with advancing age due to degeneration of the conduction system.
• In individuals over 65 years, AV block attributable to conduction tissue degeneration is much more frequent.

First-Degree AV Block

• May be seen in healthy adults and often remains asymptomatic.
• Incidence rises with age:
  • At age 20 years, prolonged PR interval (>200 ms) is seen in 0.5–2% of healthy people.
  • By age 60 years, more than 5% of healthy individuals demonstrate PR intervals >200 ms.
• In a large Chinese cohort of 10,926 adults aged ≥40 years, prevalence of first-degree AV block was 3.4%.
• A Finnish cohort (Mini-Finland Health Survey, 6,146 participants) reported a 0.9% incidence of AV block developing over 20 years.
• A study of 625 asymptomatic, heart disease–free individuals found transient type I second-degree AV block in 2.2%, more common when resting heart rate was <60 bpm.
• First-degree AV block is associated with a twofold risk of atrial fibrillation, a threefold risk of pacemaker implantation, and an increased all-cause mortality.

Second-Degree AV Block

• Mobitz I (Wenckebach) can occur physiologically, observed in 1–2% of healthy young people, especially during sleep.
• Mobitz II is rare in healthy individuals and usually indicates pathological disease of the His–Purkinje system.

Third-Degree AV Block

• Congenital complete AV block is diagnosed most often between 18 and 24 weeks’ gestation.
• It has a female predominance (60%) in congenital cases, with autoantibody-mediated injury being the primary mechanism.
• Mortality in utero or early life is approximately 20%, and most surviving children require permanent pacing.
• Acquired complete heart block shows a male predominance (60%).

Race, Sex, and Age Differences

• A study comparing African-American and Caucasian populations found higher prevalence of first-degree AV block in African-American patients in nearly all age groups except the eighth decade.
• In both groups, the incidence increases after age 50 years, peaking in the 10th decade for African-American patients and in the ninth decade for Caucasian patients.
• Overall, no strong racial predisposition is noted for higher-degree blocks.

Advanced and Infranodal Disease

• Advanced AV block (usually Mobitz II or complete block) is typically infranodal and associated with His–Purkinje system degeneration.
• In the Framingham study, QRS durations >0.12 seconds were significantly linked with coronary artery disease, hypertension, heart failure, AV block, left ventricular hypertrophy, and ventricular ectopy.
• Prolonged QRS complexes (>0.12 seconds) were rare before age 50–60 but found in 11% of older men and 5% of older women.
• Intraventricular conduction delay does not always lead to AV block but frequently precedes the development of advanced block.

General Aspects of History Taking

• Important to elicit a history of both congenital and acquired heart disease.
• A detailed review of all prescribed and non-prescribed medications should be obtained, especially beta-blockers, calcium channel blockers, digoxin, and antiarrhythmic drugs.
• Any recent cardiac procedures, including valve surgery, ablations, or device implantation, should be documented.
• Symptoms suggesting systemic disease should be sought, particularly those pointing towards amyloidosis, sarcoidosis, or connective tissue disease.
• Baseline exercise capacity should be assessed, since impaired chronotropic response may indicate clinically relevant AV block.
• History of tick bites is important in endemic areas because of the link between Lyme disease and reversible AV block.

Symptom Patterns by Degree of Block

First-Degree AV Block

• Often asymptomatic and identified incidentally.
• May occur in the context of high vagal tone, acute inferior myocardial infarction, use of antiarrhythmic drugs, athletic conditioning, or electrolyte disturbance (hypokalaemia, hypomagnesaemia).
• Symptoms, when present, include exertional shortness of breath, fatigue, and exercise intolerance.

Second-Degree AV Block

• Important associations include inflammatory and infiltrative diseases, hyperkalaemia, acute myocardial infarction, and post-cardiac interventions such as ablation or valve surgery.
• Symptoms can include fatigue, dizziness, dyspnoea, syncope, chest pain, and reduced exercise tolerance.
• Mobitz I is often asymptomatic or mildly symptomatic, whereas Mobitz II carries a higher risk of syncope and progression to complete block.

Third-Degree AV Block

• Frequently associated with degenerative conduction disease, infiltrative cardiomyopathy, myocarditis, neuromuscular disorders, ischaemia or infarction, hypoxia, and drug effects.
• Symptoms include fatigue, exertional dyspnoea, presyncope, syncope, chest pain, neck palpitations, and occasionally confusion.

Risk Factors and Diagnostic Clues from History

• Increasing age (>50–60 years) markedly raises risk due to degenerative changes in conduction tissue (Lenègre or Lev disease).
• Male sex is more frequently associated with His–Purkinje disease and QRS widening.
• A history of recurrent syncope is suggestive of high-grade or complete AV block, sometimes manifesting as Stokes–Adams attacks.
• Very slow ventricular rates (<40 bpm) in the history are clinically significant and often necessitate admission and pacing.
• Presyncope, fatigue, and exertional dyspnoea should be explored, especially in correlation with heart rate changes.
• Features of acute coronary syndrome (chest pain, palpitations, nausea, vomiting) may indicate ischaemia as a proximate and reversible cause.
• Family history is relevant, as hereditary conduction disorders and maternal autoimmune conditions (systemic lupus erythematosus) are associated with congenital AV block.
• Enquiry about systemic conditions:
  • Neuromuscular disorders (myotonic dystrophy, Kearns–Sayre syndrome, Erb dystrophy, peroneal muscular atrophy).
  • Sarcoidosis (syncope may be the first manifestation; accounts for up to one-quarter of unexplained AV block in patients <55 years).
  • Infectious causes such as Lyme disease (endemic exposure), tuberculosis, myocarditis, or infective endocarditis.
• History of hypoxaemia, acid–base disturbance, or severe electrolyte imbalance is essential, as these are potentially reversible causes.
• Trauma (blunt cardiac injury) and use of indigenous medicines (such as “mad honey”) should also be considered.

General Principles

• Physical examination alone is rarely diagnostic of AV block but provides important clues about haemodynamic impact and associated structural heart disease.
• The focus should be on assessing heart rate, rhythm, blood pressure, jugular venous pressure, and signs of low cardiac output or congestion.

First-Degree AV Block

• Routine physical examination is typically normal.
• No specific findings are usually attributable to the conduction abnormality itself.

Second-Degree AV Block

• Mobitz I: may present with an irregular pulse reflecting dropped beats.
• Mobitz II: may manifest with bradycardia and a regular or irregular pulse depending on conduction pattern.
• Jugular venous distension may be variable.

Third-Degree (Complete) AV Block

• Often associated with profound bradycardia.
• Jugular venous distension may be present, and cannon A waves can be seen when the right atrium contracts against a closed tricuspid valve.
• Pulmonary oedema and heart failure signs may occur if structural disease coexists.
• Variable intensity of the second heart sound (S2) and variable pulse strength may be noted due to AV dissociation.

Key Diagnostic Indicators from Examination

• Bradycardia is a consistent finding in higher-grade blocks; a ventricular rate <40 bpm indicates severe compromise and usually requires urgent intervention.
• Syncope or pre-syncope associated with slow ventricular rates implies significant risk, such as in Stokes–Adams attacks, and is an indication for pacing unless a reversible cause is identified.
• Elevated systolic blood pressure and wide pulse pressure are commonly seen with slow ventricular rates; hypotension occurs if escape rhythms fail or if ventricular rates are critically low.
• Fatigue and dyspnoea on exertion correlate with inadequate chronotropic response and low cardiac output.
• Chest pain, palpitations, nausea, or vomiting in the acute setting may point towards acute coronary syndrome as a proximate cause of AV block.
• Prominent cannon A waves are strongly suggestive of AV dissociation, typically in complete block.
• Hypoxaemia, electrolyte disturbance, or systemic illness may occasionally be reflected in the physical state and should be considered as potentially reversible contributors.

Approach Considerations

• A thorough review of comorbidities and medication history is essential, as many patients have underlying structural heart disease, coronary artery disease, or are on AV nodal–blocking drugs that may exacerbate conduction disturbance.
• Initial bedside evaluation should always include a 12-lead ECG and cardiac monitoring to assess the relationship between P waves and QRS complexes and to classify the block.

Laboratory Studies

• Useful particularly in second- or third-degree AV block.
• Electrolytes: abnormalities in potassium or calcium can precipitate AV block.
• Serum pH: marked acidosis or alkalosis may represent a reversible cause.
• Cardiac biomarkers (troponin, CK-MB): should be measured when myocardial infarction is suspected.
• Serum digoxin levels: indicated when patients taking digoxin present with new conduction abnormalities.
• Additional serology: Lyme disease titres when exposure risk is high; thyroid function tests in suspected myxoedema; autoimmune markers for connective tissue disease when systemic illness is suspected.

Electrocardiography and Ambulatory Monitoring

• Standard 12-lead ECG is the cornerstone for diagnosis and classification of AV block.
• Transient or intermittent blocks may require extended evaluation:
  • 24-hour Holter monitoring.
  • Event or loop recorders for intermittent symptoms.
  • Implantable loop recorders for unexplained or infrequent syncope (monitoring possible for years).
• ECG features help differentiate:
  • First-degree block – PR >210 ms with constant conduction.
  • Mobitz I – progressive PR prolongation with grouped beating.
  • Mobitz II – fixed PR with occasional dropped QRS.
  • Complete block – no consistent relation between P waves and QRS complexes.

Electrophysiology Testing

• Indicated when AV block is suspected as a cause of syncope but diagnosis cannot be established by ECG alone.
• Helps determine site of block, predict progression, and assess pacing requirements.
• Indications include:
  • Asymptomatic Mobitz I with bundle branch block.
  • Questionable Mobitz II with narrow QRS.
  • Inferior MI with suspected infranodal disease.
  • Third-degree block with accelerated ventricular rate.
  • Progressive conduction disease in neuromuscular disorders or suspected genetic mutations (e.g., SCN5A).
• A prolonged HV interval (>100 ms) is predictive of advanced conduction disease.

Imaging Studies

• Echocardiography: evaluates left ventricular function, wall motion, valvular abnormalities, and congenital lesions.
• Chest X-ray: may show cardiomegaly, valvular or coronary calcification, hilar lymphadenopathy in sarcoidosis, or signs of heart failure.
• Coronary angiography or myocardial perfusion imaging: appropriate if ischaemia is suspected.
• FDG-PET: has prognostic value in unexplained high-grade block; abnormal scans correlate with higher risk of adverse cardiac outcomes.
• Cardiac MRI: useful in young and middle-aged patients with advanced block; identifies infiltrative disease, myocarditis, or congenital anomalies.

Exercise Testing

• Can shorten the PR interval in first-degree AV block related to high vagal tone, but does not alter conduction delay in His–Purkinje disease.
• Used to differentiate Mobitz I (improves with exercise) from Mobitz II (often worsens).
• Contraindicated in complete heart block.
• Severe PR prolongation may manifest as exercise intolerance or pacemaker syndrome.

Other Specialised Tests

• Tilt-table testing: may be used in suspected neurocardiogenic syncope with associated AV block, though sensitivity and specificity are variable.
• Stress testing: in cases of suspected ischaemia outside acute coronary syndromes. Can also demonstrate chronotropic competence in vagotonia.
• Serological testing: indicated when reversible causes such as Lyme disease are suspected.

General Considerations

• All patients with suspected AV block should undergo detailed work-up to exclude alternative rhythm disturbances and to confirm the level of block.
• A 12-lead ECG and, when required, extended rhythm monitoring are central to differentiating AV block from other arrhythmias.
• Careful inspection of P wave morphology, PR interval dynamics, and the relationship of atrial to ventricular activity are critical.

Atrioventricular Dissociation

• AV dissociation occurs when atria and ventricles beat independently, often because of competing pacemaker activity rather than conduction block.
• In AV block, P waves fail to conduct despite an opportunity, whereas in AV dissociation, atrial activity does not influence ventricular activation.
• Differentiation requires rhythm strips of adequate length and correlation with sinus node function.

Junctional Rhythm

• Profound first-degree AV block with a very prolonged PR interval may mimic junctional rhythm if the P wave overlaps or appears close to the QRS complex.
• Retrograde P waves in true junctional rhythm are inverted in inferior leads (II, III, aVF), whereas in sinus rhythm with prolonged PR intervals they remain upright.
• Comparison with prior ECGs demonstrating prolonged PR intervals aids distinction.

Supraventricular Tachycardia (SVT)

• In cases of markedly prolonged PR interval, P waves may appear retrograde and be mistaken for SVT.
• Retrograde P waves in SVT are typically inverted in inferior leads.
• Variability in heart rate and PR/RP intervals argues against SVT when assessing for AV block.
• Serial ECGs and rhythm strip analysis can clarify the diagnosis.

Atrial Fibrillation and Multifocal Atrial Tachycardia (MAT)

• Mobitz I block may present with irregular RR intervals, which could be misinterpreted as atrial fibrillation or MAT.
• Presence of uniform P waves and grouped QRS complexes in Mobitz I distinguishes it from atrial fibrillation (which lacks discrete P waves) and MAT (which shows varying P wave morphologies).

Sinus Rhythm with Intact AV Conduction

• In complete AV block, if the ventricular escape rhythm rate is close to the sinus rate, the tracing may superficially resemble sinus rhythm with AV conduction.
• Careful review of long rhythm strips will reveal absence of correlation between atrial and ventricular activity, confirming AV block.

Tachy-Brady Syndrome

• Alternating tachyarrhythmias and bradyarrhythmias due to sinus node dysfunction can mimic AV block.
• Following termination of atrial fibrillation or flutter with rapid ventricular response, a long sinus pause may occur, resulting in a slow ventricular rate.
• Unlike AV block, this represents sinus node failure rather than impaired atrioventricular conduction.

Key Differentials to Exclude

• Junctional rhythm.
• Supraventricular tachycardia with retrograde atrial activation.
• Atrial fibrillation or multifocal atrial tachycardia.
• Sinus rhythm with intact conduction but apparent pseudo-block due to rate similarity.
• Tachy-brady syndrome (sinus node disease).

Goals of Therapy

• Relieve symptoms related to bradycardia and conduction delay.
• Prevent syncope, haemodynamic compromise, and sudden cardiac death in advanced AV block.
• Correct reversible causes and avoid unnecessary permanent pacing when possible.

First-Degree and Mobitz I (Wenckebach) Second-Degree AV Block

Asymptomatic

• No specific treatment required.
• Low risk of progression to advanced block.
• Routine follow-up only; repeat ECGs if new symptoms develop.

Symptomatic

• Symptoms may occur in patients with very prolonged PR intervals (>300 ms) or with Mobitz I block.
• First step: discontinue AV nodal–blocking medications (beta-blockers, calcium channel blockers, digoxin).
• If symptoms persist or are severe, consider permanent pacemaker implantation.
• Dual-chamber pacing is preferred; biventricular pacing considered if LVEF ≤35%.

Mobitz II and Third-Degree AV Block

Asymptomatic or Mildly Symptomatic

• Stop AV nodal–blocking drugs and manage any reversible causes (e.g., revascularisation in acute coronary syndrome, digoxin antibodies for digitalis toxicity, glucagon for beta-blocker overdose, calcium for calcium-channel blocker toxicity, correction of electrolyte or pH disturbances, or treatment of hypoxaemia).
• In the absence of a reversible cause, permanent pacemaker implantation is recommended.
• ICD considered when LVEF ≤35%.
• CRT may be beneficial in patients with high-degree or complete block and LVEF 36–50%, improving symptoms, quality of life, and reducing mortality.

Severely Symptomatic

• Manifestations include syncope, severe presyncope, or profound bradycardia.
• Immediate discontinuation of AV nodal–blocking agents and treatment of reversible causes.
• Temporary pacing (preferably transvenous over transcutaneous) should be initiated in haemodynamically unstable patients.
• Permanent pacemaker implantation or ICD follows if conduction disturbance is irreversible.
• CRT indicated in those with reduced LV function.

Acute Management

• Identify and treat reversible causes (drug toxicity, ischaemia, myocarditis, Lyme disease, electrolyte disturbance).
• Atropine is useful in supra-Hisian block.
• Dopamine or isoproterenol infusion may be used for symptomatic high-degree block in acute ischaemia.
• Temporary pacing reserved for unstable patients not responding to medical therapy; should be used for the shortest possible duration to reduce risk of infection, thromboembolism, immobility, and perforation.

Chronic Management

• Permanent pacing is the cornerstone of management for irreversible, symptomatic higher-grade blocks.
• Asymptomatic first-degree or Mobitz I block typically does not require pacing but should be monitored for progression.
• Pacemaker is mandatory in Mobitz II and third-degree block without reversible causes.
• Device type:
  • Dual-chamber pacing generally preferred over single-chamber pacing.
  • Single-chamber pacing reserved for patients with permanent atrial fibrillation or when dual-chamber systems provide limited benefit due to comorbidities.
  • ICD plus pacemaker indicated in patients with neuromuscular disease or infiltrative cardiomyopathies who are at increased risk of sudden death.
• CRT pacing may be superior to right ventricular pacing in those with reduced LVEF, as demonstrated in the BLOCK-HF trial, which showed reverse remodelling, improved ejection fraction, and reduced mortality and hospitalisations.

Activity Restriction and Monitoring

• Patients with significant AV block should restrict activities until adequately evaluated and treated to reduce risk of syncope-related injury.
• Asymptomatic first-degree and Mobitz I block do not require long-term monitoring.
• Intermittent Mobitz II, high-grade, or complete AV block benefit from event monitoring to identify periods of asystole or symptomatic bradycardia to guide pacemaker timing.

Specialist Referral

• Consultation with a cardiologist or electrophysiologist is warranted in cases of advanced AV block, unexplained syncope, or when electrophysiological testing is required to define site and severity of block and guide pacing decisions.

General Prognostic Principles

• Prognosis depends on the degree of block, symptom severity, underlying cardiac disease, and comorbidities such as hypertension, ischaemic heart disease, diabetes, or chronic kidney disease.
• AV block is the most common worldwide indication for pacemaker implantation.
• Untreated third-degree AV block carries poor outcomes, with reported 5-year survival as low as 37%.
• Men with third-degree AV block generally have a worse prognosis compared to women.

First-Degree AV Block

• Once considered benign, first-degree AV block is now recognised to confer risk.
• In the Framingham Heart Study (7,575 individuals), prolonged PR interval (>200 ms) was associated with increased risk of atrial fibrillation, pacemaker implantation, and all-cause mortality.
• Other cohort studies confirm a twofold risk of atrial fibrillation, a threefold risk of pacemaker requirement, and higher overall mortality.
• Prognosis worsens in the presence of concomitant heart failure or structural disease.

Mobitz I (Wenckebach)

• Traditionally viewed as benign, but symptomatic Mobitz I carries a higher risk if untreated.
• A retrospective study of 299 elderly patients (mean age 75 years) showed pacemaker implantation reduced mortality by 46% compared to no device therapy.
• Other studies support improved survival with pacing in symptomatic patients.

Mobitz II and High-Degree AV Block

• Mobitz II block and higher-grade blocks carry a substantial risk of progression to complete AV block and sudden cardiac death if untreated.
• In a PCI cohort of 3,115 patients with STEMI, 1.5% developed high-grade block. Mortality was significantly increased at 30 days, 1 year, and 3 years (HRs ranging from 2.78 to 4.37).
• Prognosis is especially poor with wide QRS or infranodal disease.

Third-Degree (Complete) AV Block

• Without pacing, prognosis is poor, with high rates of syncope, asystole, and sudden cardiac death.
• Permanent pacemaker implantation markedly improves survival and quality of life, reducing symptoms and complications.
• Non-randomised data consistently show pacing improves outcomes, particularly when syncope has occurred.
• Prognosis after acute myocardial infarction differs by territory:
  • Inferior MI: AV block often transient and reversible.
  • Anterior MI: AV block usually persistent, reflecting extensive myocardial damage, and associated with high mortality.

Congenital AV Block

• Autoimmune-mediated congenital complete AV block carries ~20% mortality.
• Most surviving children require pacemakers.
• Foetuses with congenital heart disease and advanced AV block have particularly poor outcomes.

Special Conditions Affecting Prognosis

• Cardiac sarcoidosis: AV block with sarcoid involvement is associated with high risk of sudden cardiac death, particularly when accompanied by ventricular arrhythmias or LV dysfunction. One in four cases of unexplained AV block in adults <55 years is attributable to sarcoidosis.
• Amyloidosis: prognosis depends on severity of cardiac involvement; advanced AV block indicates poor outlook.
• Neuromuscular diseases and infiltrative cardiomyopathies also worsen outcomes when associated with advanced block.

Prognosis with Pacemaker Therapy

• Symptomatic patients receiving a permanent pacemaker generally have an excellent prognosis.
• Complication rates are low, and pacing prevents syncope, sudden cardiac death, and haemodynamic deterioration.
• CRT pacing in patients with reduced LV function reduces mortality and hospitalisations compared to right ventricular pacing alone.

Complications of Untreated AV Block

• Asystole and sudden cardiac death.
• Torsade de pointes due to bradycardia-induced QT prolongation.
• Cardiovascular collapse with syncope.
• Worsening of heart failure, ischaemic heart disease, and renal disease.

Complications of Untreated AV Block

Syncope

• Common in high-grade blocks due to pauses in ventricular activity.
• Stokes–Adams attacks may occur, characterised by sudden transient loss of consciousness from abrupt AV block.

Heart failure

• Results from prolonged bradycardia and reduced cardiac output.
• More pronounced in patients with underlying structural heart disease or impaired left ventricular function.

Atrial fibrillation

• First-degree AV block is linked with atrial remodelling and increased risk of atrial fibrillation.
• AF further compounds haemodynamic compromise.

Ventricular arrhythmias

• Severe bradycardia may precipitate bradycardia-induced polymorphic ventricular tachycardia or torsade de pointes.

Sudden cardiac death

• A recognised risk in untreated Mobitz II or complete AV block.
• Particularly high in patients with structural heart disease or myocardial infarction.

Complications Related to Pacemaker Implantation

Short-term

• Periprocedural risk is low (2–3%).
• Complications include bleeding, infection, vascular trauma, pneumothorax, tamponade, lead dislodgement, and pocket haematoma.
• Major events such as myocardial infarction, stroke, or death occur in fewer than 1% of implantations.

Long-term

• Lead or generator malfunction is a recognised late complication.
• Device-related infection may require lead extraction, which carries high risk and should be performed in specialist centres.
• Battery depletion occurs every 7–10 years, requiring generator replacement.
• Chronic right ventricular pacing may worsen LV systolic function, predisposing to pacing-induced cardiomyopathy.
• Venous obstruction or thrombosis of subclavian or innominate veins may occur with chronic lead presence.

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