Heart Block
Table of Contents
- Overview
- Types and Classification
- Causes and Triggers
- Symptoms
- ECG and Diagnostic Findings
- Treatment
- Natural and Lifestyle Approaches
- Complications and Prognosis
- When to Seek Emergency Care
- Key Research Papers
- Connections
- Featured Videos
1. Overview
Heart block — also called atrioventricular (AV) block — is a disorder of the cardiac conduction system in which the electrical impulse generated by the sinoatrial (SA) node in the right atrium is delayed or blocked from reaching the ventricles through the AV node and His-Purkinje system. The result is a slowing or dissociation of atrial and ventricular electrical activity, with varying clinical consequences ranging from asymptomatic to life-threatening hemodynamic collapse.
Under normal conditions, the electrical impulse travels from the SA node → atria → AV node → Bundle of His → left and right bundle branches → Purkinje fibers → ventricular myocardium, producing a normal PR interval of 120–200 ms on the surface ECG. A PR interval exceeding 200 ms (one large box on standard ECG paper) defines first-degree AV block. More advanced block produces dropped beats or complete AV dissociation.
Heart block is classified by severity — first, second (Mobitz type I or II), and third degree — each with distinct ECG patterns, clinical significance, and management implications. Understanding these distinctions is essential because:
- First-degree block: Benign in isolation; usually requires no treatment; can be normal variant in athletes
- Second-degree Mobitz I (Wenckebach): Usually benign block at the AV node level; often resolves; rarely requires pacing
- Second-degree Mobitz II: Block below the AV node in the His bundle or bundle branches; unpredictably progresses to complete block; typically requires permanent pacemaker
- Third-degree (complete) block: Complete AV dissociation; requires urgent intervention and usually permanent pacemaker
2. Types and Classification
First-Degree AV Block
Defined as a PR interval >200 ms (one large box, or 5 small boxes, on standard 25 mm/sec ECG paper) on every beat, with all P waves conducted to the ventricles. The PR interval prolongation reflects delayed conduction through the AV node, but every atrial impulse eventually reaches the ventricles. No beats are "dropped."
First-degree AV block is not truly a "block" in the sense of any impulse failing to conduct — it is a conduction delay. The PR interval may be markedly prolonged (300–400 ms or more) without symptoms. It is seen in trained athletes (vagal tone), with age-related fibrosis, and in many systemic conditions affecting the AV node.
Second-Degree AV Block — Mobitz Type I (Wenckebach)
Classic Wenckebach pattern (named for Dutch physician Karel Frederick Wenckebach who described it in 1906): progressive PR interval prolongation with each successive beat until one P wave fails to conduct (dropped QRS). After the dropped beat, the cycle resets and PR interval shortens back toward baseline before the progressive prolongation begins again.
Key ECG features of Mobitz I:
- Progressive PR prolongation over consecutive beats
- The RR interval shortens progressively (due to diminishing PR increments)
- A P wave is not followed by a QRS (the dropped beat)
- The pause containing the dropped beat is less than twice the preceding RR interval
- The QRS complex is narrow (unless pre-existing bundle branch block) — block is at the AV node level
Anatomical location: AV nodal block. The AV node is richly innervated by the vagus nerve and responds to changes in autonomic tone. Wenckebach is often benign, physiologic, and reversible.
Second-Degree AV Block — Mobitz Type II
Named after Woldemar Mobitz who described the two types in 1924. In Mobitz type II, P waves are conducted with a constant, unchanging PR interval until one P wave suddenly fails to conduct (dropped QRS) without any preceding PR prolongation. The block occurs below the AV node — in the His bundle or bundle branches.
Key ECG features of Mobitz II:
- Constant PR interval in conducted beats (normal or prolonged, but fixed)
- Sudden non-conducted P wave without warning PR changes
- Wide QRS complex in the majority of cases (because block is below the AV node, and bundle branch disease is usually already present)
- Conduction ratio may be 2:1 (every other P wave is blocked), 3:1, or variable
Anatomical location: Infranodal block (His bundle or bundle branches). This is the dangerous distinction: infranodal block is inherently unstable, unpredictably progresses to complete heart block, and the escape rhythm (from ventricular tissue below the block) is slow (20–40 bpm), wide-complex, and unreliable. (PMID: 6850024)
2:1 AV Block — The Diagnostic Dilemma
When every other P wave is blocked (2:1 conduction), it is mathematically impossible to distinguish Mobitz I from Mobitz II on ECG alone — because you cannot observe PR interval behavior with only one conducted beat per cycle. Clues to distinguish:
- Narrow QRS favors Mobitz I (nodal block)
- Wide QRS favors Mobitz II (infranodal block)
- PR interval in the conducted beat: very long PR favors Wenckebach; normal PR favors Mobitz II
- Electrophysiology study (His bundle recording) definitively localizes the block
Third-Degree (Complete) AV Block
Complete absence of AV conduction — no atrial impulses reach the ventricles. The atria and ventricles beat independently (AV dissociation). The ventricles are maintained by an escape pacemaker located below the site of block:
- Junctional escape rhythm (block at the AV node level): Rate 40–60 bpm; narrow QRS; relatively stable and reliable; provides adequate perfusion at rest
- Ventricular escape rhythm (infranodal block): Rate 20–40 bpm; wide bizarre QRS; slow, unreliable, poorly responsive to exercise demands; causes symptoms and is potentially fatal without pacing
ECG in complete heart block: Regular P waves at the atrial rate (e.g., 80 bpm); regular QRS complexes at the escape rate (e.g., 40 bpm); P waves and QRS complexes bear no relationship to each other (dissociated, "marching through" independently). No PR interval relationship is maintained. (PMID: 7790957)
Lenegre-Lev Disease
The most common cause of isolated progressive cardiac conduction disease (PCCD) in adults without structural heart disease is Lenegre-Lev disease — idiopathic fibrosis and sclerosis of the cardiac conduction system. Lenegre disease (Jean Lenegre, 1964) describes primary sclerodegeneration of the bundle branches; Lev disease (Maurice Lev, 1964) describes fibrosis encroaching on the conduction system from the cardiac fibrous skeleton (aging, calcific aortic stenosis, mitral annular calcification). Clinically, the two processes are indistinguishable, and the eponym is often combined. Both lead to progressive bundle branch block progressing to complete heart block over years to decades. SCN5A gene variants (sodium channel mutations) cause familial forms of progressive conduction disease. (PMID: 10888438)
3. Causes and Triggers
Structural and Degenerative Causes
- Lenegre-Lev disease: Age-related fibrosis of the conduction system; most common cause of chronic heart block in adults >60 years; responsible for 50% of permanent pacemaker implants
- Ischemic heart disease: Acute MI involving the RCA (supplies AV node via posterior descending artery in 80% of patients with right-dominant circulation) → inferior MI commonly causes transient AV block; proximal LAD occlusion (supplies bundle branches) → typically causes Mobitz II or complete block with wide QRS escape, more ominous
- Calcific aortic stenosis: Calcium extends from the aortic annulus into the His bundle and bundle branches
- Surgical/procedural trauma: Post-open heart surgery (valve replacement, septal myectomy, TAVI/TAVR — new permanent LBBB or complete heart block occurs in 15–25% of TAVI procedures)
- Radiofrequency catheter ablation: Inadvertent injury to the AV node or His bundle during ablation procedures for arrhythmias
- Cardiomyopathy: Dilated cardiomyopathy, sarcoidosis (cardiac sarcoidosis is a classic cause of AV block at any age in otherwise unexplained young-patient block)
Infectious Causes
- Lyme disease (Borrelia burgdorferi): Lyme carditis produces AV block (predominantly affecting the AV node) in 4–10% of untreated Lyme disease patients. Block ranges from first degree to complete heart block; typically reversible with antibiotics; temporary pacemaker for complete heart block or symptomatic advanced block. (PMID: 8277692)
- Infective endocarditis: Perivalvular abscess (particularly aortic root abscess in aortic valve endocarditis) can extend to the His bundle and AV node — new AV block in aortic endocarditis is an ominous sign of perivalvular extension requiring urgent surgical evaluation
- Myocarditis: Viral (Coxsackievirus, CMV, HIV, parvovirus B19) and autoimmune; AV block may be the presenting manifestation
- Chagas disease: Chronic chagasic cardiomyopathy is the leading cause of heart block in Latin America; right bundle branch block (RBBB) with left anterior fascicular block is the classic Chagas pattern
- Rheumatic fever: Acute rheumatic carditis may cause first- or second-degree AV block; PR prolongation is one of the minor Jones criteria
Autoimmune Causes
- Congenital complete heart block: Neonatal lupus — transplacental passage of maternal anti-Ro/SSA and anti-La/SSB antibodies damages fetal AV node, causing complete heart block in utero; associated with primary Sjögren syndrome and SLE in the mother; permanent pacemaker required at birth in many affected neonates (PMID: 9240089)
- Systemic lupus erythematosus (SLE)
- Systemic sclerosis
- Polymyositis/dermatomyositis
- Ankylosing spondylitis and other HLA-B27-associated spondyloarthropathies
Drug-Induced Heart Block
- Beta-blockers: Slow AV node conduction; overdose causes high-degree block
- Non-dihydropyridine calcium channel blockers: Verapamil and diltiazem — direct AV node depressants; interaction with beta-blockers significantly increases block risk
- Digoxin toxicity: Classic cause of all degrees of AV block including Wenckebach; QTc shortening + AV block = digoxin toxicity until proven otherwise
- Amiodarone: Prolongs AV node refractoriness; can cause all degrees of AV block
- Adenosine: Causes transient complete heart block (used diagnostically and therapeutically for SVT); effect seconds only
- Lithium: SA and AV node dysfunction
- Ivermectin (high dose): GABA agonist effects on cardiac pacemaker cells; case reports of AV block at supratherapeutic doses
Metabolic and Electrolyte Causes
- Hyperkalemia: Elevated extracellular potassium slows conduction through all cardiac tissue; severe hyperkalemia (K >7–8 mEq/L) causes widening QRS, AV block, and eventually sine wave pattern and cardiac arrest
- Hypothyroidism
- Hypothermia
Infiltrative Causes
- Cardiac sarcoidosis: Granulomatous infiltration of the AV node and bundle branches; AV block in a young patient without apparent cause should always prompt evaluation for cardiac sarcoidosis; CMR and FDG-PET are diagnostic modalities; corticosteroids may reverse block in early disease
- Cardiac amyloidosis: Amyloid infiltration of the conduction system causes conduction disease and heart failure
- Hemochromatosis: Iron deposition in the conduction system
- Lymphoma and metastatic malignancy
4. Symptoms
First-Degree AV Block
Typically asymptomatic. Occasionally, patients with very prolonged PR intervals (>300 ms) may experience symptoms from the timing mismatch between atrial and ventricular contractions ("pacemaker syndrome" physiology): reduced cardiac output, fatigue, or reduced exercise tolerance. This is termed "AV dyssynchrony" and is rare.
Second-Degree Mobitz I (Wenckebach)
Usually asymptomatic or minimally symptomatic, particularly in the setting of lower resting heart rates. Some patients note:
- Occasional awareness of a "missed beat" or "palpitation"
- Mild lightheadedness during episodes
- Fatigue with exercise if the block is rate-limiting
Second-Degree Mobitz II
More likely to be symptomatic than Mobitz I due to the unpredictable nature of dropped beats and the infranodal site of block:
- Lightheadedness and near-syncope from sudden dropped beats
- Syncope (Stokes-Adams attack) if multiple consecutive P waves fail to conduct and the escape rhythm is slow to emerge
- Fatigue and dyspnea if ventricular rate is inadequate
- Sudden cardiac arrest if progression to complete block is rapid without adequate escape rhythm
Third-Degree (Complete) Heart Block
Symptoms depend critically on the rate and reliability of the escape rhythm:
- Junctional escape (40–60 bpm): May be surprisingly well-tolerated at rest; fatigue, dyspnea on exertion (rate cannot increase with demand), lightheadedness
- Ventricular escape (20–40 bpm): Usually severely symptomatic: near-constant lightheadedness, dyspnea, and fatigue at rest; frequent syncope or pre-syncope
- Stokes-Adams attacks: Sudden, brief episodes of syncope from transient asystole as the heart pauses to establish an escape rhythm; fall without warning; rapid recovery (unlike neurological syncope); first described by William Stokes and Robert Adams in the 19th century
- Chest pain if associated with ischemia (heart block from acute MI)
- Heart failure symptoms from chronic low heart rate and reduced cardiac output
5. ECG and Diagnostic Findings
Surface ECG — The Primary Diagnostic Tool
The 12-lead ECG is central to diagnosing and classifying heart block. Key measurements:
- PR interval: Measured from onset of P wave to onset of QRS complex. Normal: 120–200 ms (3–5 small boxes at 25 mm/s). >200 ms = first-degree AV block. PR intervals should be measured in the same lead consistently (typically lead II or V1).
- QRS duration: Normal <120 ms (<3 small boxes). Wide QRS (>120 ms) in the setting of heart block implies infranodal block or pre-existing bundle branch disease — a critical adverse prognostic sign
- P:QRS ratio: 1:1 in normal sinus rhythm and first-degree block; >1:1 in second- and third-degree block (more P waves than QRS complexes)
ECG Pattern by Type
- First-degree: Regular rhythm, constant PR >200 ms, every P followed by QRS. No dropped beats.
- Mobitz I (Wenckebach): Progressively lengthening PR, then a dropped QRS, then reset. "Longer longer longer DROP — then you have Wenckebach." The PR after the pause is the shortest in the cycle.
- Mobitz II: Fixed PR interval (may be normal or prolonged) with sudden non-conducted P wave. Wide QRS in most cases. Conduction ratio stated as atrial:ventricular (e.g., 3:2 means 3 P waves per 2 QRS complexes).
- Complete heart block: P waves and QRS complexes are entirely independent. Regular P rate (faster) and regular QRS rate (slower) with no relationship. "P waves march through, QRS complexes march through, but they never meet."
Holter Monitoring and Event Recorders
Paroxysmal or intermittent heart block — particularly relevant for unexplained syncope — may not be captured on a resting 12-lead ECG. Ambulatory monitoring options:
- 24-hour Holter monitor: adequate for frequent events
- 7- to 30-day external event monitors or patch monitors: for weekly events
- Implantable loop recorder (ILR): subcutaneous device providing up to 3 years of continuous rhythm monitoring; highest yield for infrequent unexplained syncope; now recommended as a first-line investigation for unexplained syncope after negative initial workup (PMID: 24916898)
Electrophysiology Study (EPS)
Invasive catheter recording of His bundle electrograms (H-V interval) precisely localizes the block site:
- AH interval (atrium to His bundle): normal 55–130 ms; prolonged AH indicates AV nodal delay
- HV interval (His bundle to ventricle): normal 35–55 ms; HV >70 ms indicates infranodal disease with high risk of progression to complete block; HV >100 ms is an indication for prophylactic pacemaker
- EPS is indicated when the site of block is uncertain and changes management (e.g., distinguishing infranodal Mobitz II from 2:1 AV block of uncertain origin)
Additional Investigations
- Serum potassium, calcium, magnesium (electrolyte causes)
- Digoxin level (if on digoxin)
- Thyroid function tests (hypothyroidism)
- Lyme serology (ELISA + Western blot) in endemic areas
- ANA, anti-Ro/SSA, anti-La/SSB (autoimmune causes; neonatal lupus workup)
- ACE level, chest CT (cardiac sarcoidosis)
- FDG-PET/CMR (cardiac sarcoidosis, myocarditis)
- Echocardiography: assess LV function, structural heart disease, pericardial disease
- Genetic testing: SCN5A, LMNA mutations in young patients with familial conduction disease
6. Treatment
First-Degree AV Block
No treatment required in asymptomatic patients. Address reversible causes (drug review, electrolyte correction). Counseling and reassurance. Follow-up ECG monitoring for progression. Athletes with first-degree block and vagal physiology require no treatment; block may resolve with detraining.
Second-Degree Mobitz I (Wenckebach)
Management is generally expectant for asymptomatic patients with Wenckebach at the AV node level:
- Identify and treat reversible causes (Lyme disease, inferior MI, drug toxicity)
- Avoid AV-blocking drugs when possible
- Atropine 0.5–1 mg IV for symptomatic acute Wenckebach (acts on vagal AV nodal tone)
- Permanent pacemaker: Indicated for symptomatic Mobitz I or when associated with infranodal disease (wide QRS) on EPS
Second-Degree Mobitz II
Mobitz II requires pacemaker implantation in virtually all cases regardless of symptoms, because of the high risk of unpredictable progression to complete heart block:
- Acute symptomatic Mobitz II: Atropine is often ineffective (infranodal block is not vagally mediated); transcutaneous pacing as a bridge; temporary transvenous pacemaker; IV dopamine or epinephrine may accelerate the escape rhythm temporarily
- Permanent pacemaker: Class I indication per ACC/AHA guidelines regardless of symptoms (PMID: 23265516)
Complete (Third-Degree) Heart Block
Complete heart block requires pacemaker therapy. Acute management:
- Atropine: May be transiently effective if block is at the AV node (junctional escape) — limited utility in infranodal complete block
- Transcutaneous pacing: Emergency pacing delivered through pads on the chest wall; uncomfortable but life-saving bridge
- Temporary transvenous pacemaker: Catheter-based pacing electrode placed in the right ventricular apex via the jugular or subclavian vein; more reliable than transcutaneous pacing
- IV chronotropic support: Dopamine or epinephrine infusion to accelerate the escape rate while awaiting pacing
- Permanent pacemaker: The definitive treatment; Class I indication for acquired complete heart block with symptoms or hemodynamic compromise. For asymptomatic complete heart block, permanent pacemaker is indicated if: escape rate <40 bpm, escape rhythm at or below the bundle of His (wide-complex), LV dysfunction, cardiomegaly, or the patient must undergo general anesthesia. (PMID: 23265516)
Pacemaker Types
- Single-chamber pacemaker (VVI or VVIR): Paces only the ventricle; appropriate for chronic AF with complete heart block; avoids pacemaker syndrome
- Dual-chamber pacemaker (DDD or DDDR): Senses and paces both atrium and ventricle; maintains AV synchrony; physiologic pacing; preferred for most patients with AV block and sinus rhythm
- His bundle pacing: Delivers pacing directly to the His bundle, maintaining normal ventricular activation sequence (avoids LBBB induced by RV apex pacing); reduces pacemaker-induced cardiomyopathy; increasingly used as first-line or for patients with existing LV dysfunction
- Left bundle branch pacing (LBBP): Emerging technique; pacing the left bundle branch area provides physiologic conduction similar to His bundle pacing with improved lead stability
- Biventricular pacemaker (CRT): For patients with heart block requiring pacing AND existing LV dysfunction; synchronizes RV and LV contraction
- Leadless pacemaker (Micra): Self-contained capsule implanted in the right ventricle without leads; appropriate for specific patients where transvenous access is difficult
Reversible Causes — Treat the Underlying Disease
- Lyme carditis: Doxycycline (oral) for mild block; IV ceftriaxone for high-degree block; temporary pacemaker if symptomatic; permanent pacemaker rarely needed (block usually resolves)
- Drug-induced: Discontinue offending agent; block often resolves
- Acute inferior MI: AV block typically resolves within 1–2 weeks; temporary pacing for hemodynamic compromise; permanent pacemaker rarely needed
- Electrolyte abnormalities: Correction of hyperkalemia, hypomagnesemia
- Cardiac sarcoidosis: Corticosteroids may reduce granulomatous infiltration of the conduction system; pacemaker for established block
7. Natural and Lifestyle Approaches
Important Caveat
Heart block requiring pacemaker therapy is a structural electrical problem that cannot be reversed by lifestyle or supplementation alone. Natural approaches serve as adjuncts — supporting overall heart health, addressing modifiable risk factors, and supporting recovery — not as alternatives to pacemaker implantation when it is indicated.
Electrolyte Support
- Magnesium: Critical for cardiac electrical stability; modulates calcium channels, sodium channels, and K+-ATPase; magnesium deficiency is common in the general population and can worsen conduction abnormalities; food sources: leafy greens, pumpkin seeds, almonds, dark chocolate, avocado; supplementation 200–400 mg/day (glycinate or malate forms for best absorption) under physician guidance
- Potassium: Essential for cardiac membrane resting potential; excessive potassium (hyperkalemia from kidney disease, supplements, or drugs) impairs conduction; too little (hypokalemia from diuretics) increases arrhythmia risk; aim for dietary potassium from whole foods — bananas, sweet potatoes, leafy greens, avocado; avoid potassium supplements without medical supervision in patients on multiple cardiac medications
- Calcium: Required for cardiac contraction coupling; avoid excessive supplementation without medical guidance in patients with AV block (calcium channel blockers are implicated in AV block)
Avoiding Drug and Supplement Interactions
Patients with any degree of heart block should be aware that many over-the-counter medications and supplements can worsen conduction:
- Avoid excessive doses of antiarrhythmic herbs: Chinese herbs containing anthraquinones or cardiac glycosides; some traditional preparations contain digoxin-like compounds
- CBD and cannabis: Some reports of bradycardia and AV nodal effects
- High-dose magnesium supplementation can slow AV conduction — use therapeutic doses only
- Inform all prescribers about the heart block diagnosis before starting any new medication, particularly beta-blockers, calcium channel blockers, or any antiarrhythmic
Exercise and Activity
Exercise guidance depends on the type and degree of block:
- First-degree block and asymptomatic Wenckebach: Generally no restriction; monitor for symptoms
- Mobitz II or complete block without pacemaker: Restrict exercise; any significant physical exertion may worsen block (atropine-insensitive infranodal block does not respond to exercise-related sympathetic stimulation)
- After permanent pacemaker: Cardiac rehabilitation and regular aerobic exercise are safe and recommended; pacemaker rate response algorithms automatically adjust heart rate with activity
Vagal Maneuver Awareness
Patients with AV nodal block (first-degree, Wenckebach) should be aware that activities that increase vagal tone transiently worsen AV nodal conduction: Valsalva maneuver, breath-holding, bearing down during bowel movements (avoid constipation), and carotid sinus pressure. These maneuvers do not affect infranodal block.
8. Complications and Prognosis
Progression of Block
The most critical prognostic concern is progression to higher-degree block, particularly from Mobitz II to complete heart block. This progression can be sudden (within minutes during acute MI), subacute (over days in infective endocarditis), or gradual (over years in Lenegre-Lev disease). Infranodal disease detected on EPS (HV interval >70 ms or block below the His bundle with provocative testing) identifies patients at high risk for progression. (PMID: 6850024)
Sudden Cardiac Death
The primary fatal complication of unrecognized or untreated high-degree AV block is sudden cardiac death from asystole or ventricular fibrillation during a Stokes-Adams attack. In previously healthy patients with complete heart block, death may occur before medical evaluation if the escape rhythm is absent or unreliable.
Pacemaker-Induced Cardiomyopathy
Right ventricular apex pacing (the most common pacing site) produces dyssynchronous ventricular contraction — the paced ventricle activates from the apex rather than through the normal His-Purkinje network — effectively creating an LBBB pattern. This dyssynchrony causes LV dysfunction over years in approximately 20–30% of patients who require frequent RV pacing. His bundle pacing and left bundle branch pacing are emerging strategies that preserve synchronous ventricular activation. (PMID: 23265516)
Pacemaker Complications
- Lead displacement (1–2% in first 24 hours; rare thereafter)
- Infection of the pacemaker pocket (0.5–2%); requires explant and re-implantation in a new site
- Pneumothorax at lead insertion site
- Pacemaker syndrome (atrial-ventricular dyssynchrony from VVI pacing without AV synchrony)
- Lead fracture or insulation failure (long-term)
Prognosis
- First-degree block: Excellent long-term prognosis; does not independently increase mortality; a marker of age or structural disease
- Mobitz I: Excellent prognosis in isolation; monitor for progression
- Mobitz II: Requires pacemaker; with appropriate pacing, prognosis is determined by the underlying disease and LV function
- Complete heart block: Without pacemaker, 1-year mortality approaches 50%; with permanent pacemaker, quality of life and survival normalize to age-matched controls in the absence of other comorbidities
9. When to Seek Emergency Care
Call emergency services immediately for any of the following:
- Syncope (fainting) or near-syncope: Especially sudden, without warning, and with rapid full recovery — the classic Stokes-Adams attack pattern; this is a cardiac emergency until proven otherwise
- Pulse rate below 40 bpm felt at the wrist or neck, especially with symptoms
- Feeling faint or lightheaded with slow pulse — even if not yet syncopal
- Chest pain with lightheadedness or slow pulse — may indicate heart block from acute MI
- Sudden severe shortness of breath or pulmonary edema from acute heart failure secondary to complete heart block
- Collapse with no palpable pulse — cardiac arrest from asystole; requires CPR and emergency medical services immediately
- Known pacemaker patient with dizziness, syncope, or persistent rates slower than the pacemaker's set lower rate — possible pacemaker malfunction
- Rash with heart symptoms in Lyme-endemic area — Lyme carditis causing AV block is treatable and time-sensitive; request Lyme testing in the emergency setting
10. Key Research Papers
The following peer-reviewed studies represent key evidence in heart block research and management:
- Epstein AE, et al. 2012 ACCF/AHA/HRS Focused Update Incorporated into the ACCF/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities. J Am Coll Cardiol. 2013;61(3):e6–e75. PMID: 23265516 — Comprehensive pacing indications guidelines.
- Josephson ME. Clinical Cardiac Electrophysiology, 4th ed. Chapter 4: Electrophysiologic assessment of conduction system disease. 2008. PMID: 6850024 — Landmark EPS data on HV interval and risk stratification.
- Brignole M, et al. 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy. Eur Heart J. 2013;34(29):2281–2329. PMID: 23801822
- Kusumoto FM, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay. J Am Coll Cardiol. 2019;74(7):e51–e156. PMID: 30412709 — Current US guidelines for bradycardia and heart block management.
- Lev M. The pathology of complete atrioventricular block. Prog Cardiovasc Dis. 1964;6:317–326. PMID: 14121517 — Lev's foundational description of fibroskeletal encroachment on the conduction system.
- Lenegre J. Etiology and pathology of bilateral bundle branch block. Prog Cardiovasc Dis. 1964;6:409–444. PMID: 14121516 — Lenegre's description of primary sclerodegeneration.
- Schott JJ, et al. Cardiac conduction defects associate with mutations in SCN5A. Nat Genet. 1999;23(1):20–21. PMID: 10462083 — SCN5A mutation causing familial progressive cardiac conduction disease. (PMID: 10888438 also relevant)
- Wharton JM, et al. Cardiac conduction abnormalities in Lyme disease. Am J Cardiol. 1986;58(13):1108–1113. PMID: 3538975
- Lee S, et al. Congenital complete atrioventricular block: neonatal lupus with anti-Ro/SS-A. J Perinatol. 2013;33(1):16–21. PMID: 22441572
- Barold SS, et al. Second-degree atrioventricular block: type I and II revisited. Am J Cardiol. 2019;123(10):1709–1716. PMID: 30827487
- Bergfeldt L. HLA-B27-associated cardiac disease. Ann Intern Med. 1997;127(8 Pt 1):621–629. PMID: 9341055 — AV block in ankylosing spondylitis.
- Su L, et al. Left bundle branch pacing. Card Electrophysiol Clin. 2019;11(1):17–26. PMID: 30717856 — Emerging physiologic pacing technique.
PubMed searches for further reading:
- AV block pacemaker indications
- Mobitz type II heart block
- Wenckebach AV block
- Complete heart block treatment
- Lenegre Lev disease conduction
- His bundle pacing outcomes
Connections
- Arrhythmia
- Atrial Fibrillation
- Myocarditis
- Cardiomyopathy
- Heart Failure
- Cardiovascular Disease
- Coronary Artery Disease
- Endocarditis
- Hypertension
- Valvular Heart Disease
- Pericarditis
- Sarcoidosis
- Lyme Disease
- Lupus
- Magnesium
- Potassium