Hemiblocks Revisited

Authors, Journal, Affiliations, Type, DOI

• Marcelo V. Elizari, Rafael S. Acunzo, Marcela Ferreiro
• Circulation. 2007;115:1154–1163
• Division of Cardiology, Ramos Mejía Hospital, Buenos Aires, Argentina
• Review article with original epidemiological data
• DOI: 10.1161/CIRCULATIONAHA.106.637389

Overview

A Circulation review from Elizari — co-author with Mauricio Rosenbaum on the original 1968 monograph that introduced the trifascicular conduction system and hemiblock concepts. The review re-examines anatomy, ECG and VCG criteria, masking/simulation of MI, epidemiology, and clinical significance of left anterior hemiblock (LAH) and left posterior hemiblock (LPH). Key original contributions: detailed Argentinian population epidemiology, 7 distinct MI-masking/simulation patterns, the masquerading RBBB phenomenon (LAH concealing RBBB), and the near-trifascicular nature and grave prognosis of RBBB + LPH.

Keywords

Epidemiology; heart septal defects; myocardial infarction; heart block; bundle-branch block

Key Takeaways

Anatomy — Trifascicular LBB System and Septal Fascicle

• The intraventricular conduction system has 3 terminals: RBB + anterior division LBB + posterior division LBB (Rosenbaum 1968); midseptal fibers may originate from posterior division (most common), anterior division, or both, or independently from the bifurcation of the main LBB
• Theoretical vulnerability order (most to least): RBB > anterior division LBB > posterior division LBB > main LBB; clinical incidence order of conduction disturbances: LAH > RBBB > LBBB > LPH (explains why LPH is rare)
• Middle/septal fascicle exists anatomically but isolated left septal fascicular block is extremely difficult to recognize by surface ECG; AHA 2009 labels it "not recommended" — ECG recognition requires transient/rate-dependent changes or comparison of serial tracings
• Posterior division LBB is the least vulnerable: short and wide structure; located in the inflow tract (less turbulent than outflow tract); dual blood supply from LAD and posterior descending artery; not adjacent to dangerous anatomic structures

LAH ECG and VCG Criteria (Elizari/Rosenbaum)

• AQRS: −45° to −90° (complete LAH); −30° to −44° is incomplete LAH; AQRS may be −45° or less; degrees of −45°, −60°, −75° represent increasing completeness
• Initial 20ms vector: Inferior and rightward (+120°) → small Q in I and aVL; small sharp R in II, III, aVF
• Main forces: Superior and to the left → deep S in II, III, aVF; S III is deeper than S II (key diagnostic sign)
• QRS duration: Widens no more than 20ms in pure uncomplicated LAH (total QRS ≤110ms); MI or LVH may cause more widening
• Precordial leads: Deeper S waves in V5–V6; normal Q waves in left chest leads may be absent; small Q waves in V2–V3 possible (from initial inferior-rightward forces — can simulate anteroseptal MI)
• qR in aVL (AHA 2009 criterion confirmed)
• VCG frontal plane: Small initial forces inferior-rightward; main forces superior-leftward; wide-open counterclockwise (CCW) rotated loop — pathognomonic of LAH; differentiates LAH from all other causes of LAD

LPH ECG and VCG Criteria (Elizari/Rosenbaum)

• AQRS: +100° to +180° (complete); requires absence of: right ventricular hypertrophy, vertical heart in slender subjects, large lateral infarction
• S1Q3 pattern in limb leads
• QRS duration: <110ms
• rS in leads I and aVL; qR in leads II, III, aVF
• VCG: initial forces superior-leftward (small R in I/aVL, small Q in II/III/aVF); main and terminal forces inferior-rightward (+100°); wide-open clockwise (CW) rotated loop in frontal plane
• LPH VCG is the exact mirror image of LAH in the frontal plane

LAH and Myocardial Infarction — 7 Masking/Simulation Patterns

1. Inferior MI concealed by LAH: LAH creates initial R in II, III, aVF via early inferior LV activation; this R masks the pathological Q of inferior MI if the necrotic zone includes areas of early activation; if infarction spares early activation areas, initial R persists and MI is concealed

   • Negative T in II, III, aVF in the presence of LAH = strong sign of inferior ischemia or concealed inferior MI (LAH secondary T changes normally produce positive T in inferior leads)
   • VCG: initial 25ms vector rightward (not inferiorward) with CCW remaining loop; if septum preserved, initial vector first rightward then superior-leftward with inferior concavity

2. LAH concealed by inferior MI: Extensive inferior necrosis eliminates the initial R in inferior leads, making LAH invisible

3. Anterior MI concealed by LAH: Recording below normal chest lead level may produce small R waves masking Q waves; horizontal heart in stocky patients compounds effect

4. LAH simulates anteroseptal MI: Initial inferior-rightward forces → small Q waves in V2–V3 (especially at higher electrode positions); if Q waves persist 1 interspace below standard level, real anteroseptal MI is more likely

5. LAH simulates lateral MI: Q waves in I and aVL from early rightward vector + secondary T wave inversion → mimics lateral MI pattern

6. Extensive inferolateral necrosis simulates LAH: AQRS shifts to −60°, mimicking LAH — key differentiator: frontal plane QRS loop rotation; LAH = CCW; inferolateral necrosis = CW loop; additionally, Qr (not QS) in lead II excludes LAH — the presence of Qr means the terminal depolarization loop rotates CW into the positive hemifield of lead II

7. Transient LPH conceals inferior MI: LPH-induced inferior-rightward forces mask inferior infarction Q waves; subtle ST elevation in III and marked ST depression in I and V5-V6 may be the only sign of severe inferolateral injury during LPH

Masquerading RBBB (LAH Concealing RBBB)

• LAH causes the S waves of RBBB to disappear from leads I and aVL (standard masquerading RBBB) and from left precordial leads V5–V6 (precordial masquerading RBBB)
• When S wave disappears in I and V5–V6, RBBB configuration becomes so atypical it may resemble LBBB; RBBB may be totally missed even in right precordial leads
• Conditions required: (1) high-degree LAH superimposed with RBBB; (2) LVH and/or LV focal block from myocardial fibrosis/necrosis
• Clinical importance: failure to diagnose RBBB obscures recognition of bifascicular block and its risk of AV block progression
• Precordial chest lead mapping (recording at higher positions V1H, V3RH) can unmask RBBB when standard leads are misled by LAH

LPH Clinical Significance and Prognosis

• Isolated LPH is extremely rare; almost invariably associated with RBBB
• RBBB + LPH in acute MI:
  • Mortality 80–87% during first weeks after coronary event
  • Progression to complete AV block: 42% (effectively trifascicular block)
  • 75% of those with AV block die from pump failure
• Elizari cohort (29 cases RBBB + LPH): AV conduction disturbances in 82.7%; prolonged PR in 26/29; complete or high-degree AV block during follow-up in 18/29 (62%); Adams-Stokes seizures in 17/29 (58.6%)
• Dhingra et al (21 patients RBBB + LPH; 671±68 days follow-up): 6 had prolonged HV intervals; 3 required permanent pacemaker
• Posterior LBB involvement implies extensive conduction system disease — because the posterior division is the most protected, its block implies that more vulnerable structures (RBB, anterior division) are almost certainly also affected
• Mechanism of high AV block rate: lesions extensive enough to block the posterior fascicle virtually always also affect the RBB and anterior division → trifascicular block → complete heart block

LAH — Clinical Significance and Epidemiology

• Hospital data (1658 consecutive cardiology patients): LAH in 4.58%; RBBB 3.19%; LBBB 1.02%
• Healthy population — Argentine civilian pilots (8915 subjects, age 17–79 years): LAH prevalence 2.77% (247 cases); 152/247 (62%) in age group 17–39; low associated pathology: hypertension 10.5%, CAD 3.2% (mean age 50.7 years); not a single case of LPH found
• General population prevalence: 0.9% to 6.2% depending on series, diagnostic criteria, and ethnic diversity
• LAH more common in men; increases with advancing age
• Main causes in hospital populations: CAD (41% unequivocally); arterial hypertension; cardiomyopathies; Lev and Lenègre diseases; aortic valve disease; congenital heart disease
• Spontaneous VSD closure — underrecognized cause in young patients: 70% of 14 documented spontaneous membranous/perimembranous VSD closures developed LAH; 50% of neonatal VSD closures developed LAH by 6 months of follow-up
• Chagas disease: Endemic cause of LAH ± RBBB in Latin America
• Isolated LAH prognosis in healthy population: Does NOT imply adverse cardiac risk; should be regarded as incidental ECG finding; Biagini et al (1187 patients with suspected CAD): LAH (159 patients) associated with increased cardiac death over 6 years (P=0.004) — but this is in a suspected CAD population, not healthy individuals
• LAH in acute MI: prognosis controversy — some studies no worse than without LAH; one study showed slightly higher death rate

Lev vs Lenègre Disease

• Lenègre disease: Genetic/hereditary disorder; sclerodegenerative lesions and fibrosis isolated to conduction system; suspected in middle-aged patients with RBBB + LAH progressing to AV block without CAD or myocardial disease; LAH typically precedes RBBB → further involvement of LBB or posterior division → complete heart block
• Lev disease: Sclerosis of the left side of the cardiac skeleton at the pseudobifurcation of the His bundle; responsible for most cases of RBBB + LAH in elderly without other cardiac involvement → complete heart block over many years

Limitations of the Document

• Much of the epidemiological data (Argentine pilot study) is from selected populations (aviators) not representative of general population; prevalence data from 1960s–1990s studies
• Original pathological and experimental data predates modern genotyping and imaging — mechanistic interpretations rely on older correlation methods
• Limited prospective mortality data on isolated LAH; most prognostic data for LPH comes from small series (29 cases, 21 cases)
• Review reflects a specific theoretical framework (trifascicular system) that, while widely accepted, is contested regarding the septal fascicle

Key Concepts Mentioned

• concepts/Fascicular-Blocks — LAH and LPH criteria, masking patterns, epidemiology, prognosis
• concepts/ECG-Conduction-Disturbances — LAFB and LPFB AHA 2009 criteria; broader IVCD context

Key Entities Mentioned

• entities/Vectorcardiography — VCG frontal plane loop rotation as key differentiator for LAH vs MI vs LPH

Wiki Pages Updated

• wiki/sources/hemiblock-circ-2007.md — Created (this file)
• wiki/concepts/Fascicular-Blocks.md — Created
• wiki/concepts/ECG-Conduction-Disturbances.md — Updated LAFB/LPFB sections with clinical context
• wiki/concepts/RBBB.md — Added masquerading RBBB section
• wiki/sourceindex.md — New entry prepended
• wiki/wikiindex.md — New Fascicular-Blocks entry added
• log.md — Ingest entry prepended