Left posterior fascicular block, state-of-the-art review: A 2018 update

Figures

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  Fig. 1. LAFB (Fig. 1-A) causes left axis deviation in the frontal plane (usually between −45° and −90°); LPFB (Fig. 1-B) causes right axis deviation in the frontal plane (QRS axis ≈+120°, between +80 and +140°); while left septal fascicular block (Fig. 1-C) causes prominent anterior QRS forces in the horizontal plane.

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  Fig. 2. Example of LPFB + complete RBBB Kennedy type III + hyperacute phase of inferior MI by obstruction of RCA. FP: QRS axis +150°, VCG QRS loop with clockwise rotation and located in inferior quadrants (>40% area in inferior right quadrant), injury vector pointed to III suggesting proximal obstruction of RCA, ST segment depression in I and aVL, ST segment elevation (STE) in inferior leads (STEIII > STEII). HP: QRS loop located in the anterior quadrants, CW rotation, right end conduction delay (RECD) in the right anterior quadrant, complete RBBB Kennedy type III. LSP: all QRS loop located in anterior and inferior quadrants, QRS loop with counterclockwise rotation. Conclusion: LPFB + complete RBBB + acute inferior MI.

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  Fig. 3. QRS axis +115°, I and aVL rS; III qR; II, III and aVF qR with inferoapical post-ischemic T wave; V2—V3 deep S waves. LPFB and inferior MI accounted for Q waves in leads II, III and aVF (arrows). However, the R-wave amplitude in these leads is increased after LPFB but decreased after inferior MI. The mean QRS axis in the FP was shifted toward the vertical in LPFB but little changed or slightly shifted away from the vertical in inferior MI.

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  Fig. 4. A: Upwards concave STE followed by positive T waves across the precordial leads (hyperacute phase of anterolateral MI). B: Right axis deviation, LPFB and a QS pattern from V2 to V6 suggesting transmural MI, higher precordial STE and qR pattern followed of negative T wave suggesting RBBB associated.

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  Fig. 5. Clinical features: 85-year-old female. Autopsy diagnosis: Lev's disease. ECG diagnosis: 1st degree AV block + LPFB + RBBB: probable trifascicular block + digitalis effect.

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  Fig. 6. ECG performed before the percutaneous septal ablation. Clinical diagnosis: obstructive hypertrophic cardiomyopathy with a gradient in LVOT of 80 mmHg and NYHA IV, even with medication. ECG diagnosis: left atrial enlargement + left ventricular hypertrophy (LVH) with strain.

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  Fig. 7. ECG/VCG correlation immediately after percutaneous procedure. ECG/VCG: LPFB + acute septal MI + LVH + RBBB.

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  Fig. 8. VCG/ECG correlation in isolated LPFB. FP-ECG: initial 10–20 ms vector heading upward and to the left; rS pattern in I and aVL; qR in inferior leads; RIII > RII; middle final notch in the descending limb of the R wave of lead III; QRS loop of clockwise (CW) rotation and broadened morphology. Clinical absence of RVH, vertical heart or extensive lateral MI (the diagnosis of LPFB must obligatorily be clinical-electrocardiographic). A definite diagnosis should be made only in absence of RVH, “vertical heart” or lateral MI. FP-VCG: Initial 10–20 ms vector heading above and to the left (near −45°) with delay (initial 10–25 ms); broad QRS loop, CW rotation; maximal vector ≈ +110°; almost all the QRS loop located below the X orthogonal lead predominantly in the inferior quadrants; QRS loop duration 110 ms; T loop with CW rotation, heading below and to the left near +10°. HP-ECG: rS pattern in V1 –V2, deep S wave in V2 (consequence of posterior dislocation and to the right of the final forces), scant progression of growth of R wave, transition zone in V4 and Rs in V6, prolonged R-wave peak time (≥50 ms) in V5—V6 and disappearance of q wave in these leads. HP-VCG: Initial 10–20 ms vector…

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  Fig. 9. Typical RBBB pattern associated with LPFB, septal infarction (qR in V1) and anterior ischemia.

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  Fig. 10. Right axis deviation (QRS axis in +115°), rS pattern in leads I and aVL, tall R waves in lead III > RII, and qR pattern (embryonic q) in lead III. This ECG pattern in the limb leads, in the absence of clinical and echocardiographic evidence of RVH, lateral infarction and/or vertical heart associated with significant left ventricular hypertrophy, suggests LPFB. In the chest leads, prominent anterior QRS forces: R wave in V2 > 15 mm. In the absence of RVH, laterobasal MI, RBBB, pre-excitation with a posterior anomalous pathway, hypertrophic cardiomyopathy, endomyocardial fibrosis, muscular dystrophy, and dextroposition, strongly suggests LSFB.

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  Fig. 11. Admission ECG. Sinus tachycardia, rate-independent transient alternating LPFB associated with complete RBBB (qR pattern from V1—V4) + acute extensive anterior STEMI, caused by occlusion of the LAD after the first septal perforator and before the first diagonal branch of the LAD, because the injury vector points to the left leads (I and aVL) with reciprocal ST depression in the inferior leads. In precordial leads, the injury vector points to the front and minimally leftward, causing STE from V2—V5 (Fig. 12).

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  Fig. 12. ECG/VCG correlation in the FP and HP. FP: ST injury vector directed to left and upward (ST segment elevation in I and aVL and ST depression in III, aVF and II). HP: St injury vector directed to front and leftward near +60°. ST segment elevation from V2 to V5, qR from V1—V4 (anterior MI complicated with RBBB).