Fascicular VT and Bundle Branch Reentrant VT
Two ventricular tachycardias that live entirely within the conduction system. Both produce relatively narrow QRS complexes, and both are curable with ablation.
Most ventricular tachycardias arise from diseased myocardium. The wavefront grinds through zones of scar, producing wide, bizarre QRS complexes that bear no resemblance to the conducted beat.
The two VTs in this chapter break that rule. Their circuits run through the His-Purkinje network itself. Because the wavefront uses the heart's own highway system, the resulting QRS is far narrower than you would expect from a ventricular rhythm. This narrow morphology is a trap: it frequently leads to misdiagnosis as supraventricular tachycardia.
Understanding where these circuits live explains everything: the ECG morphology, the drug response, and the ablation target.
Fascicular VT: The Verapamil-Sensitive Circuit
The left ventricle's Purkinje network fans out from the left bundle branch into two major divisions: the left anterior fascicle and the left posterior fascicle. In some patients, abnormal Purkinje tissue forms a small pathway connecting septal fibers back to one of these fascicles. False tendons, thin fibromuscular bands stretching across the left ventricular cavity, often harbor this tissue.
This creates a micro-reentrant circuit. One limb is the fascicle itself, conducting rapidly through normal sodium channels. The other limb is the abnormal Purkinje tissue, which conducts slowly through calcium-dependent channels. The difference in conduction velocity between the two limbs is what allows the circuit to sustain itself.
The most common form involves the left posterior fascicle. A premature beat finds the posterior fascicle refractory, conducts antegradely through the slow calcium-dependent pathway, then reenters the posterior fascicle retrogradely once it has recovered. The circuit spins continuously.
Because the wavefront exits through the left posterior fascicle (which normally activates the inferoposterior left ventricle), the activation sequence during tachycardia resembles left anterior fascicular block: the ECG shows an RBBB morphology with left axis deviation. The QRS is relatively narrow (120-140 ms) because the exit point is already within the Purkinje system.
Variants of Fascicular VT
The posterior fascicular form accounts for roughly 90% of cases. Two rarer variants exist:
Left anterior fascicular VT uses a circuit involving the left anterior fascicle. The wavefront exits anteriorly and superiorly, so the ECG shows RBBB morphology with right axis deviation. This is the mirror image of the posterior form.
Upper septal fascicular VT originates near the bifurcation of the left bundle branch. It produces a narrow QRS with a normal axis or slight rightward axis, sometimes with a pattern that mimics septal depolarization abnormalities. This variant is the least common and the hardest to distinguish from SVT.
Why Verapamil Works
The slow limb of the fascicular VT circuit depends on L-type calcium channels for conduction. This is an unusual property for ventricular tissue. Most ventricular myocytes and Purkinje fibers conduct through fast sodium channels. The abnormal septal tissue in this circuit behaves more like AV nodal tissue: slow, decremental, calcium-dependent.
Verapamil blocks L-type calcium current. When administered intravenously, it suppresses conduction through the slow limb and terminates the tachycardia. This response is so reliable that it has become a diagnostic criterion. A wide-complex tachycardia that terminates with verapamil in a young patient with a structurally normal heart is fascicular VT until proven otherwise.
This drug sensitivity is unique among ventricular tachycardias. Scar-related VT does not respond to verapamil. Outflow tract VT does not respond to verapamil. The calcium-dependent slow limb is the singular vulnerability of this circuit.
In the emergency department, fascicular VT is frequently misdiagnosed as SVT with RBBB aberrancy because the QRS is narrow and the patient is young and hemodynamically stable. The left axis deviation is the key differentiator. SVT with true RBBB aberrancy produces a normal or rightward axis. An RBBB-morphology tachycardia with marked left axis deviation in a young patient should raise immediate suspicion for posterior fascicular VT.
Bundle Branch Reentrant VT: The Macro-Circuit
Bundle branch reentrant VT (BBRVT) is an entirely different animal. Where fascicular VT uses a tiny circuit within the left ventricle, BBRVT uses the entire His-Purkinje system as its racetrack.
The circuit is large: the wavefront descends one bundle branch, activates ventricular myocardium at the apex, crosses the interventricular septum, and then ascends the other bundle branch retrogradely. It passes through the His bundle and re-enters the descending limb. This is macro-reentry through the conduction system.
BBRVT almost always occurs in patients with dilated cardiomyopathy and pre-existing conduction disease. The substrate is a diseased His-Purkinje system with prolonged conduction times. A long HV interval (≥60 ms) at baseline is the hallmark. The slowed conduction through damaged bundle branches provides the time necessary for the tissue ahead to recover excitability, allowing the circuit to sustain.
In the typical form, the wavefront travels down the right bundle branch (antegradely), crosses the ventricular myocardium at the apex, and ascends the left bundle branch (retrogradely). Because ventricular activation begins via the right bundle branch, the resulting QRS has an LBBB morphology.
The ECG Clue: VT That Looks Like Sinus
Here is the diagnostic trap. Because BBRVT uses the same bundle branch for antegrade ventricular activation that the patient uses during sinus rhythm, the QRS morphology during tachycardia is often identical to the patient's baseline QRS.
A patient with baseline LBBB who develops BBRVT will have a VT that looks exactly like their sinus rhythm LBBB. The only difference is the rate. This makes the arrhythmia easy to dismiss as sinus tachycardia or SVT with pre-existing LBBB.
The less common form runs the circuit in reverse: down the left bundle branch and up the right bundle branch. This produces an RBBB-morphology VT and is seen in patients with baseline RBBB.
EP Lab Diagnosis of BBRVT
The intracardiac electrogram provides definitive proof. During BBRVT, a His bundle electrogram precedes every QRS complex. The HV interval during VT is equal to or longer than the HV interval in sinus rhythm. This confirms that the His-Purkinje system is part of the circuit, driving ventricular activation.
Additional findings: the right bundle branch potential precedes ventricular activation on the RBB recording catheter. Changes in the bundle branch electrogram timing directly correlate with changes in the tachycardia cycle length. If the RBB interval fluctuates, the VV interval fluctuates in lockstep.
Programmed stimulation (the formal protocol is covered in Volume VI, Chapter 6) typically induces the tachycardia with relative ease in these patients. The induction often requires only a single extrastimulus from the right ventricle.
Ablation: Cutting the Circuit
BBRVT is one of the most satisfying ablation targets in electrophysiology. The right bundle branch serves as the antegrade limb of the circuit in the typical form. A single radiofrequency lesion on the right bundle branch permanently eliminates the circuit.
Why the right bundle branch? The left bundle branch is the dominant pathway for normal antegrade ventricular activation. Ablating it would worsen conduction and likely require a pacemaker. The right bundle branch, by contrast, contributes relatively little to normal ventricular depolarization in these patients (who already have diseased conduction). Its ablation is tolerated well.
After successful ablation, the patient develops complete RBBB on the surface ECG. The VT is no longer inducible. However, these patients still have severe cardiomyopathy with a substrate capable of generating scar-related VT through different mechanisms. Most will still require an implantable cardioverter-defibrillator (ICD) for protection against other arrhythmias.
Fascicular VT ablation targets the slow calcium-dependent pathway at the midseptum of the left ventricle. Activation mapping during tachycardia (Volume VI, Chapter 3) identifies a diastolic potential (the "P1 potential") along the septum. Ablation at this site eliminates the slow limb and cures the arrhythmia. Because these patients have structurally normal hearts, no ICD is needed.
The typical BBRVT circuit: antegrade down the right bundle branch, across the ventricular myocardium, retrograde up the left bundle branch, through the His bundle, and back down the RBB. Ablation of the right bundle branch eliminates the circuit.
Key Takeaways
- Fascicular VT (Belhassen VT): A micro-reentrant circuit using the left posterior fascicle and abnormal calcium-dependent Purkinje tissue. ECG shows RBBB with left axis deviation. Terminates with IV verapamil.
- The Slow Limb: The calcium-dependent pathway in fascicular VT is what makes it uniquely sensitive to verapamil among all ventricular tachycardias.
- BBRVT: Macro-reentry through the His-Purkinje system, typically in patients with dilated cardiomyopathy and prolonged HV intervals. The QRS during VT often looks identical to the patient's baseline conducted QRS.
- EP Proof: A His bundle electrogram preceding every QRS complex during VT, with an HV interval equal to or exceeding the sinus HV, confirms BBRVT.
- Ablation Targets: RBB ablation cures BBRVT. Midseptal ablation at the slow pathway (P1 potential) cures fascicular VT. Both have high success rates.
- The Diagnostic Trap: Both arrhythmias produce narrow or relatively narrow QRS complexes and are commonly misdiagnosed as SVT. The ECG morphology and clinical context (young patient vs. cardiomyopathy) point to the correct diagnosis.