Transition from Narrow to Wide QRS Tachycardia: What is the Mechanism?

Vora, Amit; Lokhandwala, Yash

doi:10.1046/j.1460-9592.2001.00374.x

Cited by 3 publications

(2 citation statements)

References 2 publications

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“…[1][2][3][4][5][6][7][8] The tachycardia-induced tachycardia, or so-called double tachycardia, appears to be a relatively rare condition and three possibilities should be considered: (1) the NCT and WCTs are related to a single mechanism (i.e., NCT with transient right or left BBB aberrancy), (2) a PT, or (3) an NCT inducing VT. 1,9 In the PT, the WCT occurs with the gradual fusion between activation over the His Purkinje system (HPS) and the ventricles, as evident from the progressive decrease in HV interval until the HB is no longer visible. 6,10 Comparison of QRS morphology and HV interval between SR and WCT, and the distinguishing between an antegrade His bundle (HB) signal and the retrograde HB potential are therefore critical in the interpretation of pacing maneuvers or complex cases involving WCT. 2,4,8,11 Antegrade HB activation and normal HV interval suggest that the mechanism of the WCT is the BBB, whereas retrograde HB activation or subnormal HV interval is consistent with either VT or ART.…”

Section: Discussionmentioning

confidence: 99%

Widening of the QRS complex during the wide complex tachycardia: What is the mechanism?

Aslan¹,

Merovci

Tunçez

et al. 2022

Cardiovasc electrophysiol

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Section: Discussionmentioning

confidence: 99%

Widening of the QRS complex during the wide complex tachycardia: What is the mechanism?

Aslan¹,

Merovci

Tunçez

et al. 2022

Cardiovasc electrophysiol

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“…However, tachycardia‐induced tachycardia is rare. The following associations have been reported: (1) LIVT inducing typical or atypical AVNRT, 3–5 (2) VT originating in the RVOT or pulmonary artery inducing typical or atypical AVNRT, 6–9 and (3) typical AVNRT inducing LI 10–12 or RVOT 13 VT. However, AVNRT entraining VT 14 or VT entraining AVNRT 15 is extremely rare.…”

Section: Discussionmentioning

confidence: 99%

Reciprocal Induction of Long RP and Wide QRS Tachycardias

Irie

Kaneko

Nakajima

et al. 2011

Pacing Clinical Electrophis

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Figure 1. (A) Twelve-lead ECG during sinus rhythm. (B) Limb leads of the 12-lead ECG recorded during transition from tachycardia 1 to tachycardia 2 following a bolus injection of ATP. The fifth QRS complex widens, consistent with fusion of AVNRT and LIVT, following a slight prolongation of the RP interval immediately after fourth complex. The subsequent QRS morphology and absence of visible P waves is consistent with LIVT. (C) Limb leads of the 12-lead ECG recorded during transition from tachycardia 2 to tachycardia 1. The fourth QRS complex narrows and is followed by a P wave, consistent with fusion of AVNRT and VT, while all subsequent QRS complexes are consistent with AVNRT. (D) Precordial leads recorded during tachycardia 1. See the text for further explanations.to our hospital for electrophysiologic studies and catheter ablation. The physical examination, chest roentgenogram, and transthoracic echocardiogram were unremarkable. His baseline 12-lead electrocardiogram (ECG) showed sinus rhythm, with a normal PR interval, atypical right bundle branch block (RBBB), an indeterminate QRS axis, and ST depression in inferior leads (Fig. 1A). Ischemic heart disease and cardiomyopathy were excluded by transthoracic echocardiography and cardiac catheterization. A recording during tachycardia 1 (first half of Fig. 1B, second half of Figs. 1C and D) showed a long RP tachycardia with a cycle length of 310 ms, RBBB morphology, indeterminate axis, and negative P waves in leads II, III, and aVF.

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Alternating Narrow and Wide Complex Tachycardia:

Watanabe

Okumura

Nakai

et al. 2004

Pacing Clinical Electrophis

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Case PresentationA 38-year-old man presented with a 20 year history of repeated episodes of paroxysmal palpitations, terminating spontaneously or with verapamil. Clinical examination and 12-lead electrocardiography (ECG) during sinus rhythm were normal, and echocardiography showed a structurally normal heart. The patient was referred for electrophysiological study and radiofrequency ablation (RFA). During electrophysiological study, tachycardia was induced; the ECG (leads I and V 1 ) is shown in top panel of Figure 1. What is the best explanation for this rhythm? CommentaryThe bottom panel of Figure 1 shows narrow QRS tachycardia recorded just before the top panel of Figure 1. The initial part of tracing of the top panel of Figure 1 shows a narrow QRS tachycardia with cycle length of 325 ms that transitions to a wide QRS tachycardia with right bundle branch block morphology and cycle length of 320 ms. The wide QRS tachycardia then changes again to narFigure 1. (Top panel) Surface leads I and V 1 depict transition from a narrow to right bundle branch block with inferior axis QRS complex tachycardia, and back to narrow complex tachycardia. Note the variable fusion beats of narrow and wide complex tachycardia (beats 4,5, and 10). (Bottom panel) Surface leads I and V 1 depict a segment of more pure narrow QRS tachycardia recorded just before the top panel of Figure 1.row QRS tachycardia in the last part of the tracing, and only the last beat shows entirely narrow QRS. The clinical tachycardia of this patient always showed a right bundle branch block with inferior axis pattern. At electrophysiological study, three multipolar catheters were positioned via the right and left femoral veins at the high right atrium, right ventricle, and the His-bundle region, and another was positioned in the coronary sinus via the right internal jugular vein. Atrial premature stimulation at baseline did not reveal dual atrioventricular (AV) nodal physiology. The narrow QRS tachycardia was induced with right atrial and right ventricular premature stimuli (Figure 2 A). A His bundle depolarization preceded each tachycardia beat with an HV interval of 46 ms, and 1:1 ventriculoatrial (VA) conduction was present with the site of earliest retrograde conduction located at the distal coronary sinus. An identical retrograde activation pattern was present during right ventricular pacing without decremental retrograde conduction. The mechanism of this tachycardia was confirmed to be AV reentrant tachycardia (AVRT) based on the fact that the retrograde earliest atrial electrogram was recorded at the left lateral wall and because of the absence of dual AV nodal pathway physiology, with induction of tachycardia upon reaching a critical AH delay. On multiple occasions, tachycardia converted from a narrow to wide QRS morphology, or vice versa. An example of this transformation is 246

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Transition from Narrow to Wide QRS Tachycardia: What is the Mechanism?

Cited by 3 publications

References 2 publications

Widening of the QRS complex during the wide complex tachycardia: What is the mechanism?

Widening of the QRS complex during the wide complex tachycardia: What is the mechanism?

Reciprocal Induction of Long RP and Wide QRS Tachycardias

Alternating Narrow and Wide Complex Tachycardia:

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