Dual Atrioventricular Nodal Non–Re-Entrant Tachycardia

Corresponding Author

Dual atrioventricular nodal non–re-entrant tachycardia (DAVNNT), or dual atrioventricular node (AVN) conduction, has been recognized as a rare phenomenon that can mimic almost all cardiac arrhythmias and deceive both noninvasive practitioners and invasive electrophysiologists alike. This phenomenon could be considered the ideal protagonist of a clinical scenario titled the electrocardiographic chameleon of the atrioventricular node¹ In this issue of JACC: Case Reports, Cholagh et al² present a textbook example of this deception.

A 69-year-old woman spent 1 year being treated for presumed atrial fibrillation with β-blockers while her ejection fraction deteriorated to 22%. Only when the “double fire bigeminy” phenotype of DAVNNT was correctly recognized did the true diagnosis emerge, enabling targeted slow pathway ablation and a remarkable recovery of ventricular function to 54%. This case is a powerful reminder that to see the forest, one must first recognize the chameleon hiding among the trees of P waves and QRS complexes.

The Electrophysiological Substrate

DAVNNT is dependent on the unique electrophysiological characteristics of the AVN that enable a double antegrade conduction of sinus rhythm via both the fast pathway and the slow pathway. Therefore, DAVNNT is typically recognized when a single P-wave is followed by 2 narrow QRS complexes, the so-called double fire. The easiest way to identify it is to recognize the second interpolated QRS complex after a single P-wave, preceded by an impulse conducted via the fast pathway, resulting in a narrow QRS complex conducted via the fast pathway.

In other, more complex scenarios, the “second fire” via slow conduction induces several typical, atypical, intermittent, or reproducible conduction aberrancies due to phase III or phase IV block in the His-Purkinje system, as the electrical wave front encounters myocardial tissue during different depolarization phases. The result is a spectrum of QRS morphologies within a single recording, ranging from narrow complexes to progressively more pronounced bundle branch block patterns, creating a chaotic electrocardiographic (ECG) picture that mimics polymorphic arrhythmias. What appears overwhelmingly complex at first glance becomes much simpler once the underlying mechanism is understood. Although DAVNNT is usually an isolated phenomenon, the intermittent reappearance of retrograde AVN conduction enables the induction of typical and atypical atrioventricular nodal re-entry tachycardia, which makes the ECG diagnosis even more complex and diagnostically challenging.

The Diagnostic Pathway

The history of DAVNNT is a history of misdiagnosis. A landmark review by Peiker et al¹ identified 68 cases accumulated between 1950 and 2014, of which 48 (71%) were initially misdiagnosed. The most common erroneous diagnosis was atrial fibrillation, but sinus tachycardia, nonspecific supraventricular tachycardia, and ventricular tachycardia were also reported. A subsequent multicenter observational study by Hartmann et al³ demonstrated the real-world consequences: in 17 patients with confirmed dual antegrade conduction, the mean delay to correct diagnosis exceeded 1 year, and patients received nonindicated oral anticoagulation and inappropriate implantable cardioverter-defibrillator shocks. The case reported by Cholagh et al² follows this unfortunate pattern precisely.

Continuous, simultaneous 12-lead ECG recording, or ideally 12-lead Holter monitoring, is the best noninvasive option for differentiating the absence of hidden P waves from true hidden second AVN conduction (from an ECG point of view). However, the final diagnosis of DAVNNT is made during an invasive electrophysiology study by excluding other very rare phenomena, such as His-Purkinje system ectopy. The electrophysiology study should include assessment during conscious sedation at baseline, without drugs, to reliably document the “double fire” phenomenon, with intracardiac recordings showing similar HV intervals preceding each QRS complex after a single P-wave.

Why Correct Diagnosis Matters

This is crucial for appropriate diagnosis and, above all, for avoidance of inappropriate therapeutic decisions. DAVNNT may induce arrhythmia-induced cardiomyopathy, which represents the only arrhythmia-related cardiomyopathy occurring during sinus rhythm below 100 beats/min, because the additional QRS complexes effectively double the ventricular rate while the sinus rate itself remains unremarkable. Misidentification leads to unnecessary implantable cardioverter-defibrillator implantation for presumed ventricular arrhythmia or futile pulmonary vein isolation for mistaken atrial fibrillation. The case reported by Cholagh et al² serves as a cautionary tale: 1 year of wrong treatment, progressive cardiomyopathy, and ultimately recovery once the correct rhythm was identified and ablated.

Slow pathway catheter ablation is highly effective in the treatment of DAVNNT, as demonstrated by both the accumulated literature and the present case. Yet despite this favorable therapeutic profile, DAVNNT is not mentioned in current guidelines on supraventricular arrhythmias,⁴ and as of 2026, it is estimated that fewer than 200 cases have been reported in the literature. Only specialized case reports and small series document this phenomenon. Noninvasive cardiologists and invasive electrophysiologists should consider DAVNNT in their differential diagnosis because the treatment is curative and the consequences of missing it are severe.

To arrive at the correct diagnosis amid the complexities of DAVNNT, clinicians should learn to recognize this ECG chameleon within the forest of P waves and QRS complexes (Figure 1). What looks overwhelmingly complex at first glance becomes simpler once the chameleon reveals itself. It is not easy to see the forest for the trees, but it is far worse to lose sight of the diagnosis for the ECG chameleon.

Figure 1.

Electrophysiological Mechanism, Electrocardiographic Manifestation, and Novel Graphical Notation of His-Purkinje Conduction in Dual Atrioventricular Nodal Non-Re-Entrant Tachycardia

(Top) Modified ladder diagram illustrating the mechanism of dual atrioventricular nodal non–re-entrant tachycardia. (Middle) The ECG is adapted from the original case report.² (Bottom) A novel proposed graphical notation of His-Purkinje conduction. A = atrium; AVN = atrioventricular node; ECG = electrocardiogram; FP = fast pathway; HPS = His-Purkinje system; LAF = left anterior fascicle; LPF = left posterior fascicle; LSF = left septal fascicle; RBB = right bundle branch; SP = slow pathway.

Funding Support and Author Disclosures

The authors have reported that they have no relationships relevant to the contents of this paper to disclose.