Speech-induced atrial tachyarrhythmias represent a very rarely described phenomenon, with only a few previous reports. Understanding the precise mechanisms underlying speech-triggered paroxysmal atrial tachyarrhythmias is challenging, because of the complexity of the systems involved in vocalization (neural and muscle activation, respiratory activity, and autonomic control of all physiological variations occurring during speech).
In recent years, studies have shown that the vagus nerve is involved in the occurrence of arrhythmias. The preganglionic neurons of the vagus nerve are located in the dorsal nucleus and nucleus ambiguus of the vagus nerve in the medulla oblongata. After intermingling with other nerves, the preganglionic fibers converge into the cervical vagus trunk and descend to the heart, forming a ganglionated plexi (GP) on the surface of the heart, mainly distributed in the fat pad on the surface of the left atrium and the Marshall ligament. The atrial ganglion plexus can independently regulate cardiac contraction, conduction, and automaticity, while the ganglion plexus in the left atrial wall is mainly distributed at the root of four pulmonary veins, atrial sulcus, and other parts [1]. The successful ablation site of this patient was located at the posterior wall of the left atrium (near the opening of the right lower pulmonary vein), which is the common part of the cardiac ganglia plexus in the left atrium. This report describes a case of atrioventricular node reentrant tachycardia triggered by atrial premature contraction. Atrial tachycardia occurs after successful ablation of the dual atrioventricular node pathway and is related to speech. It may be related to the vagal reflex mediated by the left recurrent laryngeal nerve in the pharynx and larynx while speaking. The vocal cords vibrate when speaking, stimulating the recurrent laryngeal nerve under the glottic fissure, thus mediating the vagal reflex and triggering the occurrence of atrial tachycardia. The ablation of cardiac ganglia plexus has been studied extensively [2–3], and can significantly reduce bradycardia and syncope caused by vagal reflex, along with a decrease in the triggering of tachycardia. In this case, the heart rate and blood pressure decreased upon ablation of the right lower pulmonary vein opening, which was considered to be related to the abundance of the vagus nerve and vagal reflex during ablation.
Vagal nerve stimulation activates the release of acetylcholine, leading to the release of catecholamine from chromaffin cells in the heart muscle. When the stimulation stops, acetylcholine rapidly degrades, and catecholamine in the heart immediately plays a role, causing temporary tachycardia, shortening the refractory period of the atrium, hyperpolarizing the resting membrane potential, inhibiting 4-phase depolarization, and shortening the time limit of the action potential [4–5]. Vagus nerve stimulation can change the electrophysiological characteristics of pulmonary veins by significantly shortening the effective refractory period of various parts of pulmonary veins, especially the distal portion of the pulmonary veins, rendering them prone to tachycardia induction [6]. Some cases of triggered atrial tachycardia occurrence in the left pulmonary vein and the right pulmonary vein opening have been reported previously. Therefore, we speculated that circumferential pulmonary vein isolation (PVI) could be performed for speech-induced atrial tachycardia to reduce the onset of tachycardia.