ST-Segment Elevation Associated with Mobitz II Atrioventricular Block During Transseptal Puncture for Atrial Fibrillation Ablation

Pulmonary veins electrical isolation as an invasive treatment of atrial fibrillation has been widely used in electrophysiology laboratories. This case report presents a rare and transient complication, during transseptal puncture for atrial fibrillation ablation. ST-segment elevation, hypotension and bradyarrhythmia related to catheterization were observed despite cineangiocoronariography without obstructive lesions. Clinical stability was achieved after administration of intravenous atropine and saline solution. It is speculated that the phenomenon is attributed to an increased vagal tone after the mechanical effect of transseptal puncture in the interatrial vagal network. The procedure was completed despite the phenomenon.


INTRODUCTION
Access to the left atrium by transseptal puncture is a common practice in electrophysiology laboratories in the treatment by radiofrequency of cardiac arrhythmias. The ST segment elevation during transseptal puncture is mostly described as a sudden and transient alteration on the electrocardiogram, accompanied or not by symptoms with vagal action characteristics.The main pathophysiological mechanisms are vasospasm, due to the imbalance in autonomic innervation; coronary hypoperfusion secondary to reflex action; or air embolism. The incidence of this phenomenon is not well defined, and its description comes from case reports or retrospective records. Despite the diversity of clinical findings in the literature, there are two characteristics in common in the published series: the transience of the phenomenon and the normal angiographic findings.

CASE REPORT
A 67-year-old man with paroxysmal atrial fibrillation refractory to the use of antiarrhythmics, a candidate for radiofrequency ablation, received oral anticoagulation for three weeks before the procedure, maintaining the international normalized ratio (INR) between 2 and 3, and underwent transesophageal echocardiography, who demonstrated a left atrium with an indexed volume of 39 mL/m 2 , a left ventricular ejection fraction of 62%, without an intracavitary thrombus.
He underwent sinus rhythm catheter ablation. The confirmation of the proper position was defined by the operator's opposition and by not pointing to the left (posterior) or to the right (anterior). In addition, the needle was positioned posteriorly and inferiorly to the plane of the aorta. In the right side view, it was turned posteriorly between the spine and the catheter positioned in the coronary sinus (Fig. 1). In LAO, it was between the final two thirds between the curvature of the right atrium and the coronary sinus catheter (Fig. 2).
In this position, the septum was punctured, and, right after the transseptal puncture with a drop-off signal observed in fluoroscopy, it was recorded on the electrophysiology polygraph (EP-TRACER V 1.0®) elevation of the ST segment of 4 mm in DIII, in addition to junctional bradycardia with a heart rate of 35 bpm, blood pressure 93 × 37 mmHg and sweating. The junctional rhythm evolved to 2:1 conduction, followed by second-degree atrioventricular block (AVB) type Mobitz II (Fig. 3), with an infusion of atropine to reverse the sinus rhythm ( Fig. 4) and saline to maintain blood pressure levels.
The disappearance of ST elevation occurred after resolution of the clinical picture. The cinecoronariography performed immediately after the onset of the phenomenon proved to be normal. After the normalization of the ST segment with hemodynamic stability and the absence of coronary changes, the procedure was successfully concluded.    The Bezold-Jarisch reflex is an inhibitory reflex originating from sensory cardiac receptors with vagal afferent fibers that are influenced by chemical or mechanical stimuli. This stimulation increases parasympathetic activity and inhibits sympathetic activity, producing bradycardia, vasodilation and hypotension 5,8,9 . Right coronary dilation, hypotension and bradycardia would result in coronary hypoperfusion and regional and transient myocardial ischemia, which can generate electrocardiographic changes in the ST segment during transseptal puncture 2,5 , however, the hypothesis of the reflex similar to that of Bezold-Jarisch leading to ST change does not explain the fact that, after a few minutes of septal puncture, the clinical and electrocardiographic changes disappear, despite the continuous stimulation of the septum by the presence of the sheath used during the puncture.

Contrast AE
The hypothesis that the electrocardiographic and clinical picture observed during the puncture is secondary to vasospasm of the coronary artery is based on the presumption that manipulation of the intrasseptal plexuses and left atrial ganglia by the needle and transeptal sheath may cause imbalance in the autonomic innervation and lead to the hypervagotonic state 3,7,10 . The induced hypervagotonia would result in the release of acetylcholine, which would cause spasm in the coronary circulation 6 . The right coronary artery is more susceptible to cholinergic action and vasospasm 3 .
Another possible mechanism is the introduction of air emboli through the transeptal sheath, which would migrate to the coronary artery, resulting in acute gas embolism 3,6,11 , however, there are several explanations that make the procedure unlikely: • The coronary arteries have a predominant diastolic perfusion and origin perpendicular to the laminar flow at the root of the aorta; • Thrombi of the left atrium usually go to the cerebral circulation and less commonly to the coronary arteries 8 ; • Changes in the ST segment have a predominant location in the lower wall, but air embolism should occur with an identical predominance between the right and left coronary arteries;