Anterior Mitral Line Ablation-Induced Complete Heart Block: A Cautionary Case Study

Introduction

Cardiac arrhythmias are associated with substantial morbidity and mortality, with atrial flutter being one of the most common cardiac rhythm disorders [1,2]. The incidence of atrial flutter ranges from 5 to 500 per 100 000, depending on patient age, leading to more than 200 000 cases of new-onset atrial flutter per year in the United States alone [3]. Due to cardiovascular disease complications, it is imperative to treat atrial flutter. Usual treatment can involve medications for rate and rhythm control, but cardiac ablation is sometimes necessary. Although cardiac ablation is successful most of the time, complications can arise, such as complete heart block, as was demonstrated in this case.

Case Report

A 73-year-old woman with a medical history of paroxysmal atrial fibrillation, recurrent atypical atrial flutter status after ablation, moderate mitral regurgitation, hypertension, hypothyroidism, and coarctation of the aorta repair in childhood presented to the hospital for an ablation of persistent atypical atrial flutter (Figure 1). Electro-anatomic mapping demonstrated counterclockwise mitral annular flutter. An anterior ablation line was initially created from the right superior pulmonary vein to the mitral valve annulus. As the line was extended to the anterior mitral valve annulus at the 9 o’clock position, complete heart block occurred, and ablation was immediately terminated. Complete recovery of atrioventricular (AV) conduction occurred within 1 min. The catheter tip was noted to be within 1.8 cm from the His bundle, as denoted by the yellow tag on the CARTO map (Figure 2). A second mitral line was created more anteriorly, at the 11 o’clock position on the mitral valve annulus, and extended to the left atrial roof line, with the termination of atrial flutter, using a power of 35 W, 50°C, and the creation of a bi-directional mitral isthmus block guided by signal suppression. Following ablation, the patient remained in sinus rhythm with PR prolongation and no AV block. The atrial His bundle interval was measured at 106 ms (reference range, 50–125 ms), and the Wenckebach interval was 350 ms (reference range, 500–350 ms). The AV node function was assessed after ablation, and there was no dual AV node physiology identified, and no echo beats were recorded. Following ablation, the conduction time across the trans-isthmus line was 213 ms.

Due to successful ablation, the patient was sent home that evening, only to develop dizziness and lightheadedness that was aggravated with standing and associated with bradycardia, which she noted on her pulse oximeter. She subsequently presented to the Emergency Department after having worsening symptoms and a pre-syncopal episode. On presentation, her vital signs were notable for a blood pressure of 156/53 mmHg and a heart rate of 43 beats/min. She reported light-headedness and generalized weakness, but on physical examination, she was lying comfortably in her bed, without signs of discomfort or head lacerations. Potential differential diagnoses were considered, and the initial evaluation showed normal levels of electrolytes and thyroid stimulating hormone, and a chest X-ray without acute cardiopulmonary processes. In contrast, she had elevated high sensitivity troponin levels and NT-proBNP, along with other laboratory test results (Table 1). Once the patient was evaluated, cardiac telemetry was noted to show a complete heart block with a heart rate in the low 40s, and ECG showed complete heart block, QRS escape, and heart rate of 43 beats/min (Figure 3). The elevated cardiac enzymes were concerning because they are indicative of the amount of myocardial injury after ablation is performed, but it is not specific to ischemia. Despite the abnormalities in her laboratory test results, she was hemodynamically stable and did not receive transvenous pacemaker placement. Furthermore, the patient did not have ischemic findings on the ECG, was chest pain-free, and it was thought she did not have acute coronary syndrome, for which a catheterization was not performed. The following day, she underwent placement of a dual-chamber permanent pacemaker.

Discussion

Initial evaluation of an individual with suspected atrial flutter includes an ECG, which generally shows an atrial rate of 240–300 beats/min, absent typical P waves, negative sawtooth pattern of atrial activity in inferior leads, and discordance in flutter wave polarity between inferior leads and lead V1 [3]. This classical finding on ECG is associated with typical atrial flutter, a cavotricuspid isthmus-dependent macroreentrant tachycardia that circuits around the tricuspid annulus [4]. Typical circuits can be further divided into clockwise and counterclockwise dysrhythmia. Typical counterclockwise circuits present on ECG as negative flutter waves in the inferior leads and positive flutter waves in the precordial leads that transition to inverted waves by V6 [5,6]. Atypical atrial flutter is a non-cavotricuspid isthmus-dependent macroreentrant circuit that can originate in either the atrium, usually presenting around atrial scars in patients with underlying structural heart disease, congenital malformations, or prior surgical procedures or cardiac ablations [5,6].

Treatment of atrial flutter involves maintaining sinus rhythm with medical management, cardioversion, and catheter ablation, along with anticoagulation. Cavotricuspid isthmus-dependent atrial flutter can be treated with radiofrequency or cryoablation continuously along the full thickness of the cavotricuspid isthmus, to ensure a bidirectional conduction block [5,7]. Successful ablation ends posteriorly toward the tricuspid annulus, laterally by the 6 o’clock position on the left anterior oblique view, or anteriorly toward the coronary sinus ostium [5]. Furthermore, the risk of AV node damage or free right atrial wall rupture is low in cavotricuspid isthmus-dependent atrial flutter ablation [6]. However, when catheter ablations are conducted toward the septum, there is an increased risk of right coronary artery damage or complete heart block from AV nodal damage [5]. Specifically, a peri-mitral flutter can occur either proximally or distally and in a clockwise or counterclockwise direction. The peri-mitral circuit is ablated between the left inferior pulmonary vein and mitral annulus or across the anterior wall located anterior to the atrial appendage and to the left of the right superior pulmonary vein. This approach is known as the anterior line approach and is associated with a reduced risk of cardiac tamponade but an increased risk of left atrial anterior wall flutter. Ablation along the anterior wall can lead to left atrial appendage activation after the QRS complex, resulting in delayed atrial contribution during systole [5].

Nevertheless, despite ablation being successful with low rates of complications, a complete heart block can be seen with ablations near the normal conduction system [5]. In the present case, we report the unfortunate sequela of complete heart block or AV dissociation after ablation of persistent atypical atrial flutter. The patient’s AV nodal conduction was likely impacted during the anterior line ablation at the 9 o’clock position between the right superior pulmonary vein and the mitral valve annulus. However, a bidirectional mitral isthmus conduction block was achieved with a more anterior approach at the 11 o’clock position. Therefore, we recommend providers consider performing the anterior line peri-mitral ablation in a more anterior location to minimize the risk of AV node dysfunction and complete heart block.

Conclusions

We present a case of a patient who developed a complete heart block likely due to the anatomical location of the AV node, requiring pacemaker implantation following anterior mitral line ablation for treatment of recurrent atypical mitral annular flutter. Anterior mitral line ablation should be performed in a more anterior location away from the septum to minimize the risk of damage to the AV node.