Gerbode-Type Defect Induced by Catheter Ablation of the Atrioventricular Node
A 72-year-old man with a history of dilated cardiomyopathy, prosthetic aortic valve, biventricular intracardiac pacemaker, and permanent atrial fibrillation presented with uncontrolled ventricular response from atrial fibrillation despite pharmacological therapy. He underwent radiofrequency (RF) catheter ablation of the atrioventricular (AV) node to achieve optimal biventricular pacing.
AV node ablation was performed via the right femoral vein with a 4-mm tip ablation catheter (EPT, Boston-Scientific) positioned at the AV node just proximal to the His bundle region. RF energy was applied at this site for 60 seconds (55°C) resulting in complete heart block with an escape rhythm of 32 bpm. The next day he was discharged uneventfully. An echocardiogram at 5 months follow-up showed a left ventricular to right atrial (LV-RA) shunt across the membranous septum immediately above the tricuspid valve (online-only Data Supplement Movies I and II and Figure 1A and 1B). This LV-RA shunt (Gerbode-type defect) had a 76-mm Hg gradient across the defect (Figure 1C). Left ventricular ejection fraction was depressed (25% to 30%) and the right ventricle was mildly to moderately dilated. The mechanical aortic prosthetic valve functioned normally with a mean gradient of 17 mm Hg. Review of the patient’s preablation echocardiographic studies did not show any evidence of LV-RA shunt. He remained stable with New York Heart Association class I to II and >85% biventricular pacing. A repeat echocardiographic study 14 months after the ablation procedure did not show any progression in the size of iatrogenic Gerbode-type defect or shunting.
In a second case, a 68-year-old man with a history of severe chronic obstructive pulmonary disease and symptomatic permanent atrial fibrillation underwent RF catheter ablation of the AV node because of ineffective ventricular rate control by medical therapy. Three days after the procedure, the patient developed ventricular fibrillation and could not be resuscitated. Autopsy findings showed lesions at the RF ablation sites. Although he did not develop a frank defect, the ablation lesions extended to the left ventricular side of the membranous septum (Figure 2) at a site similar to the Gerbode-type defect in the first patient.
LV-RA communications (Gerbode-type defect) are rare intracardiac defects in the superior membranous septum.1 The septal leaflet of the tricuspid valve is 5 to 10 mm more apically located than the mitral valve attachment. This anatomic feature of the septal leaflet divides the membranous ventricular septum into 2 portions: a superior atrioventricular portion and an inferior interventricular portion. Thus, defects in the superior portion of the membranous septum can result in a direct LV-RA communication. Figure 3 illustrates the anatomic relationship of the membranous septum with the right atrium (A and B) and left ventricle (C).
LV-RA communications are mostly congenital, extremely rare (accounting for <1% of all congenital heart disease) and were first classified by Gerbode et al.1 Acquired LV-RA communications can arise from endocarditis, trauma, valve replacement, or myocardial infarction.1 However, there are no reports of this happening after RF ablation procedures. RF ablation can cause tissue necrosis, and an unfortunately placed ablation lesion in the thin superior membranous region, a site in close proximity with the AV node during AV nodal ablation, could result in a LV-RA communication. Autopsy data on patients with AV nodal ablation are rare; our second patient provides a rare opportunity to assess the damage after such procedures and suggests that damage to this superior membranous area (a precursor to Gerbode-type defect) is quite likely after AV nodal ablation, even after using conservative ablation parameters.
The clinical implications of Gerbode-type defects are variable and depend on the degree of shunting and biventricular volume overload. Large defects can cause biventricular volume overload, whereas smaller LV-RA defects can remain clinically silent for an extended period of time. Most symptomatic patients come to attention because of congestive heart failure. The prominent physical finding of LV-RA shunt is a loud and harsh pansystolic murmur often associated with a thrill along the left sternal border. Gerbode-type defects can also be prone to infective endocarditis.2 Our first patient has remained stable without significant volume overload and is being managed conservatively.
In conclusion, this is the first reported case of a Gerbode-type defect after an AV node ablation. Although rare (the only known case in 118 AV node ablations performed for ventricular rate control at our institution since 1998), it should be considered, especially in cases of a new murmur or signs of worsening heart failure after AV node ablation procedure.