Left atrial intramural hematoma during radiofrequency catheter ablation for atrial fibrillation: The important role of intracardiac echocardiography

Key Teaching Points.

• •Intracardiac echocardiography is important for monitoring the formation of radiofrequency lesions during atrial fibrillation catheter ablation.
• •Prompt recognition of a left atrial intramural hematoma is crucial, as it is a rare but serious complication of atrial fibrillation catheter ablation.
• •Calcification of the mitral annulus and left atrial posterior wall might facilitate the rupture of the atrial endothelium adjacent to the calcification, initiating the process of left atrial wall dissection and the formation of the intramural hematoma.

Introduction

Radiofrequency catheter ablation (RFCA) has become a method of treating atrial fibrillation (AF) worldwide.1, 2, 3 Intracardiac echocardiography (ICE) is used during various steps of RFCA because it can show the real-time anatomy of the heart and related structures, namely during transseptal puncture; monitor catheter position and contact; titer radiofrequency delivery; promptly recognize complications, such as thrombus formation, pericardial effusion, and pulmonary veins (PVs) encroaching; and help esophageal temperature monitoring.4, 5, 6 It has been reported recently that ICE may increase safety and efficacy and reduce procedure time and need for radiography.^7,8

We report a rare case of left atrial intramural hematoma (IMH) detected by ICE during an ablation of AF.

Case report

A 70-year-old man with a history of long-standing, persistent AF and tachycardiomyopathy (left ventricular ejection fraction of 28%) underwent successful RFCA in 2018 with complete recovery of left ventricle function in the subsequent months. He remained free of arrhythmias until 2023, when AF recurred and he once again developed decreased left ventricular ejection fraction (23%) and a redo ablation was proposed.

The procedure was performed using an electroanatomic CARTO3 Mapping System and CARTOSOUND Module (Biosense Webster, Diamond Bar, CA) under uninterrupted anticoagulation with warfarin (international normalized ratio of 2.6 on the day of the procedure). Heparinization with 100 IU/kg was used to achieve activated clotting time >350 seconds before double transseptal puncture. A 20-mm circular catheter was used for mapping. The left PVs were reconnected (Figure 1) and the strategy adopted was re-isolation of the left PVs and posterior wall (PW) isolation. ICE views found a heavy calcification of the mitral isthmus at the inferior lateral region, extending to the left atrium (LA) PW, close to the floor of the left inferior PV ostium (Figure 2). Except for this calcification, no other unexpected imaging was noticed via ICE before the transseptal puncture.

Figure 1.

Electroanatomic CARTO3 Mapping System (Biosense Webster, Diamond Bar, CA) showing reconnection of the left pulmonary veins.

Figure 2.

Intracardiac echocardiography showing calcification of the mitral isthmus at the inferior lateral region, extending to the left atrial posterior wall, close to the left inferior pulmonary vein ostium floor. abla = ablation catheter; DESC AO = descending aorta; LA = left atrium; LASSO = circular catheter; LIPV = left inferior pulmonary vein.

Ablation was performed in a power-controlled mode at 40 W with a temperature cutoff of 43°C with a ThermoCool SmartTouch SF^TM irrigated, force-sensing ablation catheter (Biosense Webster) using a flow of 15 mL/min and contact between 8 g and 25 g and VISITAG SURPOINT® Module (Biosense Webster) target of 400–500. Esophageal temperature monitoring was performed as described previously. Briefly, a 4-mm tip deflectable ablation catheter was positioned into the esophagus guided by ICE, and an elevation of 2°C determined prompt termination of ablation until it returned to baseline.⁵

Left wide circumferential ablation was achieved, followed by the roofline and inferior line to isolate PW. However, a significant steam pop occurred instantly during the first third of the inferior line, close to the calcification (Figure 3 and Supplemental Video 1). No pericardial effusion was noted, and PW isolation was achieved in 10 minutes. At this time, ICE showed an image formation, heterogeneous, filled with layers, suggesting a dissection within the LA PW, extending between the inferior PVs (Figure 4 and Supplemental Video 2). Color Doppler detected a low-velocity blood flow inside the image formation, and a 2.4-mm entering orifice was visualized (Figure 5 and Supplemental Video 3).

Figure 3.

A significant steam pop (yellow arrow) occurred instantly during the first third of the inferior line, close to the calcification.

Figure 4.

Intracardiac echocardiography showed an image formation, heterogeneous, filled with layers, suggesting a dissection within the left atrium posterior wall, extending between the inferior pulmonary veins (yellow arrows).

Figure 5.

Color Doppler detected a low-velocity blood flow inside the image formation, and a 2.4-mm entering orifice was visualized (yellow arrow).

As an IMH was suspected, heparinization was immediately reverted after the line completion, and electroanatomic CARTO3 LA remapping showed completed PW isolation (Figure 6A and 6B). After heparin reversion, increased echogenicity and a reduction of low blood flow inside the IMH were noticed (Supplemental Video 4). No pericardial effusion was visualized at the end of the procedure or via transthoracic echocardiography 6 hours later. The patient remained hemodynamically stable and computed tomography scans were performed on the first day after the procedure, confirming the diagnosis of IMH. No blood flow was noted in the late contrast-enhanced computed tomography images (Figure 7A–7D). The patient was discharged, and computed tomography scans performed 3 months later showed total regression of the IMH (Figure 8A–8D).

Figure 8.

Computed tomography scans performed 3 months after the procedure showed total regression of the hematoma. Two-chamber (A) and 4-chamber (C) views precontrast. Two-chamber (B) and 4-chamber (D) views postcontrast images.

Figure 6.

Electroanatomic CARTO3 (Biosense Webster, Diamond Bar, CA) LA remapping showing (A, B) linear lesions with the application data from the steam pop and location and the hematoma under CARTOSOUND Module (Biosense) visualization and (C, D) remapping showed completed posterior wall and posterior wall isolation. Yellow arrow: intramural hematoma (on CARTOSOUND Module).

Figure 7.

Computed tomography scans performed on the first day after the procedure, confirming the diagnosis of intramural hematoma (yellow arrows). No blood flow was noted in the late contrast-enhanced computed tomography images. Two-chamber (A) and 4-chamber (C) views pre contrast when the hematoma has increased density. Two-chamber (B) and 4-chamber (D) views post-contrast images when the hematoma shows reduced density and its relationship with the left atrium.

Discussion

Left atrial IMH is defined as a false, blood-filled cavity or lumen from the mitral annular area to the LA free wall or interatrial septum. This cavity, which is a rare complication of left atrial procedure, may or may not have communications with the LA. In a review by Fukuhara and colleagues⁹ comprising 87 patients reported from 1979 to 2014, left atrial IMHs were associated with mitral valve cardiac surgery in approximately 56% of the cases, followed by spontaneous etiology associated with cardiac amyloidosis or infectious endocarditis (10.3%). RFCA was the third cause of left atrial IMH, accounting for 7 cases (8%). There have been reports of this complication related to other pathologies or interventional procedures, such as percutaneous coronary intervention, aortic valve surgery, myocardial infarction, coronary artery bypass grafting, cardiac mass excision, cardiac blunt trauma, pulmonary vein cannulation, and left ventricular aneurysm repair.⁹ Left atrial IMH has a different clinical presentation and, if not recognized, can be fatal.

The hypothesized mechanism is that IMH begins with an initial insult to the left atrial endocardium, and the pressurized blood creates the dissection within the LA wall. In mitral valve surgery, debridement of the posterior annulus or subvalvular apparatus, oversizing of the prosthesis, inappropriate suturing, or intense traction applied on the annulus might all be contributory as a cause of laceration of the annulus or bleeding from the AV groove. Inadequate reversal of anticoagulation may exacerbate the dissection. We could transport this mechanism to RFCA, when needles, wires, and catheter manipulation could create a LA wall lesion and an endocardial flap. Some studies described that severe calcification of the mitral annulus may be a predictor factor for the occurrence of left atrial IMH.^10,11 Calcification of the mitral annulus and LA PW was a finding in our patient, raising suspicion of being a facilitator for the rupture of the atrial endothelium adjacent to the calcification, initiating the process of LA wall dissection, and formation of the hematoma.

There are few reports of left atrial IMH associated with RFCA. In the case reported by Sah and colleagues,¹² IMH occurred after combined PV isolation, cavotricuspid isthmus ablation, and atypical flutter ablation within the coronary sinus. After the procedure, the patient was hypotensive and transthoracic echocardiography revealed a large pericardial effusion and cardiac tamponade, requiring pericardiocentesis. The left atrial IMH was noted in subsequent transthoracic echocardiography and resolved spontaneously in a few weeks. In the case reported by Kelly and colleagues,¹³ the IMH occurred 2 days after the patient was discharged from the hospital. The main symptoms were nonspecific, including fatigue, lethargy, weakness, and headaches. The authors speculated that damage to the LA wall occurred during a transseptal puncture performed under fluoroscopic guidance.

In the present report, the use of ICE allowed early identification of the initial formation of the left atrial IMH, detection of the low-velocity blood flow inside it, measurement of the entering gap orifice, and a prompt start to heparinization reversal. This complication can only be recognized by ICE, and the possible worsening of the scenario can be avoided. Reverse heparinization might be useful to avoid progression to tamponade, which is an important cause of death in AF ablation. During posterior wall isolation, additional lesions may be required to close any gaps in the roof or inferior line. However, if an undiagnosed IMH is present, particularly when ICE is not used, these additional lesions may exacerbate the IMH and increase associated risks.

Kashou and colleagues¹⁴ recently published a case of AF recurrence when ICE showed a focal dissection of the LA wall. This area was associated with localized voltage abnormalities that were serving as a driver for AF. The authors hypothesized this area to be the AF trigger likely resulting from a 1-year prior ablation, which caused an iatrogenic left atrial dissection, thereby creating a localized region of fibrillating tissue with the ability to trigger AF. As in our case, ICE was able to recognize left atrial IMH as a complication of RFCA.

Conclusion

Our case demonstrates a left atrial IMH after a steam pop in proximity to calcification of the mitral annulus and LA PW, in which the lesion formation and subsequent left atrial IMH were promptly diagnosed, highlighting the importance of ICE during AF ablation.

Disclosures

The authors have no conflicts of interest to disclose.