Deadly Heart-Esophagus Fistula Seen Directly on Angiography After AF Ablation

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The case described here illustrates how quickly an atrioesophageal fistula can convert from an apparently stable clinical picture into a life-threatening emergency. On arrival, the patient was in sinus rhythm with normal cardiac troponin, and her only complaint was recurrent palpitations. Within hours she had lost consciousness, developed fever and abnormal breathing, and shown inferior ST-segment elevation. This trajectory is consistent with what is known about the natural history of fistula formation: the lesion begins as thermal injury to the esophageal wall, progresses through ulceration, and only later establishes a patent communication between the esophageal lumen and the left atrium. Once that communication opens, swallowed air, oropharyngeal secretions, and commensal bacteria can be drawn or forced into the left atrium, particularly during increases in intraluminal esophageal pressure such as swallowing, vomiting, or endoscopic insufflation. From the left atrium, gas and infected material enter the systemic arterial circulation directly, because the left-sided chambers are normally connected to the systemic arteries without any filtering bed. This explains the otherwise puzzling combination of cerebral gas foci, gas in all four cardiac chambers, gas in the aorta and pulmonary arteries, and a right coronary artery occluded by visible gas with no distal flow.

The coronary angiographic findings deserve particular emphasis. Coronary air embolism is a recognized but uncommon event, usually described in the context of cardiac surgery, percutaneous procedures, or right-to-left shunts, and it is exceptionally rare as the presenting manifestation of an atrioesophageal fistula. In this patient, the operator could see gas as a mobile, lucid filling defect in the mid right coronary artery on the very first contrast injection, with TIMI grade 0 flow distally. Aspiration with the catheter removed a large volume of gas without any thrombus, and antegrade flow immediately returned to TIMI grade 3. That sequence is diagnostically powerful: the absence of thrombus or atherosclerotic occlusion, the instantaneous restoration of flow after aspiration, and the simultaneous presence of intravascular gas elsewhere on imaging together rule in gas embolism as the mechanism of the inferior ST elevation rather than plaque rupture or coronary spasm. It also demonstrates a practical point for interventional cardiologists, namely that aspiration can be both diagnostic and therapeutic in suspected coronary air embolism, restoring perfusion even when the underlying source of the gas cannot be corrected at the same sitting.

The electrocardiographic distribution of injury adds another layer of plausibility. The right coronary artery supplies the inferior wall in most individuals, and the ST-segment elevation in leads II, III, and aVF matched the angiographic location of the gas. Transient ST elevation from air embolism has been reported before, but it is easily mistaken for acute plaque rupture, which can lead to inappropriate delays while anticoagulation, loading with antiplatelet agents, or plans for percutaneous intervention are considered. In a patient weeks after left atrial ablation, the combination of abrupt neurologic depression, fever, and ST elevation should immediately raise suspicion for systemic air embolism from a fistula, and emergency angiography in this setting can be justified both to treat the ischemic event and to document its mechanism.

The microbiology in this case reinforces the pathophysiologic model. Blood cultures grew Streptococcus constellatus together with small quantities of other streptococci. S. constellatus belongs to the anginosus group, organisms that colonize the oropharynx, gastrointestinal tract, and genitourinary tract and are well known for abscess formation and bacteremia arising from mucosal disruptions. Isolation of such organisms from the bloodstream shortly after the abrupt clinical deterioration is difficult to explain by any mechanism other than translocation of esophageal or oral contents into the left atrium. It also helps distinguish fistula-related sepsis from the low-grade fevers that can accompany uncomplicated pericarditis or esophageal ulceration after ablation. In practice, when blood cultures from a post-ablation patient with neurologic findings grow oral or enteric streptococci, the pretest probability of an atrioesophageal fistula rises substantially, and empiric broad-spectrum antibiotic coverage covering streptococci and anaerobes should be started without waiting for definitive imaging.

The imaging strategy in this case reflects the delicate balance between diagnostic certainty and patient safety. Non-contrast computed tomography of the head and chest was performed rapidly and showed gas in the cortical sulci, along the superior sagittal sinus, in all cardiac chambers, and in the aorta, coronary arteries, pulmonary arteries, and cervical vessels. Retrospective review identified a suspected tract between the posterior left atrial wall and the adjacent esophagus. Contrast-enhanced computed tomography, which would have provided the strongest direct evidence of a fistulous connection, was not performed because the patient was hemodynamically unstable. Upper gastrointestinal endoscopy and transesophageal echocardiography were deliberately avoided, consistent with the widely held view that endoscopic insufflation can propel additional gas and esophageal contents through the fistula into the arterial circulation and worsen neurologic injury. This is a recurring dilemma in the literature: the tests that would confirm the diagnosis are the same tests that may accelerate the disease. Most experts therefore recommend that when the clinical syndrome and non-invasive imaging are sufficiently suggestive, treatment should proceed on the presumptive diagnosis, with surgical consultation obtained immediately, rather than waiting for endoscopic or contrast confirmation that may never be safely obtainable.

Timing is another consistent theme. The fistula in this patient declared itself approximately one month after ablation, which falls squarely within the typical window. Published series describe symptom onset most often in the second to fourth week after the procedure, with a mean interval of roughly two to three weeks, and the esophageal ulceration that precedes fistulization has been documented endoscopically within days of radiofrequency delivery. The delay occurs because the thermal injury must deepen through the esophageal mucosa and muscularis before the wall is breached. This latent period has two practical consequences. First, patients and clinicians should not consider the danger period over at hospital discharge; symptom education must extend for at least a month, and any new fever, chest pain, dysphagia, odynophagia, hematemesis, seizure, stroke, or altered mental status in that window warrants urgent evaluation. Second, the delayed onset means the causal connection to the ablation is easy to miss, particularly when the patient presents to a facility that did not perform the procedure, as happened here. Procedural details were unavailable to the treating team, which likely contributed to diagnostic uncertainty during the first hours.

Prevention remains the most effective intervention, because survival once the fistula is established is poor even with prompt surgery. Radiofrequency energy is not tissue selective, and the esophagus lies immediately posterior to the left atrium in many patients, sometimes separated by only a few millimeters of tissue. The distance between the esophagus and the posterior left atrial wall has been identified as an important risk factor, and esophageal ulcers have been found in a small but meaningful fraction of patients screened endoscopically after ablation. Strategies to reduce risk include limiting posterior wall radiofrequency power and duration, monitoring esophageal temperature during ablation, and using active esophageal cooling devices, which have been proposed to lower the risk of fistula formation. Mechanical esophageal displacement, luminal esophageal temperature probes, and the choice of energy source, including cryoablation or pulsed field ablation with its theoretical tissue selectivity, are areas of ongoing study. Post-procedural acid suppression and treatment of gastroesophageal reflux may also matter, because reflux is thought to promote the progression from superficial ulcer to deep fistula.

The hemodynamic and laboratory evolution in this patient tracks the expanding injury. Early point-of-care testing showed only modest myoglobin elevation with near-normal troponin, but by ten hours the high-sensitivity troponin had risen to more than 6,000 ng/L and ultimately exceeded 25,000 ng/L, reflecting extensive myocardial necrosis from coronary embolism and prolonged shock. Interleukin-6 above 5,000 pg/mL signaled a profound systemic inflammatory response driven by bacteremia and tissue injury. Recurrent bradycardia and hypotension preceded cardiac arrest, and death occurred approximately twenty-seven hours after admission despite antibiotics, anticoagulation, antiplatelet therapy, statin, and vasopressor support. Surgical repair was considered but deferred because refractory shock made perioperative survival unlikely. This outcome mirrors the published experience, in which mortality for atrioesophageal fistula remains high even in surgically treated patients, and delays of more than twenty-four hours between symptom onset and repair are associated with markedly worse survival. The lesson is that the window for salvage is measured in hours, and the decision to operate must often be made on clinical suspicion alone.

Finally, the authors’ caution about diagnostic certainty is worth underscoring. The case demonstrates direct angiographic visualization of intracoronary gas and successful catheter aspiration, and it shows multisite intravascular gas on non-contrast imaging together with bacteremia from organisms characteristic of the oropharyngeal and gastrointestinal flora. These findings together make the diagnosis of an atrioesophageal fistula complicated by systemic air embolism highly probable, but the fistulous tract itself was only a retrospective suspicion on non-contrast imaging, never confirmed by contrast-enhanced cross-sectional imaging, endoscopy, or surgery. Reporting the case with that limitation intact is scientifically honest and clinically useful, because it models the epistemic situation clinicians actually face: the evidence is often strong but incomplete, the confirmatory tests are hazardous, and the cost of waiting is death. For clinicians, the practical synthesis is straightforward. In any patient within several weeks of atrial fibrillation ablation who presents with fever, new neurologic deficits, altered consciousness, seizures, or acute ST-segment elevation, atrioesophageal fistula with systemic air embolism belongs at the top of the differential diagnosis. Immediate computed tomography of the head and chest, blood cultures, empiric antibiotics, avoidance of endoscopy and esophageal instrumentation, urgent cardiothoracic surgical consultation, and consideration of hyperbaric oxygen therapy where available constitute the appropriate initial response, and coronary angiography with aspiration can play a defined role when myocardial ischemia is the dominant manifestation.

Subject of Research: Cardiovascular Medicine

Article Title: Suspected atrioesophageal fistula complicated by coronary air embolism after catheter ablation for atrial fibrillation: direct angiographic visualization and catheter aspiration in a case report

Article References: Yang, C., Zeng, X., Wang, S., Wang, C., Lan, J., Wen, Y., & Zheng, Z. (2026). Suspected atrioesophageal fistula complicated by coronary air embolism after catheter ablation for atrial fibrillation: direct angiographic visualization and catheter aspiration in a case report. Frontiers in Cardiovascular Medicine, 13, Article 1985470. https://doi.org/10.3389/fcvm.2026.1985470

Image Credits: AI Generated

DOI: 10.3389/fcvm.2026.1985470

Keywords: atrial fibrillation, catheter ablation, atrioesophageal fistula, coronary air embolism, case report, radiofrequency ablation, Streptococcus constellatus, coronary angiography, left atrium, esophageal injury, cardiac arrest, Frontiers in Cardiovascular Medicine