Tracheopericardial fistula in lung cancer masquerading as acute myocardial infarction: a case report

Abstract

Tracheopericardial fistula is an extremely rare clinical condition caused by lung disease penetrating the tracheal wall and extending to the pericardial cavity, forming a fistula between the airway and the pericardial cavity. Since the pericardial cavity communicates with the respiratory tract, gases, airway secretions and pathogens can enter the cavity, leading to pneumopericardium, effusion and abscess. In severe cases, it can result in cardiac tamponade and cardiogenic shock. Only a few cases of TPF have been reported in the literature. In this report, a 72-year-old man with recurrent lung cancer presented with fever, chest tightness and chest pain. Electrocardiogram showed ST-segment elevation in multiple leads, resembling an acute myocardial infarction. Emergency coronary angiography did not reveal significant stenosis. Further examination with chest computed tomography and bronchoscopy revealed pericardial effusion and a tracheal fistula, leading to the final diagnosis of TPF as a complication of lung cancer. This case aims to enhance understanding and recognition of this clinical entity to reduce misdiagnosis.

Introduction

Tracheopericardial fistula (TPF) is an uncommon and serious complication that can occur in patients with lung cancer [1]. It is characterised by abnormal communication between the trachea and the pericardial cavity, which can lead to significant clinical consequences. Due to its rarity and nonspecific presentation, TPF is often misdiagnosed [2, 3]. Here, we present a case of TPF in a patient with recurrent lung cancer, initially mistaken for acute myocardial infarction (AMI).

Case report

A 72-year-old male patient presented to our hospital in June 2024 with fever, chest tightness and chest pain for 4 h. He had a fever with a maximum temperature of 38 °C, accompanied by chest tightness and dull precordial chest pain, which was not relieved by rest or nitroglycerin. The patient was admitted to our hospital for further evaluation and treatment.

The patient had a medical history of lung cancer. In November 2016, he underwent a right upper lobectomy, which identified adenocarcinoma (T2aN1M0, stage IIB), and subsequently received six cycles of postoperative chemotherapy. Genetic testing on the postoperative pathological specimen did not reveal any gene mutations. Based on this result, targeted therapy was not pursued when recurrence was detected.

In October 2018, a follow-up chest computed tomography (CT) showed enlargement of the mediastinal 4R group lymph node with an elevated carcinoembryonic antigen level. Recurrence of the postoperative lung cancer was considered, and the patient was given three cycles of cisplatin and pemetrexed chemotherapy. The choice of cisplatin combined with pemetrexed was based on the absence of actionable gene mutations and aimed to provide a platinum-based regimen in line with standard care for recurrent adenocarcinoma. However, despite the initial stabilisation of the disease, the patient declined further chemotherapy due to personal reasons, opting instead for self-administration of traditional Chinese medicine.

The patient remained under follow-up until 2024. In February 2024, he experienced haemoptysis, and flexible bronchoscopy revealed tumour involvement in the trachea, causing airway stenosis (about 70%). Cryotherapy and argon plasma coagulation therapies via rigid bronchoscopy were performed twice. In March 2024, the patient underwent radiotherapy. However, by May 2024, he experienced further disease progression with metastatic lesions compressing the main airway, leading to a critical narrowing that was not amenable to surgical intervention. Given the extensive tumour burden and failure of previous treatments, a combination regimen of pemetrexed, carboplatin and bevacizumab monoclonal antibody was initiated. The decision to include bevacizumab was based on its anti-angiogenic properties, which are particularly effective in preventing tumour growth and metastasis in advanced non-squamous non-small cell lung cancer. By 2024, bevacizumab had become available at our hospital, making it a viable option that was previously inaccessible during the initial recurrence in 2018. This regimen was administered for three cycles, and the patient responded favourably.

Physical examination showed a temperature of 39.7 °C, pulse rate of 136 beats/min, respiratory rate of 23 breaths/min and blood pressure of 98/67 mmHg (1 mmHg = 0.133 kPa). His lungs were slightly coarse on auscultation without moist rales. His heart rate was 136 beats per minute, with a normal rhythm, but heart sounds were distant and dull, with no pathological murmurs. All other physical examination results were normal.

Laboratory tests showed a white blood cell count of 10.05 × 10⁹/L, a neutrophil percentage of 93.2%, haemoglobin of 110 g/L, platelet count of 187 × 10⁹/L, C-reactive protein of 130 mg/L and D-dimer level of 7.83 mg/L. Cardiac enzyme markers (creatine kinase, creatine kinase isoenzyme, myoglobin, lactate dehydrogenase, alanine transaminase and troponin I) and B-type natriuretic peptide levels were all normal. An electrocardiogram (ECG) demonstrated sinus tachycardia, abnormal Q waves, ST-segment elevation (> 0.1 mV in leads II, III and aVF) and ST-segment changes in leads I and aVL (Fig. 1).

Fig. 1.

The electrocardiogram shows sinus tachycardia with a heart rate of beats/minute, and ST segment elevation of 0.1mv ∼ 0.5 mv in leads II, III, and aVF (black arrows), along with abnormal Q waves and ST segment changes in leads I and aVL

Considering the typical ST-segment manifestations on ECG and his chest pain symptoms, AMI was highly suspected. An immediate loading dose of aspirin (300 mg), clopidogrel (300 mg) and continuous intravenous nitroglycerin for 24 h were administered. Four hours after admission, a repeat ECG still showed ST-segment elevation without dynamic changes compared with the previous ECG, and cardiac enzyme markers remained normal. The patient’s chest pain also did not improve. He was then transferred to the cardiac catheterisation laboratory for coronary angiography 6 h after admission, which revealed a normal left main coronary artery, 50% stenosis in the mid-segment of the left anterior descending artery, diffuse plaque infiltration without significant stenosis in the circumflex branch of the left coronary artery and 50% stenosis in the mid-segment of the right coronary artery. A lucent zone was noted between the visceral and parietal layers of the pericardium during coronary angiography, suggestive of pneumopericardium. Acute myocardial infarction was excluded, and pneumopericardium was considered a possible cause. A chest X-ray then showed a gas shadow around the heart (Fig. 2). To explore the cause of the pneumopericardium, a chest-enhanced CT the next day revealed an irregular diverticulum at the carina, pneumopericardium, patchy density shadows under the bilateral pleura and no signs of pulmonary embolism (Fig. 3).

Fig. 2.

Chest X-ray showed a gas shadow (red arrow) around the heart

Fig. 3.

A: Chest CT scan shows an irregular cystic band protrusion (red arrow) in the tracheal lumen near the carina, adjacent to the aorta, with gas density shadows seen. Increased patchy density shadows are seen under the bilateral pleura. B: An arcuate gas shadow (red arrow) is seen within the pericardial cavity

The diagnosis of pneumopericardium was confirmed, and urgent pericardiocentesis with catheter drainage was performed, resulting in a continuous release of gas into the drainage bag. Considering the CT imaging findings, tracheal rupture was suspected. To determine the cause of the pneumopericardium, the patient underwent bronchoscopy on the 3rd day, which revealed a fistula in the lower right wall of the trachea, communicating externally with the tracheal wall, with no abnormalities in the rest of the lung segments (Fig. 4). A diagnosis of TPF was confirmed. The patient received continuous drainage of the pneumopericardium and anti-infection treatment and was scheduled for a planned closure of the fistula. On the 5th day, the patient suddenly experienced massive haemoptysis (approximately 1500 ml), followed by loss of consciousness and cardiac and respiratory arrest. Unfortunately, the patient could not be saved despite resuscitation efforts.

Fig. 4.

Flexible bronchoscopy examination shows a fistula (red arrow) in the lower right wall of the trachea that communicates with the outside of the tracheal wall. The fistula presents with leukoplakia-like changes

Discussion

Lung cancer remains the most prevalent and deadly malignancy in China, often presenting at a late stage with the potential to metastasise to the trachea. Tracheopericardial fistula, characterised by a channel forming between the trachea and pericardium, primarily arises from thoracic surgery [4], trauma [5, 6], infection [7], lung cancer [8], spontaneous mediastinal emphysema [9] and mechanical ventilation [10]. Lung cancer complicated by TPF is highly infrequent, with scant documentation in the literature. In June 2024, the patient presented with fever and angina-like symptoms due to recurrent lung cancer. The marked ST-segment elevation on ECG led to a strong suspicion of AMI. To save time for coronary artery revascularisation, coronary angiography was prioritised, but the differential diagnosis was overlooked. Finally, the diagnosis of postoperative lung cancer recurrence complicated by TPF was confirmed by chest CT and bronchoscopy.

Tracheopericardial fistula is a rare complication of lung cancer that is predominantly documented through case reports. Pneumopericardium discerned on ECG can easily be mistaken for AMI, leading to potential misdiagnosis. Pneumopericardium and AMI share similar clinical features, both showing ST-segment elevation on ECG. However, normal cardiac injury biomarkers and the absence of the dynamic evolution typical of myocardial infarction serve as key differentiators. Chen W et al. [11] reported a case where lung carcinoma invading the right main bronchus resulted in TPF. The initial diagnosis of AMI with cardiogenic shock, based on multilead ST-segment elevation on ECG, was revised after chest radiography revealed pneumopericardium and coronary angiography ruled out abnormalities. Similarly, Chen Q et al. [12] described a case of a patient with lingual carcinoma metastasised to the lungs, presenting with acute chest pain and dyspnoea. The initial misdiagnosis of AMI, based on ST-segment elevation detected in leads I, aVL and V1–V5 on the ECG, was corrected after pneumopericardium was confirmed by emergency coronary angiography and chest CT.

The formation of TPF in this case was primarily attributed to structural damage of the tracheal wall induced by tumour invasion and interventional treatment. We initially planned to perform stent implantation to seal the fistula. However, during the preparation for this procedure, the patient experienced sudden massive haemoptysis, which ultimately led to death. Had the sealing procedure been successfully implemented, it is possible that this fatal outcome could have been averted. The use of bevacizumab, a vascular endothelial growth factor inhibitor, may have potentially exacerbated the risk of fistula formation due to its association with impaired wound healing and the development of fistulas. However, its role remains unclear and likely minimal in this context. The consequent formation of a tracheal fistula traversing the diaphragm culminated in a connection between the respiratory tract and the pericardial cavity. The severity of pneumopericardium correlates with the rate of gas formation and the volume within the pericardial cavity. Most patients manifest no symptoms and closely monitor gas absorption, provided that the pneumopericardium does not induce tension pericardial tamponade. Conversely, large gas volumes alongside unstable haemodynamics predict imminent occurrences of cardiac tamponade, obstructive shock and potentially sudden death – conditions mandating emergent pericardiocentesis. Zhang T et al. [13] reported improvement following pericardial puncture and drainage in a case of tension pneumopericardium caused by thin-walled cavitary lung cancer. In the current case, persistent chest pain triggered anxiety that pneumopericardium-induced cardiac compression could escalate pericardial cavity pressure, reduce cardiac output and consequently increase the risk of shock. Thus, emergent pneumopericardium drainage was implemented, temporarily stabilising the patient’s condition. Regrettably, sudden haemoptysis induced by pulmonary vascular invasion from lung cancer led to the patient’s death before our planned fistula repair.

In conclusion, TPF as a complication of lung cancer is seldom encountered in clinical practice. When lung cancer patients present with symptoms of chest tightness and pain, coupled with ST-segment elevation on ECG but unsupported by coronary angiographic findings pointing to myocardial infarction, TPF should also be considered. Chest imaging and bronchoscopy should underpin confirmation, with treatment hinging on the impact on haemodynamics and severity of symptoms.

Abbreviations

CT

Computer tomography

ECG

Electrocardiography

AMI

Acute myocardial infarction

TPF

Tracheopericardial fistula

Author contributions

Cao SY conceived of the study, and An R participated in its design and data analysis and statistics and Wang CH helped to draft the manuscript. All authors read and approved the final manuscript.

Funding

Shandong Province Medical Health Science and Technology Project.

Data availability

All data generated or analysed during this study are included in this article. Further enquiries can be directed to the corresponding author.

Declarations

Ethics approval and consent to participate

This study was conducted in accordance with the Declaration of Helsinki and approved by the ethics committee of Shengli Oilfield Central Hospital. Written informed consent was obtained from the participants.

Consent for publication

Written informed consent was obtained from the patient for publication of this case report.

Competing interests

The authors declare no competing interests.

Clinical trial number

Not applicable.