Uncommon presentation of postcardiac injury syndrome induced by radiofrequency catheter ablation for atrial fibrillation: Only pulmonary parenchymal inflammation

Abstract

Postcardiac injury syndrome (PCIS) is characterized by the appearance of pericardial, pleural, or pulmonary parenchymal inflammation following a cardiac operation. The autoimmune disorder is characterized by eosinophilia, pleuritic chest pain, pleural, and pericardial effusion. It is a troublesome complication, which may prolong hospital stay and lead to severe and life-threatening conditions. Recently, its incidence appears to be declining, owing to modern immunomodulatory drug therapies. Here we report an uncommon case of PCIS, which occurred following a pulmonary vein isolation for atrial fibrillation. The patient suffered from pulmonary parenchymal inflammation but no pleuropericarditis after the operation. We describe with detailed clinical information, laboratory, and imaging tests, treatment processes, and a favorable prognosis in the content. This case illustrates that even after initially uneventful radiofrequency catheter ablation, careful, long-term follow-up is necessary to recognize the potential development of postcardiac injury syndrome.

<Learning objective: Although uncommon, physicians should keep postcardiac injury syndrome in mind following radiofrequency catheter ablation. The pattern does not always resemble the classical picture described by Dressler, but may take many forms and should be sought. Diagnosis is based on the clinical signs and symptoms and is mostly confirmed after excluding other diseases. Prognosis is usually benign, and therapeutic response to anti-inflammatory drugs and corticosteroids can aid in the diagnosis.>

Introduction

The postcardiac injury syndrome (PCIS) is characterized by inflammation of the pericardium, pleura, and pulmonary parenchyma following myocardial infarction, cardiac surgery, blunt chest trauma, percutaneous left ventricle puncture, implantation of a pacemaker, and catheter ablation [1]. The literature contains information regarding the pericardium, pleural, and pulmonary manifestations of PCIS [2]. We report a rare case in which radiofrequency ablation of atrial fibrillation led to the development of pulmonary parenchymal inflammation but no pleuropericarditis.

Case report

A 68-year-old woman with paroxysmal atrial fibrillation that was not controlled by antiarrhythmic drugs was referred for electrophysiology evaluation and treatment (Fig. 1, Fig. 2). The ablation procedure consisted of a computed tomography (CT)-, CARTO-, and Lasso-guided circumferential pulmonary vein isolation. A three-dimensional anatomy of the left atrium and the pulmonary veins were created by CARTO Sound and ICE (Intra Cardiac Echocardiogram) catheter with an incorporated navigation sensor (SoundStar™ catheter, Biosense Webster, Diamond Bar, CA, USA) (Fig. 3). After the anatomical three-dimensional model of the left atrium was prepared, ablation was performed to encircle the right and left pulmonary veins in pairs, and no atrial fibrillation was induced after ablation. The radiofrequency generator was set to a temperature limit of 43 °C and energy of 30 W, and the total procedure time was 3 h. The trauma experienced by the heart during the ablation resulted in an inflammation of the myocardium. On the second day post ablation, the patient had a body temperature of 37.6 °C. The blood leukocyte count was 10.9 × 10⁹/L (normal 4.0–10.0 × 10⁹/L). C-reactive protein (CRP) level was slightly elevated to 11 mg/L (normal 0.0–8.0 mg/L). These values normalized in 4 days and the patient was discharged. Three weeks later, the patient developed cough and mild chest discomfort. On the day of readmission, she complained of increased shortness of breath. Physical examination revealed scattered rales and strengthened respiratory voices but no heart murmur and S3 were heard on auscultation. Jugular venous pressure was not elevated. No peripheral edema was noted. The blood test showed that the leukocyte count was 6.6 × 10⁹/L, along with an increased percentage of eosinophilic granulocytes of 7.8% (normal value 0.5–5.0%). Erythrocyte sedimentation rate (ESR, 51 mm/h, normal value 0–20 mm/h) and CRP concentration (32.1 mg/L, normal value 0–8 mg/L) were both elevated. The value of D-dimer, B-type natriuretic peptide, troponin I, and cardiac enzyme remained within the normal range. Tests for antinuclear antibody (ANA), antineutrophil cytoplasmic antibody (ANCA), anti-MPO, and anti-PR3 antibody in serum were negative. With the patient breathing room air, arterial blood gas values were as follows: pH, 7.43; PaCO₂, 42.8 mmHg; PaO₂, 68.1 mmHg. Echocardiogram showed an enlarged left atrium and no pericardial effusion was detected. Posteroanterior chest X-ray film revealed patchy areas of ground-glass opacity (Fig. 1B). The CT of the chest showed the lung was scattered in high-density flake flocculent (Fig. 2B). No pericardial or pleural effusion was detected. CT angiography of pulmonary vein showed no obvious stenosis and anatomic structures were in normal places (Fig. 2C). Purified protein derivative (PPD) skin test was carried out to exclude tuberculosis. Antibiotics were used for diagnostic treatment. Nonetheless, no obvious improvement was observed under antibiotics therapy. On the basis of these laboratory and clinical findings, we diagnosed PCIS, which was related to the prior cardiac catheter ablation. She was subsequently treated with corticosteroid for half a month with great improvement of her symptoms and discharged (Fig. 1C). The eosinophilic granulocytes, CRP, and ESR levels normalized in 14 days. During a four-week follow-up period, the patient's symptoms resolved and the pulmonary parenchymal inflammation had disappeared by the CT scan (Fig. 2D).

Fig. 1.

Posteroanterior chest X-ray films before pulmonary vein isolation, during postcardiac injury syndrome, and after improvement. Enlarged cardiac silhouette (A, C) and ground-glass opacity (B) were present.

Fig. 2.

Representative images from the chest computed tomography (CT) and pulmonary vein angiography. (A) Preoperation: CT images showed that no lesions were found on bilateral lung fields. (B) Postoperation: CT images showed bilateral patchy areas of ground-glass opacity, which were distributed mainly in the inferior lobe of left lung close to heart. (C) Pulmonary vein angiography: No obvious pulmonary vein stenosis was detected and anatomic structures were in normal places. (D) Follow-up: CT scan performed 11 days later showed near-complete resolution of the lesions.

Fig. 3.

Electroanatomic mapping and ablation circle (red colored) using the CARTO Sound and ICE catheter. (A) Left lateral view. (B) Posteroanterior view. (C) Right lateral view.

Discussion

PCIS was first described by Dressler [3]. It is characterized by fever, pericardial effusion, and pleural effusion. We report the case of a 68-year-old woman who developed a syndrome of pulmonary parenchymal inflammation without pleuropericarditis accompanied by a pronounced increase in eosinophilic granulocytes, ESR, and CRP levels following initial radiofrequency ablation of atrial fibrillation.

The diagnosis of PCIS in a case following cardiac catheter intervention is difficult because patients no longer suffer from symptoms of the heart disease and general practitioners may undertake the follow-up role. Secondly, although PCIS has been clinically recognized for several decades, the lack of a confirmatory diagnostic test renders the diagnosis one of exclusion. Therefore, it would be important for clinicians to be aware of PCIS. In fact, patients with PCIS often receive unnecessary and inappropriate therapy for suspected congestive heart failure, pneumonia, or pulmonary emboli. Recently, diagnosis is based on clinical criteria – the occurrence within about a week after cardiac injury, and abnormal echocardiography and chest X-ray findings [4]. In our patient, the differential diagnosis including infectious, thromboembolic, malignant diseases, and PCIS also should be considered. After extensive work has been done for excluding the other causes of the acute inflammatory syndrome, a diagnosis of PCIS without exudative pericardial and pleural effusions as a rare complication of radiofrequency ablation was made. The possibility that the symptoms might be categorized to another new syndrome was also likely and it was hoped that this paper might prompt other physicians to report on similar patients.

A retrospective study of 35 patients with clearly defined PCIS has demonstrated that pleuropulmonary involvement is a common manifestation, since the chest X-ray film is abnormal in 94% of the patients [5]. Furthermore, investigators showed that the major clinical findings in the patients with PCIS were pulmonary parenchymal infiltrates (74%), pleurisy (91%), fever (66%), pericardial rub (63%), dyspnea (57%), roles (51%), pleural rub (46%), elevated ESR (96%), and leukocytosis (49%). Pleural effusion was present in 83%, and an enlarged cardiac silhouette in 49% [5]. In our case, the patient developed an uncommon presentation of pulmonary parenchymal inflammation without pleural and pericardiac effusion accompanied by a pronounced increase in eosinophilic granulocytes, ESR, and CRP levels. We first report that pulmonary manifestations of PCIS can be independent of pleuropericarditis.

Currently, PCIS is considered as an inflammatory process that occurs in the setting of injury to the pericardium, epicardium, or myocardium [6]. It may follow cardiac surgery, myocardial infarction, trauma, intracardiac ablation, percutaneous coronary intervention, or implantation of a pacemaker or cardioverter–defibrillator [1]. In fact, the pathophysiology of PCIS is still unclear. An autoimmune mechanism with the involvement of both cellular and humoral immune responses is postulated [7]. The most accepted hypothesis involves autoantibodies that target antigens exposed after damage to cardiac tissue [8]. Accordingly, available data suggest a beneficial profile for nonsteroidal anti-inflammatory drugs and corticosteroid administration [9]. In our case, short-term treatment with corticosteroids eventually resulted in complete clinical and imaging recovery of the pulmonary parenchymal inflammation and a normalization of inflammatory markers.

Conflict of interest

None declared.