Postcardiac injury syndrome complicating circumferential pulmonary vein radiofrequency ablation for atrial fibrillation

Postcardiac injury syndrome (PCIS) is characterized by inflammation of the pericardium, pleura and pulmonary parenchyma following a cardiac injury.1 It has been described in many patients after a variety of cardiac insults including infarction, surgery, trauma, implantation of a pacemaker, percutaneous coronary angioplasty and radiofrequency ablation of cardiac arrhythmias.2-8 We report a rare case of PCIS that occurred after circumferential pulmonary vein radiofrequency ablation for atrial fibrillation (AF). CASE REPORT A 58-year-old woman with drug-refractory paroxysmal AF underwent circumferential pulmonary vein ablation in April 2006. After trans-septal catheterization, intravenous heparin was administered to maintain an activated clotting time of 250 to 300 seconds. The left atrial geometry was reconstructed using CARTO system with a 3.5 mm tip ablation catheter (Navi-Star, ThermcoolTM, Biosense-Webster, USA). Continuously irrigated radiofre-quency ablation was performed along the pulmonary vein antrum to encircle the ipsilateral pulmonary veins with a target temperature of 43°C and maximum power of 35 W and an infusion rate of 17 ml/min. The procedural end-point was electrical isolation of all pulmonary veins under the direction of a decapolar catheter (Lasso, Biosense-Webster, USA). The total radiofrequency time was 42 minutes and the procedure time was 192 minutes. When the ablation procedure was over, the patient complained of mild chest discomfort. The fluoroscopy showed no cardiac tamponade and the blood pressure was 120/80 mmHg. After the patient was escorted to the ward, she underwent hypotension with the blood pressure 50/40 mmHg and was treated with dopamine infusion. After the ultrasonography showed trace pericardial effusion without any retroperitoneal bleeding, low molecular weight heparin (Clexane, AVENTIS Pharma Specialites, France) 1 mg/kg subcutaneous injection twice a day and 3 mg warfarin orally per day were administered. The patient's blood pressure remained normal after dopamine infusion was discontinued 12 hours later. Twenty-four hours after the procedure, the patient underwent dyspnea and dizziness. On physical examination, the blood pressure was 40/20 mmHg, respiratory rate was 30 breaths per minute, respiratory sound reduced over the bilateral lungs, the heart rate was 45 beats per minute, an S3 gallop and a pericardial friction rub were absent. When the patient breathed oxygen 4 L/min, the arterial blood gas values were as follows: pH 7.330, PCO2 41.6 mmHg, PO2 67 mmHg. Laboratory evaluation showed a white blood cell count of 12.5×109/L with 85.5 % neutrophils, troponin I 2.99 μg/L (reference range, 0-0.05 μg/L), D-dimer 268.0 μg/L (reference range, 0-300 μg/L), international normalized ratio 1.42. The electroca-rdiogram showed junctional escape beat without any sign of myocardial infarction. Magnetic resonance angiography showed moderate pericardial effusion, bilateral pleural effusion and the pulmonary artery was normal. Low molecular weight heparin and warfarin were discontinued. A pericardial drainage catheter was inserted and 150 ml of bloody fluid was drained. The patient became hemodynamically stable after pericardial drainage, however the dyspnea was not relieved and hypoxia remained. Chest X-ray showed that pulmonary marking was blurry and bilateral pleural effusions were present (Fig. 1). The pericardial drainage catheter was withdrawn twenty-four hours later without any drain. Three days postoperatively, thoracentesis was performed on both sides for diagnosis and management of the effusion, which revealed light-yellow exudative fluid with a total protein level of 33 g/L (serum 48 g/L), lactate dehydrogenase 725 IU/L (serum 132 IU/L), glucose 6.34 mmol/L, adenosine deaminase 8.80 IU/L (reference range, 4-24 IU/L), white blood cell count 6.4×105/L (mononuclear 40%, polymorphonuclear 60%). Bacteriologic studies were negative for organisms and acid-fast bacterium. No neoplastic cell was discovered in the pleural fluid. Four days postoperatively, low molecular weight heparin 0.75 mg/kg subcutaneous injection twice a day was administered. The shortness of breath and hypoxia were not relieved after the thoracentesis, however, the patient had a fever of 37.7°C and complained of pleuric pain. Rales and rubs could be heard over both sides of the lung. Computerized tomography showed bilateral inferior pulmonary atelectasis but there was no sign of pulmonary vein stenosis. Six days postoperatively, the patient underwent hypotension again with blood pressure 50/30 mmHg. Chest X-ray revealed massive left pleural fluid. Low molecular weight heparin was discontinued again. On thoracentesis 1500 milliliter bloody pleural fluid was drained, and laboratory examinations on the effusion showed that white blood cell count was 1.1×109/L, red blood cell count 2.1×1012/L, and hemoglobin 58.1 g/L. Additional laboratory evaluations showed that the results of antinuclear antibody, extractable nuclear antigen antibodies and antineutrophil cytoplasmic antibody were normal, purified protein derivative of tuberculin was negative, serum level of complement 3 was 0.4 g/L (reference range, 0.9-1.8 g/L), C-reactive protein was 9.5 mg/L (reference range, 0-8 mg/L). Considering PCIS, the patient was given infusion of methylprednisolone 40 mg for 3 days and together with prednisone 30 mg orally per day for 20 days. The patient recovered rapidly, without pericardial and right pleural fluid and with a little left pleural fluid (Fig. 2). After prednisone was tapered for six days the left pleural effusion increased. The patient was given prednisone again at a low maintenance dose for four months. The patient recovered with normal blood pressure and blood oxygen pressure when she was discharged. During the ten-month follow-up period, the patient was atrial fibrillation-free without taking any antiarrhythmic drug after the ablation.Fig. 1.: Posteroanterior chest X-ray showed that pulmonary marking was blurry and bilateral pleural effusions were present two days postoperatively.Fig. 2.: Posteroanterior chest X-ray showed that right pleural fluid was absorbed and a small amount of fluid in the left pleural cavity was left after intermittent thoracentesis and glucocorticoid treatment for 20 days.DISCUSSION Radiofrequency catheter ablation of AF has been in a dramatic increase in recent years.9,10 Post-pericardiotomy syndrome following extensive linear left atrial ablation was reported, however, PCIS occurring after the popular protocol of circumferential pulmonary vein ablation was not reported. For diagnosis of PCIS, no definitive diagnostic test is available, thus, presumptive diagnosis of PCIS based on both clinical manifestations and exclusion of other diagnoses that arise in this setting, namely pulmonary embolism, congestive heart failure, pneumonia, neoplasma, tuberculosis, autoimmune process, is currently required.1,7 The clinical manifestations of the syndrome were reported to be characterized by pleurisy, fever, dyspnea, rubs, rales, pleural effusion, leukocytosis, elevated erythrocyte sedimentation rate and pulmonary parenchymal infiltrate.1 Our findings match the observations in the other studies and lend support to our diagnosis of PCIS following catheter ablation and exclusion of those that can evoke plural effusion.1,7,11,12 The etiology of PCIS is not completely understood, but is believed to be an autoimmune reaction resulting from trauma to the heart.1 An alternative hypothesis has suggested the importance of the leakage of blood into the pericardial space.13 The higher incidence of Dressler's syndrome seen when oral anticoagulation was in common use following myocardial infarction is suggested as corroborative evidence for this theory.14 Intensive anticoagulation after catheter ablation of AF may attribute to the occurrence of PCIS in this case. Cardiac perforation is a major complication of catheter ablation of AF, which leads to bloody pericardial effusion and cardiac tamponade.10 The patient had bloody pericardial effusion and delayed tamponade, however, cardiac perforation was not likely the cause. If left atrial perforation had occurred during ablation, cardiac tamponade would have occurred soon after the procedure and larger amount of bloody effusion would have been seen. PCIS may be the cause of cardiac tamponade when effusion is accumulated rapidly, as it was described in Turitto's report.12 Pulmonary veins stenosis was a unique complication of catheter ablation of AF. Some clinical manifestations suggestive of pulmonary vein stenosis, such as pleural pain, plural effusion, cough and exertional shortness of breath were the same as those of PCIS.15 Pulmonary vein stenosis should be excluded before PCIS is diagnosed after catheter ablation of AF, however, it was not excluded objectively in Wood's study.8 Hypoxia, which was relieved more than two months later, was the major trouble of the patient. Pulmonary embolism is one of the most important clinical diagnosis that should be considered when a patient undergoes hypoxia and hypotension after the procedure. However, pulmonary embolism was excluded by pulmonary artery magnetic resonance angiography and D-dimer assay. The bilateral inferior pulmonary atelectasis may partly be attributable to hypoxia, which was not relieved when right pulmonary atelectasis recovered. Pulmonary parenchymal inflammation was a characteristic of PICS, which could lead to hypoxia. The hypoxia recovered after the three months' prednisone treatment.