INTRODUCTION: Pulmonary vein thrombosis (PVT) is an uncommon complication of lung transplantation, radiofrequency catheter ablation (RFCA) for atrial fibrillation, and lobectomy. Below is described a case of post-lobectomy PVT leading to myocardial infarction.
CASE PRESENTATION: A 60-year-old man with Buerger's disease underwent a left upper lobe lung resection for non-small-cell lung cancer. Five days post-operatively, he developed dyspnea and a non–ST-elevation myocardial infarction (NSTEMI), for which he was transferred to our hospital. He was treated with aspirin, unfractionated heparin and eptifibatide, and subsequently underwent cardiac catheterization. The coronary arteries had mild diffuse disease and a 90% stenosis of the distal right coronary artery (RCA) with distal flow via collaterals. He underwent stenting of the RCA. Post-procedure, he remained dyspneic. A chest CT showed a post-lobectomy left hydropneumothorax and a thrombus in the left upper pulmonary vein extending into the left atrium. The hydropneumothorax was drained with a pigtail catheter, and because of the extension of the thrombus and the patient's hypercoagulable state, oral anticoagulation was started. The patient was discharged and three months post-operatively, he is doing well.
DISCUSSIONS: This case highlights the importance of considering PVT in patients who have had surgeries involving the pulmonary veins. The incidence of PVT after RFCA and lobectomy are not well known. However, after lung transplantation, approximately 15% of patients have PVT within 48 hours, and among those, mortality is 38%. PVT occurs when the clotting cascade is activated at sites of surgically-induced endothelial damage. Symptoms of PVT after lung transplantation and RFCA are caused by obstruction of pulmonary venous outflow, with resultant pulmonary edema, infarction, and/or infection. In lung transplant patients, these symptoms can mimic those of acute rejection and reperfusion injury. Post-lobectomy PVT leads to a different set of clinical manifestations. Thrombosis of the pulmonary vein in this setting does not affect any lung parenchyma, and symptoms, therefore, are generally related to peripheral embolization: stroke, femoral artery occlusion, and splenic infarcts have been reported. Per “Braunwald's Heart Disease, 7th Edition,” emboli from PVT are a rare cause of myocardial infarction. We hypothesize our patient's NSTEMI may have been due to embolism of his PVT. He had chronic stable atherosclerotic disease in his RCA without angiographic evidence of plaque disruption or thrombus. An embolism from the PVT may have lodged in the RCA, causing NSTEMI, with subsequent dissolution of the embolism with anticoagulation and antiplatelet therapy prior to catheterization. Both transesophageal echocardiogram (TEE) and CT scan can diagnose PVT. TEE may be advantageous in critically ill patients since the procedure is performed at the bedside. CT scans, however are less invasive, and require less highly-trained personnel. No studies have been conducted regarding the management of PVT, but anticoagulation, antibiotics, and, in cases of large PVT, thombectomy have been used. TEE can quantify the degree of obstruction and direct therapy appropriately.
CONCLUSION: PVT represents a potentially fatal complication in patients who have undergone lung surgery or RFCA. A high index of suspicion and diagnostic confirmation with TEE or chest CT are necessary. Though uncommon at present, PVT diagnoses will increase with the rising number of lung transplants, lobectomies and RFCA being performed, in the setting of widespread use of TEE and chest CT for other diagnostic purposes. It is essential for chest physicians to become familiar with this underdiagnosed entity.
DISCLOSURE: Julio Miranda, None.