To plan appropriate treatment, PAS should be suspected whenever there are specific clinical and radiological manifestations that can differentiate it from thromboembolic disease. In our experience of differentiating between PAS and thromboembolic disease, which we termed the wall eclipsing sign, was pathognomonic for PAS. To evaluate the diagnostic value of this sign for differentiating between different types of pulmonary artery lesions, we retrospectively reviewed all the PACTA examinations performed in patients with pulmonary thromboembolic disease and PAS Most patients presented with syncope, cough, dyspnea, and right heart Isochlorogenic-acid-C failure, and some also complained of hemoptysis and chest pain. These symptoms are all characteristic of significant pulmonary vascular obstruction, and they are similar to the symptoms of thromboembolic disease, leading to misdiagnosis. PAS is usually detected at an advanced stage, making curative resection nearly impossible. The prognosis of PAS is therefore extremely poor. The natural course of the disease is determined by local tumor growth as well as superimposed thrombosis and metastasized tumor embolus, leading to progressive obstruction of the pulmonary vessels,. The median survival of time of untreated patients after diagnosis is 1.5 months,. The main cause of death is decompensated heart failure. Because of the rarity of PAS, it is often initially misdiagnosed as acute or subacute massive pulmonary Sipeimine thromboembolism or CTEPH. Anderson et al. reported a series of six cases of PAS, all of which were initially investigated for chronic thromboembolism. Parish et al. reported nine cases of PAS over a 30-year period, of which seven were originally treated for pulmonary thromboembolism. Huo et al. reviewed the reports of seven cases of PAS, of which five were 
initially thought to be chronic thromboembolism. We report here 12 cases of PAS, all of which were misdiagnosed as CTEPH before they were referred for surgical intervention. These data show that PAS should be included in the differential diagnosis of pulmonary thromboembolism. Because of the similar clinical presentations, it is very difficult to differentiate between PAS and pulmonary thromboembolism, leading to inappropriate treatments such as thrombolysis and longterm anticoagulant therapy. Such misdiagnosis and inappropriate treatment result in delays of several months before surgical intervention, increase the risk of morbidity, and reduce the survival time. In spite of improvements in imaging modalities, the diagnosis of PAS is still based on pathological examination findings, and the majority of specimens are obtained at surgery or autopsy. Preoperative histological diagnosis is usually not possible, although a biopsy specimen can sometimes be obtained by CTguided transthoracic aspiration, pulmonary angioscopy with transvenous catheter suction biopsy, or transbronchial biopsy. If PAS is diagnosed early, cure may be possible with aggressive surgical intervention. However, the diagnosis is difficult and often delayed because the symptoms are insidious and nonspecific. These characteristics suggest that clinicians should increase their awareness of this disease to increase the likelihood of early diagnosis and treatment. As PAS is rare, it has not been studied in large randomized trials, and the optimal methods of diagnosis and treatment are still unknown. There is no specific biomarker to assist in screening for PAS or differentiating it from thromboemlic disease. In our series, the hsCRP level was elevated in all patients with PAS, the LDH level was elevated in eight patients, and the ESR was elevated in nine patients. In patients with thromboembolic disease the hs-CRP level, LDH level, and ESR were usually normal.