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Patient presentation A 33-year-old man was referred to our hospital suffering fever with shivers, dyspnea, dry cough, and weakness. Initial work up Symptoms appeared three weeks until hospitalization. Laboratory results showed leukocytosis and high levels of inflammatory markers. Haematological diseases were excluded, a chest x-ray showed infiltration in the lower lobe of the right lung, antibiotics were prescribed. Diagnosis and management When clinical and laboratory results showed no signs of improvement, chest computed tomography (CT) scan was performed and bilateral pulmonary artery thromboembolism with right lung infarct-pneumonia was diagnosed (Figure 1, 2). Treatment was supplemented with intravenous anticoagulants. In the course of treatment patient’s status worsened, respiratory failure progressed, so CT scan was performed again and showed massive pulmonary artery thromboembolism without the effect of treatment. Transthoracic 2D echocardiography showed dilated right heart chambers, relative severe tricuspid valve regurgitation, increased systolic pulmonary artery pressure (Video 1, figure 3), pulmonary artery valve masses in the stem which caused obstruction with maximum gradient about 50 mmHg(Video 2, figure 4). For a detailed workup, magnetic resonance imaging (MRI) was done, that revealed tumorous masses from pulmonary artery valve to the pulmonary trunk and right pulmonary branch (Figure 5, 6, 7). The patient underwent pulmoangiography and biopsy was taken out of the masses that suspected sarcoma. The multidisciplinary team came to a conclusion to perform surgery considering worsening patient’s status. The patient underwent pulmonary artery prosthesis implantation and right pneumonectomy (Figure 8). Masses from pulmonary artery valve were examined by pathologists, surgical specimen results showed high grade poorly differentiated pulmonary artery intimal sarcoma (Figure 9, 10). Follow up Early postoperative period was complicated with cardiogenic shock and respiratory failure. Despite extracorporeal membrane oxygenation (ECMO) and high doses of vasopressors patient did not survive the 2nd postoperative day. Conclusions Pulmonary artery sarcoma (PAS) frequently can be misdiagnosed as thromboembolism. Multimodality imaging should be considered pulmonary artery filling defects persist despite proper anticoagulation therapy for early diagnosis and better survival. Abstract P1450 Figure 3.

Objective: Activation of matrix metalloproteinases and the renin/angiotensin signaling pathways is under investigation with regard to their potential pathogenesis in dilatative pathology of the aorta. The purpose of this study was to explore matrix metalloproteinase-3 5A/6A and angiotensin-converting enzyme I/D polymorphisms as predisposing factors to dilatative pathology of the aorta. Methods:We studied 107 patients who underwent aortic reconstruction surgery due to dilatative pathology of ascending thoracic aorta and a random sample of the population (n = 773), all from Lithuania. The insertion/deletion (� 1171 5A/6A) polymorphism in the promoter region of matrix metalloproteinase-3 studied by real-time polymerase-chain-reaction amplification and the D and I alleles were identified on the basis of standard polymerase-chain-reaction amplification of the respective fragments from intron 16 of the angiotensin-converting enzyme gene. Results: The frequency of the angiotensinconverting enzyme D allele was significantly higher in dilatative pathology of ascending thoracic aorta patients than in the reference group subjects (0.55 vs 0.48, respectively). The latter group had a significantly higher frequency of the angiotensin-converting enzyme I/I genotype than in dilatative pathology of ascending thoracic aorta patients (27.4% vs 16.5%, respectively). In the reference group, the frequency of combined angiotensin-converting enzyme I/I and matrix metalloproteinase-3 6A/6A genotypes was 7.5%, while in the dilatative pathology of ascendingthoracicaortapatientgroup,therewasnoonecarryingthatcombinedgenotype(p = 0.001).Conclusions:Thepresentstudyshowinga role of angiotensin-converting enzyme and matrix metalloproteinase-3 in the development of dilatative pathology of ascending thoracic aorta permits us to entertain a possible protective mechanism for the combined effects of the angiotensin-converting enzyme I/I and the matrix metalloproteinase-3 6A/6A genotypes. # 2010 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved.