Syndecan‐1 belongs to the syndecan family of cell surface transmembrane heparan‐sulfate proteoglycans, which participate in cell proliferation, cell migration and cell‐matrix interactions. Decreased expression of syndecan‐1 has been observed in some gastrointestinal malignancies, and it is thought that high levels of syndecan‐1 correlate with the maintenance of epithelial morphology and inhibition of invasiveness. In our study, we characterized the expression of syndecan‐1 in normal, chronic pancreatitis and primary and metastatic human pancreatic cancer tissues, in cultured pancreatic cancer cell lines and in esophageal, gastric, colon, and liver cancers. Pancreatic cancer cell lines expressed syndecan‐1 mRNA and protein at variable levels. In addition, these cells also released syndecan‐1 into the culture medium. Pancreatic cancer tissues markedly over‐expressed syndecan‐1 mRNA in comparison with both chronic pancreatitis (2.4‐fold increase, p < 0.01) and normal pancreatic samples (10.6‐fold increase, p < 0.01). There was no difference in syndecan‐1 mRNA expression between early and advanced tumors. By in situ hybridization and immunohistochemistry, syndecan‐1 expression was evident at relatively low levels in the ductal cells and less frequently in acinar cells of the normal pancreas. In chronic pancreatitis, syndecan‐1 was present at low to moderate levels in areas with atrophic acinar cells and ductular complexes. In contrast, in pancreatic cancer tissues, syndecan‐1 was present at moderate to high levels in the majority of the cancer cells within the tumor mass and also in metastatic lesions of pancreatic tumors. Syndecan‐1 mRNA levels in other gastrointestinal malignancies (esophageal, gastric, colon and liver cancers) were not significantly different from the levels observed in the corresponding normal samples. Together, our findings suggest that syndecan‐1 expression by pancreatic cancer cells may be of importance in the pathobiology of this disorder and that its role in pancreatic cancer seems to be different from that in other gastrointestinal malignancies. Int. J. Cancer 88:12–20, 2000. © 2000 Wiley‐Liss, Inc.

Background: Pulmonary veins isolation (PVI) is a standard treatment for recurrent atrial fibrillation (AF). Uninterrupted anticoagulation for minimum 3 weeks before the ablation and exclusion of left atrial (LA) thrombus with transesophageal echography (TEE) immediately before or during the procedure minimize peri-procedural risk. We aimed to demonstrate the utility of cardiac tomography (CT) and cardiac magnetic resonance (CMR) to rule out LA thrombus prior to PVI.Methods: Patients undergoing PVI for recurrent AF were retrospectively evaluated. Only patients that started anticoagulation at least 3 weeks prior to the CT/CMR and subsequently uninterrupted until the ablation procedure were selected. An intracardiac echo (ICE) catheter was used in all patients to evaluate LA thrombus. The results of CT/CMR were compared to ICE imaging.Results: We included 272 consecutive patients averaging 54.5 years (71% male; 30% persistent AF). Average CHA2DS2VASC Score was 0.9 and mean LA diameter was 43 mm, 111 patients on Acenocumarol and 161 on direct oral anticoagulants. Anticoagulation was started 227±392 days before the CT/CMR, and 291±416 days before the ablation procedure. CT/CMR diagnosed intracardiac thrombus in 2 cases, both in the LA appendage. A new CT/CMR revealed resolution of thrombus after 6 additional months of uninterrupted anticoagulation. No macroscopic thrombus was observed in any patients with ICE (negative predictive value of 100%; p<0.01).Conclusions: CT and MRI are excellent surrogates to TEE and ICE to rule out intracardiac thrombus in patients adequately anticoagulated prior AF ablation. This is true even for delayed procedures as long as anticoagulation is uninterrupted.