Objectives-We sought to investigate whether patients with in-stent thrombosis (IST) display altered plasma fibrin clot properties. Key Words: angioplasty Ⅲ fibrin Ⅲ fibrinolysis Ⅲ stents Ⅲ thrombosis T here are several factors associated with increased risk of in-stent thrombosis (IST) in epicardial arteries, including the procedure itself (small final lumen dimension due to stent malapposition and/or underexpansion, stent length, placement of multiple stents, dissections), patient (low left ventricular ejection fraction [LVEF], diabetes mellitus, advanced age, stenting in acute coronary syndrome) and lesion characteristics (bifurcation, in-stent restenosis), stent design and premature cessation of antiplatelet drugs. 1-3 Autopsy studies provided evidence that lack of complete endothelialization and persistent fibrin thrombi are a primary substrate underlying IST. 4,5 Thrombin-mediated fibrinogen conversion to fibrin and fibrin monomer cross-linking result in the formation of a fibrin clot. Its structure and function are modulated by several genetic and environmental factors, predominantly those affecting levels and function of fibrinogen. 6 Effective fibrinolysis is essential for removal of intravascular clots that might otherwise be manifest as thrombosis or enhance the development of atherosclerotic plaques. A more tightly packed and less porous fibrin structure reduces transport of proteins involved in fibrinolysis and anticoagulant reactions mediated by antithrombin inside the clot. These alterations might prolong the presence of fibrin in the lumen. 6 Dense clot fiber networks with reduced susceptibility to lysis have been demonstrated in survivors of myocardial infarction (MI), 7 in the acute phase of MI, 8 and in patients with a history of the no-reflow phenomenon, defined as the absence of a complete myocardial perfusion despite successful opening of the infarct-related artery. 9 Several lines of evidence 10,11 indicate that incompletely endothelialized coronary stents predispose to fibrin deposition and persistent thrombi on the stent struts. However, it is not known whether the IST is associated with unfavorably altered fibrin clot properties that might contribute to this complication regardless of platelet reactivity. Therefore, we sought to evaluate plasma fibrin clot structure/function in patients with definite IST. Methods and Results-We

The objectives of this study were to determine the relationship between carotid-femoral (cfPWV) and aortic pulse wave velocity (aPWV) and to compare their modulators and association with coronary artery disease (CAD). We studied 107 consecutive patients (68 men) with a mean age of 60.49 ± 8.31 years who had stable

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