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Despite the use of prasugrel, a significant number of patients undergoing PCI in the setting of acute coronary syndromes do not achieve optimal PR inhibition. Such patients have a higher risk for MACE after PCI.

D-Dimers are elevated in patients with AAD and provide valuable diagnostic and prognostic information. In patients with acute chest pain and elevated D-Dimer, a diagnosis of AAD should also be considered. D-Dimer might be a useful complementary tool to the current diagnostic work-up of patients with suspected AAD.

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Background-Factors leading to subacute stent thrombosis after percutaneous coronary intervention (PCI) have not been well established. We assessed the pre-and post-PCI intravascular ultrasound (IVUS) characteristics of subacute stent thrombosis. Methods and Results-We analyzed 7484 consecutive patients without acute myocardial infarction who were treated with PCI and stenting and underwent IVUS imaging during the intervention. Twenty-seven (0.4%) had angiographically documented subacute closure Ͻ1 week after PCI (median time to subacute closure, 24 hours). Subacute closure lesions were compared with a control group (selected to be 3 times the abrupt closer group) matched by procedure date (within 6 months), age, gender, stable or unstable angina, lesion location, and additional treatment (balloon angioplasty or atherectomy). Postintervention IVUS did not identify a cause in 22% and did identify at least 1 cause for abrupt closure in 78% of patients (versus 33% in matched lesions, Pϭ0.0002). In 48% of the patients, there were multiple causes in 48% (versus 3% in matched lesions, PϽ0.0001). Causes included dissection (17%), thrombus (4%), and tissue protrusion within the stent struts leading to lumen compromise lumen (4%). A total of 83% of patients with Ͼ1 of these abnormal morphologies also had reduced lumen dimensions post-PCI (final lumen Ͻ80% reference lumen). Preprocedural lesion characteristics were not different from matched lesions. Conclusions-Subacute

We aimed to assess the incidence of underexpansion and the relationship between delivery pressure and expansion with sirolimus-eluting stents. Adequate stent expansion contributes to early and late improved outcomes. In 51 patients (53 lesions) with native coronary artery narrowing, balloon-expandable sirolimus-eluting stents (Cypher) were serially expanded with gradual balloon inflations [14 atm, 20 atm, and in case of minimal stent cross-sectional area (CSA)/reference lumen CSA< 50% at 20 atm, postdilatation with 0.5 mm larger balloon]. Intravascular ultrasound (IVUS) imaging was performed before intervention and after each gradual balloon inflation. Stent expansion (minimal stent CSA/reference lumen CSA) was measured. Stent expansion was 72% +/- 16% after 14 atm balloon inflation, 90% +/- 18% after 20 atm balloon inflation (P < 0.001 vs. 14 atm), and 90% +/- 18% at the end of the procedure (including optional postdilatations with 0.5 mm larger balloon; P = NS vs. 20 atm). Stent expansion addressed by MUSIC criteria (all struts apposed, no tissue protrusion, and final lumen CSA > 80% of the reference or > 90% if minimal lumen CSA was < 9 mm2) was adequate in 15% of the cases after 14 atm balloon inflation, in 60% after 20 atm balloon inflation (P < 0.001 vs. 14 atm), and in 60% at the end of the procedure (P = NS vs. 20 atm). Sirolimus-eluting stent underexpansion is common when deployed at conventional pressures. Increasing balloon delivery pressure or assessing stent expansion with IVUS seems warranted in order to ensure adequate sirolimus-eluting stent deployment.

No abstract

Background— Late total occlusion after vascular brachytherapy (VBT) continues to be a serious complication. Delayed reendothelialization was suggested as a pivotal cause, but the time course for complete healing is unknown. Methods and Results— Seventy-two rabbit iliac arteries underwent stent implantation and were treated with γ-radiation using 192 Ir. The prescribed doses were 0 Gy (controls, n=24 arteries), 15 Gy (n=24), or 30 Gy (n=24) at 2 mm. Animals were killed at 1 month (n=24), 3 months (n=24), or 6 months (n=24) and were analyzed for histomorphometry or scanning electron microscopy. Intimal area was reduced after VBT at 3 months with 15 and 30 Gy (0.66±0.07 and 0.66±0.04 mm 2 , respectively) compared with controls (1.01±0.11 mm 2 , P <0.05) and at 6 months with 30 Gy (0.75±0.09 versus 1.28±0.26 mm 2 in controls, P <0.01). Intimal area was similar at 6 months between 15 Gy and controls. At 1 month, 92±4% of the control stented segment was covered with endothelial cells, whereas only 37±4% and 37±8% was covered in the 15- and 30-Gy arteries, respectively. Similarly, at 3 and 6 months, there was a difference in the extent of reendothelialized areas (at 3 months, 95±2%, 32±12%, and 29±13%; and at 6 months, 98±2%, 40±8%, and 35±12% in control, 15-Gy, and 30-Gy arteries, respectively). Excess platelets and leukocytes were seen in irradiated arteries without complete coverage of endothelium. Conclusions— Reendothelialization after VBT is not completed at 6 months after VBT. Special care with prolonged antiplatelet therapy should be considered beyond that time point.