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Importance: The role of vascular closure devices (VCD) for the achievement of hemostasis in patients undergoing transfemoral coronary angiography remains controversial., Objective: To compare outcomes with the use of 2 hemostasis strategies after diagnostic coronary angiography performed via transfemoral access-a VCD-based strategy with 2 types of devices, an intravascular device and an extravascular device, vs standard manual compression. The primary hypothesis to be tested was that femoral hemostasis achieved through VCD is noninferior to manual compression in terms of vascular access-site complications. A secondary objective was the comparison of the 2 types of VCD., Design, Setting, and Participants: Randomized, large-scale, multicenter, open-label clinical trial. We enrolled 4524 patients undergoing coronary angiography with a 6 French sheath via the common femoral artery from April 2011 through May 2014 in 4 centers in Germany. Last 30-day follow-up was performed in July 2014., Interventions: After angiography of the access site, patients were randomized to hemostasis with an intravascular VCD, extravascular VCD, or manual compression in a 1:1:1 ratio., Main Outcomes and Measures: Primary end point: the composite of access site-related vascular complications at 30 days after randomization with a 2% noninferiority margin. Secondary end points: time to hemostasis, repeat manual compression, and VCD failure. An α-level of .025 was chosen for primary and secondary comparisons., Results: Of the 4524 enrolled patients, 3015 were randomly assigned to a VCD group (1509 received intravascular VCD and 1506 received extravascular VCD) and 1509 patients were randomly assigned to the manual compression group. Before hospital discharge, duplex sonography of the access site was performed in 4231 (94%) patients. The primary end point was observed in 208 patients (6.9%) assigned to receive a VCD and 119 patients (7.9%) assigned to manual compression (difference, -1.0% [1-sided 97.5% CI, 0.7%]; P for noninferiority<.001). Time to hemostasis was significantly shorter in patients with VCD (1 minute [interquartile range {IQR}, 0.5-2.0]), vs manual compression (10 minutes [IQR, 10-15]; P < .001). Time to hemostasis was significantly shorter among patients with intravascular VCD (0.5 minute [IQR, 0.2-1.0]), vs extravascular VCD (2.0 minutes [IQR, 1.0-2.0]; P <.001) and closure device failure was also significantly lower among those with intravascular vs extravascular VCD (80 patients [5.3%], vs 184 patients [12.2%]; P < .001)., Conclusions and Relevance: In patients undergoing transfemoral coronary angiography, VCDs were noninferior to manual compression in terms of vascular access-site complications and reduced time to hemostasis., Trial Registration: clinicaltrials.gov Identifier: NCT01389375.

Aims: Vascular closure devices (VCD) have been introduced into clinical practice with the aim of increasing the procedural efficiency and clinical safety of coronary angiography. However, clinical studies comparing VCD and manual compression have yielded mixed results, and large randomised clinical trials comparing the two strategies are missing. Moreover, comparative efficacy studies between different VCD in routine clinical use are lacking., Methods and Results: The Instrumental Sealing of ARterial puncture site - CLOSURE device versus manual compression (ISAR-CLOSURE) trial is a prospective, randomised clinical trial designed to compare the outcomes associated with the use of VCD or manual compression to achieve femoral haemostasis. The test hypothesis is that femoral haemostasis after coronary angiography achieved using VCD is not inferior to manual compression in terms of access-site-related vascular complications. Patients undergoing coronary angiography via the common femoral artery will be randomised in a 1:1:1 fashion to receive FemoSeal VCD, EXOSEAL VCD or manual compression. The primary endpoint is the incidence of the composite of arterial access-related complications (haematoma ≥5 cm, pseudoaneurysm, arteriovenous fistula, access-site-related bleeding, acute ipsilateral leg ischaemia, the need for vascular surgical/interventional treatment or documented local infection) at 30 days after randomisation. According to power calculations based on non-inferiority hypothesis testing, enrolment of 4,500 patients is planned. The trial is registered at www.clinicaltrials.gov (study identifier: NCT01389375)., Conclusions: The safety of VCD as compared to manual compression in patients undergoing transfemoral coronary angiography remains an issue of clinical equipoise. The aim of the ISAR-CLOSURE trial is to assess whether femoral haemostasis achieved through the use of VCD is non-inferior to manual compression in terms of access-site-related vascular complications.

Background: Because of the risk of associated complications, femoral pseudoaneurysm (PSA) formation implies further treatment. Ultrasound-guided thrombin injection (UGTI) is becoming the accepted gold standard, but manual compression (MC) represents an established treatment option including PSAs not feasible for UGTI. This study aims to assess our experience in PSA treatment using MC or UGTI according to a potential algorithm based on morphological properties in a large patient cohort., Methods and Results: Between January 2007 and January 2011, a total of 432 PSAs were diagnosed in 29091 consecutive patients (1.49%) undergoing femoral artery catheterization. When compressible, small PSAs (<20 mm), PSAs without clearly definable neck, PSAs directly adjacent to vessels, and PSAs with concomitant arteriovenous fistula were referred to MC (n=145, 34%). All other PSAs were treated by UGTI (n=287, 66%). Follow-up duplex scans were performed within 12 to 14 hours after manual compression therapy and within 4 to 6 hours after UGTI or by the next morning and were available for 428 patients (99.1%). The overall success rate of our institutional therapeutic approach was 97.2%, which was achieved by 178 MC- and 357 UGTI-procedures, respectively. Procedural complications occurred in 5 cases (1.4%) after UGTI and in 3 cases (1.7%) after MC, respectively. The treatment algorithm was not successful in 12 patients, whereas 2 PSAs (0.5%) were successfully excluded by implantation of a covered stent-graft, and 10 patients necessitated surgical intervention (2.3%), which was associated with a high complication rate (30%)., Conclusions: The presented treatment algorithm facilitates effective and safe PSA elimination.

Background: Endovascular therapy of carotid artery disease has emerged as a potential alternative to endarterectomy and its clinical practise dramatically increased in many parts of the world. This study aims to determine the safety and mid-term outcome of carotid artery stenting (CAS) within a 15-year carotid program at a single-centre institution., Patients and Methods: We retrospectively analysed all CAS-procedures performed at our institution between 1995 and 2009., Results: During the observation period, a total of 497 CAS procedures were attempted in 460 patients with stenoses of the internal carotid artery of which 187 (37.6 %) were symptomatic and 310 (62.4 %) were asymptomatic. CAS was successful in 479 (96.4 %) cases and success rate significantly increased throughout the study (p < 0.001). The periprocedural complication rate for death, stroke, and transient ischemic attack (TIA) was 0.4 %, 1.2 %, and 2.6 %, respectively, and the cumulative event rate did not differ between symptomatic and asymptomatic patients (4.8 % vs. 3.9 %; p = 0.62). Age was the only significant predictor for the occurrence of any periprocedural adverse event (OR 2.08 [1.22 - 3.54]; p = 0.007). During a median follow-up of 24 [1; 141] months, the rate of stroke, TIA, and in-stent restenosis was 1.0 %, 2.2 %, and 2.7 %, respectively., Conclusions: Data from this large observation in everyday clinical patients demonstrate that endovascular therapy in carotid artery disease can be performed safely and with mid-term outcomes comparable to carotid endarterectomy.

Background: Plasminogen activator inhibitor-1 (PAI-1) has been proposed as a candidate risk factor for restenosis after coronary artery stenting. Transcription, level, and activity of PAI-1 are influenced by the 4G/5G polymorphism in the promoter region of PAI-1 gene. The polymorphism may therefore affect wound-healing processes in injured blood vessels and influence restenosis., Methods: In 1850 consecutive patients, angiographic measures of restenosis and the clinical outcome at 30 days and 1 year after stent implantation were evaluated. Angiographic restenosis was defined as > or =50% diameter stenosis determined at follow-up angiography, performed 6 months after stenting. The 4G/5G genotypes were determined with TaqMan technique., Results: Among the patients, the frequency of the 4G allele was 0.55. Follow-up angiography was done in 84% of the patients. We observed restenosis in 32.5% of 4G/4G carriers, 32.2% of 4G/5G carriers, and 35.7% of 5G/5G carriers (P =.52). The occurrence of a major adverse event (death, myocardial infarction, or target vessel revascularization due to restenosis-induced ischemia) was 5.6% in 4G/4G carriers, 5.3% in 4G/5G carriers, and 4.6% in 5G/5G carriers at 30 days (P =.80), and 24.7% in 4G/4G carriers, 23.0% in 4G/5G carriers, and 26.2% in 5G/5G carriers at 1 year (P =.45)., Conclusion: The 4G/5G polymorphism of the PAI-1 gene is not associated with an increased risk of thrombotic and restenotic events after coronary artery stenting.

Objectives: We tested the hypothesis that patients with the DD genotype of the angiotensin I-converting enzyme (ACE) gene who are treated with ACE inhibitors are at a higher risk of restenosis after coronary stent placement than patients who do not receive ACE inhibitors., Background: Two recent studies with a limited series of patients carrying the DD genotype suggested an unfavorable impact of the use of ACE inhibitors on the restenotic process after implantation of stents in coronary arteries. Because these findings may question the use of ACE inhibitors after coronary stenting, we examined this important issue in a large series of patients., Methods: We determined the ACE gene I/D genotype of 2,222 consecutive patients with symptomatic coronary artery disease who underwent stent implantation. The patients with the DD genotype (n = 612) constituted the study population. The primary end point was in-stent restenosis, which was assessed as angiographic restenosis (> or =50% diameter stenosis at six-month follow-up) and clinical restenosis (need for target vessel revascularization due to symptoms or signs of ischemia in the presence of angiographic restenosis over one year after the intervention)., Results: Of the 612 patients with the DD genotype, 403 (65.8%) were treated with ACE inhibitors and 209 (34.2%) did not receive ACE inhibitors. The angiographic and clinical restenosis rates were not significantly different between the group treated with ACE inhibitors and the group not receiving ACE inhibitors (p = 0.55). Continuous measures of restenosis, minimal lumen diameter, diameter stenosis, late lumen loss, and loss index were also similar in both groups (p > or = 0.55). In addition, one-year survival free of myocardial infarction was not significantly different between the two groups (p = 0.27)., Conclusions: In contrast to previous reports, our study provides evidence that patients carrying the DD genotype are not exposed to an increased risk of restenosis after stent placement when treated with ACE inhibitors.