Percutaneous infragenicular stent implantation after failed or unsuccessful balloon angioplasty is associated with favorable clinical results in patients with CLI. Notwithstanding limitations of primary studies, sirolimus-eluting stents appear superior to bare metal and paclitaxel-eluting stents in terms of angiographic and/or clinical outcomes.

Percutaneous intervention in acute myocardial infarction has been associated with a high incidence of "no reflow," ranging from 11% to 30%, with an increased risk of complications. The role of intracoronary adenosine for the prevention of this phenomenon has not been evaluated fully. We studied the procedural outcomes of 79 patients who underwent percutaneous intervention in the context of acute myocardial infarction. Twenty-eight patients received no intracoronary adenosine, and 51 received intracoronary adenosine boluses (24-48 microg before and after each balloon inflation). Eight patients who were not given adenosine experienced no reflow (28.6%) and higher rates of in-hospital death, while only three of 51 patients (5.9%; P = 0.014) in the adenosine group experienced no reflow. No untoward complications were noted during adenosine infusion. Intracoronary adenosine bolus administration during percutaneous intervention in the context of acute myocardial infarction is easy and safe and may significantly lessen the incidence of no reflow, which may improve the outcome of this procedure.

We have previously reported that exposure of endothelial cells to cyclic strain elicited a rapid but transient generation of inositol 1,4,5-trisphosphate (IP3), which reached a peak 10 s after the initiation of cyclic deformation. To address the effect of cyclic strain on intracellular Ca2+ concentration ([Ca2+]i) and its temporal relationship to IP3 generation, confluent bovine aortic endothelial cells were grown on flexible membranes, loaded with aequorin and the membranes placed in a custom-designed flow-through chamber. The chamber was housed inside a photomultiplier tube, and vacuum was utilized to deform the membranes. Our results indicate that the initiation of 10% average strain induced a rapid increase in [Ca2+]i which contained two distinct components: a large initial peak 12 s after the initiation of stretch which closely followed the IP3 peak, and a subsequent lower but sustained phase. Pretreatment with 5 microM GdCl3 for 10 min or nominally Ca2+-free medium (CFM) for 3 min reduced the magnitude of the initial rise and abolished the sustained phase. Repetitive 10% average strain at a frequency of 60 cycles/min also elicited a single IP3 peak at 10 s. However, there was also a large initial [Ca2+]i peak followed by multiple smaller transient [Ca2+]i elevations. Preincubation with 5 microM GdCl3 or CFM diminished the initial [Ca2+]i transient and markedly inhibited the late-phase component. Preincubation with 25 microM 2,5-di-(t-butyl)-1,4-benzohydroquinone (BHQ) attenuated the initial [Ca2+]i transient. Cyclic-strain-mediated IP3 formation in confluent endothelial cells at 10 s, however, was not modified by pretreatment with 25 microM BHQ, 500 microM NiCl2, 10 nM charybdotoxin, 5 microM GdCl3 or CFM. We conclude that in endothelial cells exposed to cyclic strain, Ca2+ enters the cytosol from intracellular and extracellular pools but IP3 formation is not dependent on Ca2+ entry via the plasma membrane.

The most consistent procedural predictor of vascular access site complications thus far has been the intensity and duration of anticoagulant therapy during and after percutaneous coronary interventions (PCI). Several devices have been developed to aid in the closure of the femoral arteriotomy. This report describes the clinical outcome of unsuccessful deployment of femoral closure devices in a cohort of 285 consecutive patients who underwent PCI and were treated with platelet glycoprotein (GP) IIb/IIIa inhibitors. Manual femoral artery compression was used in 123 patients, Perclose in 123 patients, and AngioSeal in 39 patients. Successful homeostasis was achieved in 98.4% of patients who received manual compression, in 91.9% of the Perclose-sealed arteriotomy, and in 84.6% of patients who received the AngioSeal closure device (P = 0.004). The incidence of vascular complications after successful deployment was 9%. Patients not achieving hemostasis with closure device or 1 degrees manual compression developed complications in the majority of cases (> 80%; P < 0.05). By multivariate analysis (with adjustment for baseline differences), the use of AngioSeal closure device was found to be an independent risk factors leading to primary deployment failure and all access site complications (OR 2.97; 95% CI 1.5-6.0; P = 0.006). In summary, failed hemostasis by artery closure devices in patients undergoing PCI who are treated with GP IIb/IIIa inhibitors is associated with significant vascular complications. AngioSeal may be associated with a higher failure rate, while manual compression and Perclose seem to be more effective with a lower complication rate.

The purpose of this study was to assess the effect of cyclic strain on phosphatidylinositol turnover in cultured bovine aortic endothelial cells (EC). Confluent EC grown on flexible membrane bottoms were deformed by vacuum to 24% maximum strain and subjected to two cyclic strain regimens. In the first set of experiments, EC were subjected to deformation at a frequency of 60 cycles/min for either 0 (stationary control), 1, 5, 10, 25, 50, or 100 cycles of stretch. In the second set of experiments, EC were preconditioned by deforming the membranes at 60 cycles/min for 24 h. The cycling frequency was then acutely increased to 100 cycles/min for 0, 1, 5, 10, 25, or 100 cycles. Inositol phosphate and diacylglycerol concentrations were determined at the end of each regimen. The results demonstrate that either the initiation of pulsatile stretch or an acute change in cyclic stretch frequency stimulates a sequential and transient generation of inositol trisphosphate, its metabolites inositol biphosphate and monophosphate, and diacylglycerol. Thus EC may respond to the initiation and change in cyclic stretch frequency by a signal transduction pathway involving inositol lipid metabolism.