Using the PercuSurge GuardWire® Distal Protection Device
The presence of no-reflow substantially increases the risk of major adverse clinical events (MACE) in percutaneous coronary artery interventions (PCI). Distal protection devices may eliminate both debris and soluble factors that can lead to no-reflow. This study was designed to evaluate the soluble factors released and eliminated by the PercuSurge GuardWireduring SVG intervention. Methods. Twenty-eight consecutive patients underwent PCI on 34 lesions in 31 SVGs using the PercuSurge GuardWire. Blood was taken prior to PCI for baseline measurement of: (1) Vasoconstrictive factors: endothelin (ET) and serotonin (5-HT); (2) thrombotic factors: tissue factor (TF), plasminogen activator inhibitor (PAI-1), thrombin/antithrombin III complex (TAT), and prothrombin fragment F1+2 (F1+2); and (3) inflammatory factors: soluble CD40 ligand (sCD40L) and soluble E-selectin. After stenting and before deflating the distal protection balloon, 2 aspiration runs were performed with the PercuSurge Export Catheter and sent for analysis. Results. Clinical follow-up was conducted at an average of 6 ± 3 months. SVG PCI resulted in a substantial increase in levels of vasoconstrictive factors, including ET (3 x increase; p < 0.001) and 5-HT (9.7 x increase; p = 0.031); thrombotic factors, including TF (4.5 x increase; p = 0.005), TAT (2.4 x increase; p < 0.001), and F1+2 (2.4 x increase; p < 0.001). Pro-inflammatory factors were also released during the procedure. Levels of sCD40L and soluble E-selectin increased 123% (p = 0.003) and 25% (p < 0.001), respectively. Conclusions. SVG PCI Results in an immediate increase in vasoactive factors, including vasoconstrictive, thrombotic and inflammatory factors. The PercuSurge GuardWire effectively removes these soluble factors, which may account for reduction of no-reflow and other complications during SVG interventions.
The no-reflow phenomenon is defined as a severe reduction in antegrade coronary flow in the absence of epicardial vessel obstruction. The presence of no-reflow substantially increases the risk of major adverse clinical events (MACE) in percutaneous coronary artery interventions (PCI), particularly in saphenous vein grafts (SVG). Mechanisms underlying no-reflow are not completely understood. Several hypotheses have been proposed, including microvascular spasm, in situ thrombosis and distal embolization. Distal protection devices are designed to prevent no-reflow by preventing the distal embolization of materials released during SVG PCI. Several clinical trials have shown that distal protection devices substantially reduced MACE in SVG PCI. Webb et al. reported a 3.9% MACE rate in patients in whom the PercuSurge Guardwire(PercuSurge, Minneapolis, Minnesota) distal protection device was used as compared to a historical 17.3% MACE rate in SVG PCI. The SAFER Trial randomized patients to the GuardWire device versus conventional angiogplasty wire (no distal protection devices). There was a 42% relative MACE rate reduction in patients who received the GuardWire distal protection device. Distal protection devices may be filter devices that trap debris or distal occlusion and aspiration systems, such as the GuardWire. The GuardWire is a device for transient distal vessel occlusion during balloon dilatation or stent placement that allows recovery of any liberated plaque material by aspiration of SVG contents before the restoration of flow. The GuardWire system has demonstrated its ability to recover cholesterol crystals, foam cells and other plaque constituents. One potential advantage of distal occlusion devices is that they eliminate both debris and soluble factors that can lead to no-reflow. Recent studies have indicated that soluble vasoactive compounds may contribute to the no-reflow phenomenon. Vasodilators such as calcium channel blockers, adenosine and nitroprusside reverse no-reflow in 50–80% of cases, suggesting that vasospasm plays a significant role in no-reflow. In addition, thrombotic factors released during PCI potentially increase in situ thrombosis that leads to no-reflow. Recent studies demonstrated an association between tissue factor and no-reflow in acute coronary syndrome (ACS). The release of vasoactive soluble factors and the ability of the GuardWire to recover soluble elements that could be released during SVG interventions have not been investigated before and are the focus of the present study.
The presence of no-reflow substantially increases the risk of major adverse clinical events (MACE) in percutaneous coronary artery interventions (PCI). Distal protection devices may eliminate both debris and soluble factors that can lead to no-reflow. This study was designed to evaluate the soluble factors released and eliminated by the PercuSurge GuardWireduring SVG intervention. Methods. Twenty-eight consecutive patients underwent PCI on 34 lesions in 31 SVGs using the PercuSurge GuardWire. Blood was taken prior to PCI for baseline measurement of: (1) Vasoconstrictive factors: endothelin (ET) and serotonin (5-HT); (2) thrombotic factors: tissue factor (TF), plasminogen activator inhibitor (PAI-1), thrombin/antithrombin III complex (TAT), and prothrombin fragment F1+2 (F1+2); and (3) inflammatory factors: soluble CD40 ligand (sCD40L) and soluble E-selectin. After stenting and before deflating the distal protection balloon, 2 aspiration runs were performed with the PercuSurge Export Catheter and sent for analysis. Results. Clinical follow-up was conducted at an average of 6 ± 3 months. SVG PCI resulted in a substantial increase in levels of vasoconstrictive factors, including ET (3 x increase; p < 0.001) and 5-HT (9.7 x increase; p = 0.031); thrombotic factors, including TF (4.5 x increase; p = 0.005), TAT (2.4 x increase; p < 0.001), and F1+2 (2.4 x increase; p < 0.001). Pro-inflammatory factors were also released during the procedure. Levels of sCD40L and soluble E-selectin increased 123% (p = 0.003) and 25% (p < 0.001), respectively. Conclusions. SVG PCI Results in an immediate increase in vasoactive factors, including vasoconstrictive, thrombotic and inflammatory factors. The PercuSurge GuardWire effectively removes these soluble factors, which may account for reduction of no-reflow and other complications during SVG interventions.
The no-reflow phenomenon is defined as a severe reduction in antegrade coronary flow in the absence of epicardial vessel obstruction. The presence of no-reflow substantially increases the risk of major adverse clinical events (MACE) in percutaneous coronary artery interventions (PCI), particularly in saphenous vein grafts (SVG). Mechanisms underlying no-reflow are not completely understood. Several hypotheses have been proposed, including microvascular spasm, in situ thrombosis and distal embolization. Distal protection devices are designed to prevent no-reflow by preventing the distal embolization of materials released during SVG PCI. Several clinical trials have shown that distal protection devices substantially reduced MACE in SVG PCI. Webb et al. reported a 3.9% MACE rate in patients in whom the PercuSurge Guardwire(PercuSurge, Minneapolis, Minnesota) distal protection device was used as compared to a historical 17.3% MACE rate in SVG PCI. The SAFER Trial randomized patients to the GuardWire device versus conventional angiogplasty wire (no distal protection devices). There was a 42% relative MACE rate reduction in patients who received the GuardWire distal protection device. Distal protection devices may be filter devices that trap debris or distal occlusion and aspiration systems, such as the GuardWire. The GuardWire is a device for transient distal vessel occlusion during balloon dilatation or stent placement that allows recovery of any liberated plaque material by aspiration of SVG contents before the restoration of flow. The GuardWire system has demonstrated its ability to recover cholesterol crystals, foam cells and other plaque constituents. One potential advantage of distal occlusion devices is that they eliminate both debris and soluble factors that can lead to no-reflow. Recent studies have indicated that soluble vasoactive compounds may contribute to the no-reflow phenomenon. Vasodilators such as calcium channel blockers, adenosine and nitroprusside reverse no-reflow in 50–80% of cases, suggesting that vasospasm plays a significant role in no-reflow. In addition, thrombotic factors released during PCI potentially increase in situ thrombosis that leads to no-reflow. Recent studies demonstrated an association between tissue factor and no-reflow in acute coronary syndrome (ACS). The release of vasoactive soluble factors and the ability of the GuardWire to recover soluble elements that could be released during SVG interventions have not been investigated before and are the focus of the present study.
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