85 research outputs found

    Percutaneous coronary intervention of chronic total occlusions involving a bifurcation: Insights from the PROGRESS-CTO registry

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    BACKGROUND: The impact of bifurcations at the proximal or distal cap on the outcomes of chronic total occlusion (CTO) percutaneous coronary intervention (PCI) has received limited study. METHODS: We analyzed the clinical, angiographic, and procedural data of 4,584 cases performed in patients between 2012 and 2020 in a global CTO PCI registry. We compared 4 groups according to the bifurcation location: proximal cap, distal cap, proximal and distal cap, and no bifurcation. RESULTS: The CTO involved a bifurcation in 67% cases, as follows: proximal cap (n = 1451, 33%), distal cap (n = 622, 14%), or both caps (n = 954, 21%). Proximal and distal cap cases had higher J-CTO compared with proximal cap, distal cap, and no bifurcation cases (2.9 ± 1.1 vs 2.5 ± 1.1 vs 2.4 ± 1.2 vs 2.0 ± 1.2, P \u3c 0.0001), and they were also associated with a lower technical success rate (79% vs 85% vs 85% vs 90%, P \u3c 0.0001), higher pericardiocentesis rate (1% vs 1% vs 0.2% vs 0.3%, P = 0.02), and higher emergency coronary artery bypass graft surgery rate (0.3% vs 0% vs 0% vs 0%, P = 0.01). CONCLUSION: More than two-thirds of CTO PCIs involve a bifurcation, which is associated with lower technical success and higher risk of complications

    TCT-319 Use of Limited Antegrade Subintimal Tracking Technique in Chronic Total Occlusion Percutaneous Coronary Intervention

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    Background: There are limited data on the limited antegrade subintimal tracking (LAST) crossing technique for chronic total occlusion (CTO) percutaneous coronary intervention (PCI). Methods: We analyzed the frequency of use and outcomes of LAST among 2,003 CTO PCIs performed with antegrade dissection and re-entry (ADR) in the PROGRESS-CTO Registry between 2012 and 2021 at 39 centers. Results: LAST was used in 144 cases (7.2%), primary LAST in 113 (5.6%), and secondary LAST in 31 cases (1.5%). The Stingray system was used in 905 cases (45.2%), subintimal tracking and re-entry (STAR) in 333 cases (16.6%), and contrast-guided STAR in 29 cases (1.4%). The mean patient age was 64.2 ± 10 years, 86% were men, and 34.9% had prior coronary artery bypass graft surgery. Cases in which LAST was used were less complex with a lower J-CTO score (2.50 ± 1.32 vs. 2.95 ± 1.10, P \u3c 0.001). There was no difference in technical (75.0% vs 78.4%, P = 0.337) and procedural success (72.2% vs 75.5%, P = 0.384) and major cardiac adverse events (MACEs) (2.08% vs 3.55%, P = 0.352) between LAST and non-LAST cases. However, cases in which the LAST technique was used required less procedure and fluoroscopy time (Figure 1A). A primary LAST technique was associated with higher technical and procedural success rates and a similar MACE rate compared with a secondary LAST technique (Figure 1B). Conclusion: LAST is used in 7.2% of ADR CTO PCI cases and is associated with similar technical and procedural success rates and major complication rates but lower procedural and fluoroscopy time compared with ADR cases that did not use LAST

    Vascular Endothelial Growth Factor (VEGF) isoform expression and activity in human and murine lung injury

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    <p>Abstract</p> <p>Background</p> <p>The properties of vascular endothelial growth factor (VEGF) as a potent vascular permogen and mitogen have led to investigation of its potential role in lung injury. Alternate spliced VEGF transcript generates several isoforms with potentially differing functions. The purpose of this study was to determine VEGF isoform expression and source in normal and ARDS subjects and investigate the expression and regulation of VEGF isoforms by human alveolar type 2 (ATII) cells.</p> <p>Methods</p> <p>VEGF protein expression was assessed immunohistochemically in archival normal and ARDS human lung tissue. VEGF isoform mRNA expression was assessed in human and murine lung tissue. Purified ATII cells were cultured with proinflammatory cytokines prior to RNA extraction/cell supernatant sampling/proliferation assay.</p> <p>Measurements and Main Results</p> <p>VEGF was expressed on alveolar epithelium, vascular endothelium and alveolar macrophages in normal and ARDS human lung tissue. Increases in VEGF expression were detected in later ARDS in comparison to both normal subjects and early ARDS (p < 0.001). VEGF<sub>121</sub>, VEGF<sub>165 </sub>and VEGF<sub>189 </sub>isoform mRNA expression increased in later ARDS (p < 0.05). The ratio of soluble to cell-associated isoforms was lower in early ARDS than normal subjects and later ARDS and also in murine lung injury. ATII cells constitutionally produced VEGF<sub>165 </sub>and VEGF<sub>121 </sub>protein which was increased by LPS (p < 0.05). VEGF<sub>165 </sub>upregulated ATII cell proliferation (p < 0.001) that was inhibited by soluble VEGF receptor 1 (<it>sflt</it>) (p < 0.05).</p> <p>Conclusion</p> <p>These data demonstrate that changes in VEGF isoform expression occur in ARDS which may be related to their production by and mitogenic effect on ATII cells; with potentially significant clinical consequences.</p

    Conditional deletion of epithelial IKKβ impairs alveolar formation through apoptosis and decreased VEGF expression during early mouse lung morphogenesis

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    <p>Abstract</p> <p>Background</p> <p>Alveolar septation marks the beginning of the transition from the saccular to alveolar stage of lung development. Inflammation can disrupt this process and permanently impair alveolar formation resulting in alveolar hypoplasia as seen in bronchopulmonary dysplasia in preterm newborns. NF-κB is a transcription factor central to multiple inflammatory and developmental pathways including dorsal-ventral patterning in fruit flies; limb, mammary and submandibular gland development in mice; and branching morphogenesis in chick lungs. We have previously shown that epithelial overexpression of NF-κB accelerates lung maturity using transgenic mice. The purpose of this study was to test our hypothesis that targeted deletion of NF-κB signaling in lung epithelium would impair alveolar formation.</p> <p>Methods</p> <p>We generated double transgenic mice with lung epithelium-specific deletion of IKKβ, a known activating kinase upstream of NF-κB, using a cre-<it>loxP </it>transgenic recombination strategy. Lungs of resulting progeny were analyzed at embryonic and early postnatal stages to determine specific effects on lung histology, and mRNA and protein expression of relevant lung morphoreulatory genes. Lastly, results measuring expression of the angiogenic factor, VEGF, were confirmed <it>in vitro </it>using a siRNA-knockdown strategy in cultured mouse lung epithelial cells.</p> <p>Results</p> <p>Our results showed that IKKβ deletion in the lung epithelium transiently decreased alveolar type I and type II cells and myofibroblasts and delayed alveolar formation. These effects were mediated through increased alveolar type II cell apoptosis and decreased epithelial VEGF expression.</p> <p>Conclusions</p> <p>These results suggest that epithelial NF-κB plays a critical role in early alveolar development possibly through regulation of VEGF.</p

    Angiopoietin-1 Treatment Reduces Inflammation but Does Not Prevent Ventilator-Induced Lung Injury

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    Background: Loss of integrity of the epithelial and endothelial barriers is thought to be a prominent feature of ventilator-induced lung injury (VILI). Based on its function in vascular integrity, we hypothesize that the angiopoietin (Ang)-Tie2 system plays a role in the development of VILI. The present study was designed to examine the effects of mechanical ventilation on the Ang-Tie2 system in lung tissue. Moreover, we evaluated whether treatment with Ang-1, a Tie2 receptor agonist, protects against inflammation, vascular leakage and impaired gas exchange induced by mechanical ventilation. Methods: Mice were anesthetized, tracheotomized and mechanically ventilated for 5 hours with either an inspiratory pressure of 10 cmH(2)O ('low' tidal volume similar to 7.5 ml/kg; LVT) or 18 cmH(2)O ('high' tidal volume similar to 15 ml/kg; HVT). At initiation of HVT-ventilation, recombinant human Ang-1 was intravenously administered (1 or 4 mu g per animal). Non-ventilated mice served as controls. Results: HVT-ventilation influenced the Ang-Tie2 system in lungs of healthy mice since Ang-1, Ang-2 and Tie2 mRNA were decreased. Treatment with Ang-1 increased Akt-phosphorylation indicating Tie2 signaling. Ang-1 treatment reduced infiltration of granulocytes and expression of keratinocyte-derived chemokine (KC), macrophage inflammatory protein (MIP)-2, monocyte chemotactic protein (MCP)-1 and interleukin (IL)-1 beta caused by HVT-ventilation. Importantly, Ang-1 treatment did not prevent vascular leakage and impaired gas exchange in HVT-ventilated mice despite inhibition of inflammation, vascular endothelial growth factor (VEGF) and Ang-2 expression. Conclusions: Ang-1 treatment downregulates pulmonary inflammation, VEGF and Ang-2 expression but does not protect against vascular leakage and impaired gas exchange induced by HVT-ventilatio

    Global Chronic Total Occlusion Crossing Algorithm

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    The authors developed a global chronic total occlusion crossing algorithm following 10 steps: 1) dual angiography; 2) careful angiographic review focusing on proximal cap morphology, occlusion segment, distal vessel quality, and collateral circulation; 3) approaching proximal cap ambiguity using intravascular ultrasound, retrograde, and move-the-cap techniques; 4) approaching poor distal vessel quality using the retrograde approach and bifurcation at the distal cap by use of a dual-lumen catheter and intravascular ultrasound; 5) feasibility of retrograde crossing through grafts and septal and epicardial collateral vessels; 6) antegrade wiring strategies; 7) retrograde approach; 8) changing strategy when failing to achieve progress; 9) considering performing an investment procedure if crossing attempts fail; and 10) stopping when reaching high radiation or contrast dose or in case of long procedural time, occurrence of a serious complication, operator and patient fatigue, or lack of expertise or equipment. This algorithm can improve outcomes and expand discussion, research, and collaboration.info:eu-repo/semantics/publishedVersio

    Global Chronic Total Occlusion Crossing Algorithm: JACC State-of-the-Art Review

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    The authors developed a global chronic total occlusion crossing algorithm following 10 steps: 1) dual angiography; 2) careful angiographic review focusing on proximal cap morphology, occlusion segment, distal vessel quality, and collateral circulation; 3) approaching proximal cap ambiguity using intravascular ultrasound, retrograde, and move-the-cap techniques; 4) approaching poor distal vessel quality using the retrograde approach and bifurcation at the distal cap by use of a dual-lumen catheter and intravascular ultrasound; 5) feasibility of retrograde crossing through grafts and septal and epicardial collateral vessels; 6) antegrade wiring strategies; 7) retrograde approach; 8) changing strategy when failing to achieve progress; 9) considering performing an investment procedure if crossing attempts fail; and 10) stopping when reaching high radiation or contrast dose or in case of long procedural time, occurrence of a serious complication, operator and patient fatigue, or lack of expertise or equipment. This algorithm can improve outcomes and expand discussion, research, and collaboration

    Appropriateness of percutaneous revascularization of coronary chronic total occlusions: An overview

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    Coronary chronic total occlusions (CTOs) are commonly encountered in patients undergoing coronary angiography. Several observational studies have demonstrated that successful CTO revascularization is associated with better cardiovascular outcomes and enhanced quality of life (QOL). However, in the absence of randomized trials, its prognostic benefit for patients remains debated. Over the past decade, the interest of the interventional community in CTO percutaneous coronary intervention (PCI) has exponentially grown due to important developments in dedicated equipment and techniques, resulting in high success and low complication rates. Both European and American guidelines have assigned a class IIa (level of evidence B) recommendation for CTO PCI. In the current review, we focus on the impact of CTO revascularization on clinical outcomes and QOL and on appropriate patient selection, and we provide a critical assessment of the current guidelines and recommendations on CTO PCI
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