Objectives: Venovenous extracorporeal membrane oxygenation is indicated in patients with severe refractory acute respiratory failure. Venous thrombosis due to indwelling catheters is a frequent complication. The aim of this study was to analyze the incidence of cannula-related thrombosis and its risk factors after venovenous extracorporeal membrane oxygenation. Design: Retrospective observational study. Setting: A medical ICU at the University Hospital Regensburg. Patients: We analyzed consecutive patients with severe respiratory failure (Pao 2/Fio 2 < 85 mm Hg and/or respiratory acidosis with pH < 7.25) who were successfully treated with venovenous extracorporeal membrane oxygenation in a medical ICU between 2010 and 2017. Intervention: None. Measurements and Main Results: After extracorporeal membrane oxygenation weaning, duplex sonography or CT was conducted to detect cannula-related thrombosis. Thrombosis was classified as a large thrombosis by vein occlusion of greater than 50%. The incidence of thrombosis was correlated with risk factors such as coagulation variables (mean activated partial thromboplastin time ≤ 50 s, international normalized ratio antithrombin III, fibrinogen, plasma-free hemoglobin, platelets, and decline in D-dimer ≤ 50% the day after decannulation), cannula size, time on venovenous extracorporeal membrane oxygenation, renal failure, and underlying malignant disease. Data cut-off points were identified by receiver operating characteristic analysis. One-hundred seventy-two of 197 patients (87%) were screened. One-hundred six patients (62%) showed thrombosis that was considered large in 48 of 172 (28%). The incidence of thrombosis was higher in patients with a mean aPTT of less than or equal to 50 seconds (odds ratio, 1.02; p = 0.013) and in patients with a decline in D-dimer less than or equal to 50% (odds ratio, 2.76; p = 0.041) the day after decannulation following adjustment for risk factors. Conclusions: The incidence of cannula-related venous thrombosis after venovenous extracorporeal membrane oxygenation is high. Reduced systemic anticoagulation may enhance the risk of thrombosis. Sustained elevation of D-dimer after decannulation may indicate thrombosis. Patients should undergo routine duplex sonography after extracorporeal membrane oxygenation to detect thrombosis formation in the cannulated vessel.

Objective-Angiographic indexes of restenosis after coronary stent placement in patients show a bimodal pattern suggesting the existence of two populations with different risk of restenosis. This is reflected in the arterial remodeling response of inbred mouse strains arguing for a genetic control of the mechanisms leading to lumen narrowing. As bone marrow-derived cells (BMCs) contribute to vascular healing after arterial injury, we investigated the role of BMCs in the genetic control of restenosis. Methods and Results-129X1/SvJ mice developed significantly more neointima and late lumen loss compared to C57BL/6 mice. Gene expression analysis of intimal tissue revealed major differences in the expression of inflammatory and hematopoietic stem and progenitor cell-associated genes in response to arterial injury. In 129X1/SvJ mice stronger mobilization of lin Ϫ sca-1 ϩ CXCR4 ϩ cells was observed after vascular injury. Bone marrow transplantation identified the extent of neointima formation as clearly dependent on the genetic background of BMCs (ie, mice with 129X1/SvJ BMCs developed more intimal hyperplasia). The inflammatory response and the recruitment of BMCs to the site of arterial injury were significantly increased in mice with 129X1/SvJ BMCs. 3 This process was formerly considered to be primarily directed by dedifferentiation and proliferation of medial smooth muscle cells (SMCs). 4 Recently, it has been demonstrated that recruitment of inflammatory cells and bone marrow-derived cells (BMCs) is an essential step in the pathogenesis of vascular remodeling. [5][6][7][8][9] In mice, up to 60% of intimal SMCs originate from the bone marrow. 7 In patients, a progenitor cell-associated gene expression pattern such as the induction of the stromal cell-derived factor 1␣ (SDF-1␣) receptor CXCR-4 or the granulocyte-colony stimulating factor (G-CSF) receptor in neointimal SMCs from coronary in-stent restenosis further argues for the impact of the recruitment of circulating hematopoietic stem and progenitor cells (HSPCs) to the site of vascular injury. 9 Likewise, inhibition of SDF-1␣, a key regulator of HSPC mobilization and recruitment, significantly reduces intimal hyperplasia after vascular injury in mice. 8 Conclusions-The See accompanying article on page 1407Angiographic indexes of restenosis after coronary stent placement follow a bimodal pattern, suggesting the existence of 2 populations with different risk of restenosis. 10 This finding is reflected in a wide variation in the arterial remodeling response in various inbred strains of mice after vessel ligation, arguing that the mechanisms leading to lumen narrowing in the vascular remodeling process are genetically controlled. 11 Whereas vessel ligation only leads to flow cessation, arterial injury by insertion of a standard guide wire induces endothelial denudation and dilatation of the vessel wall with injury of the media. As previously reported, wire injury yields substantial intimal hyperplasia in 129X1/SvJ mice, analogous to the situation in patients after ...

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