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Mechanisms of intrinsic force in small human airways.

Mechanisms of intrinsic force in small human airways.

Respir Physiol Neurobiol. 2012 Feb 2;

Authors: Wylam ME, Xue A, Sieck GC

Abstract
We quantified the magnitude and investigated mechanisms regulating intrinsic force (IF) in human airway smooth muscle (hASM). IF was identified by reducing extracellular calcium (Ca(2+)) concentration to nominally zero in freshly isolated isometrically mounted 2mm human bronchi. Our results show: (1) the magnitude of IF is ∼50% of the maximal total force elicited by acetylcholine (10(-5)M) and is epithelial independent, (2) IF can also be revealed by β-adrenergic activation (isoproterenol), non-specific cationic channel blockade (La(3+)) or L-type voltage gated Ca(2+) channel blockade (nifedipine), (3) atropine, indomethacin, AA-861, or pyrilamine did not affect IF, (4) IF was reduced by the intracellular Ca(2+) ([Ca(2+)](i)) chelating agent BAPTA-AM, (5) ω-conotoxin had no effect on IF. In studies in cultured hASM cells nominally zero Ca(2+) buffer and BAPTA-AM reduced [Ca(2+)](i) but isoproterenol and nifedipine did not. Taken together these results indicate that rapid reduction of [Ca(2+)](i) reveals a permissive relationship between extracellular Ca(2+), [Ca(2+)](i) and IF. However IF can be dissipated by mechanisms effecting Ca(2+) sensitivity. We speculate that an increase of IF, a fundamental property of ASM, could be related to human airway clinical hyperresponsiveness and must be accounted for in in vitro studies of hASM.

PMID: 22322114 [PubMed - as supplied by publisher]

Usefulness of Thrombophilia Testing in Venous Thromboembolic Disease: Findings From the RIETE Registry.

Usefulness of Thrombophilia Testing in Venous Thromboembolic Disease: Findings From the RIETE Registry.

Clin Appl Thromb Hemost. 2012 Feb 12;

Authors: Gabriel F, Portolés O, Labiós M, Rodríguez C, Cisneros E, Vela J, Nuñez M

Abstract
Background: Information on thrombophilia risk factors for patients with upper extremity deep vein thrombosis (UEDVT) is limited. The genetic, acquired, and coagulation risk factors of an acute episode of lower EDVT (LEDVT) or UEDVT, either isolated or associated with pulmonary embolism (PE), were studied. Materials and Methods: A total of 4503 patients participated in a thrombophilia study. Odds ratio (OR) and 95% confidence intervals (CIs) were calculated. Results: Mean age of the participants was 55 ± 19 years. The risk of LEDVT or UEDVT, isolated or associated with PE, was calculated according to thrombophilia factors. We found association between LEDVT and factor V Leiden ([FVL]; OR: 1.8; 95% CI 1.4-2.4) and resistance to activated protein C ([APC-R]; OR: 1.6; 95% CI 1.1-2.4). The LEDVT + PE presented an association with PTG20210A (OR: 1.5; 95% CI 1.1-2.1). No association was found between the thrombophilic defects studied and UEDVT or UEDVT + PE. Conclusions: Both FVL and APC-R carriers had the risk of developing LEDVT. The PTG20210A carriers had the risk of developing LEDVT + PE. No thrombophilic defects studied presented risk factors for UEDVT or UEDVT + PE.

PMID: 22327823 [PubMed - as supplied by publisher]

The future of deep venous thrombosis and post-thrombotic syndrome in 2020.

The future of deep venous thrombosis and post-thrombotic syndrome in 2020.

Phlebology. 2012;27 Suppl 1:95-102

Authors: Comerota AJ

Abstract
This manuscript addresses six major issues involving deep venous thrombosis (DVT) and post-thrombotic syndrome. Prevention will likely see modest advances in pharmacological therapy, mainly by extending prophylaxis in high-risk patients. More notable advances will be observed in mechanical means of prophylaxis, focusing on sustained application of devices that can move larger volumes of blood. Silent, large-vein thrombi continue to place patients at risk for fatal pulmonary embolism. Improved imaging techniques will permit us to identify these patients over the next eight years. In many of those patients, vena caval interruption will be required. Elimination of high-risk filters and the production of improved filters placed through low-profile systems with antithrombotic agents bound to their surface will improve the short- and long-term results for inferior vena cava filters. The long-term management of DVT will focus on establishing appropriate duration for the individual patient and will see the evolution towards direct Xa and IIa inhibitors. Patients with extensive DVT will more commonly receive treatment strategies designed to eliminate thrombus and restore patency. This will substantially reduce post-thrombotic morbidity and reduce recurrence. Post-thrombotic syndrome will see greater attention towards treating the intraluminal fibrosis, thereby eliminating post-thrombotic venous obstruction. Unfortunately, neovalves will still be searching for the appropriate application.

PMID: 22312074 [PubMed - in process]

Prevention of VTE in Orthopedic Surgery Patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.

Prevention of VTE in Orthopedic Surgery Patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.

Chest. 2012 Feb;141(2 Suppl):e278S-325S

Authors: Falck-Ytter Y, Francis CW, Johanson NA, Curley C, Dahl OE, Schulman S, Ortel TL, Pauker SG, Colwell CW

Abstract
BACKGROUND: VTE is a serious, but decreasing complication following major orthopedic surgery. This guideline focuses on optimal prophylaxis to reduce postoperative pulmonary embolism and DVT.
METHODS: The methods of this guideline follow those described in Methodology for the Development of Antithrombotic Therapy and Prevention of Thrombosis Guidelines: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines in this supplement.
RESULTS: In patients undergoing major orthopedic surgery, we recommend the use of one of the following rather than no antithrombotic prophylaxis: low-molecular-weight heparin; fondaparinux; dabigatran, apixaban, rivaroxaban (total hip arthroplasty or total knee arthroplasty but not hip fracture surgery); low-dose unfractionated heparin; adjusted-dose vitamin K antagonist; aspirin (all Grade 1B); or an intermittent pneumatic compression device (IPCD) (Grade 1C) for a minimum of 10 to 14 days. We suggest the use of low-molecular-weight heparin in preference to the other agents we have recommended as alternatives (Grade 2C/2B), and in patients receiving pharmacologic prophylaxis, we suggest adding an IPCD during the hospital stay (Grade 2C). We suggest extending thromboprophylaxis for up to 35 days (Grade 2B). In patients at increased bleeding risk, we suggest an IPCD or no prophylaxis (Grade 2C). In patients who decline injections, we recommend using apixaban or dabigatran (all Grade 1B). We suggest against using inferior vena cava filter placement for primary prevention in patients with contraindications to both pharmacologic and mechanical thromboprophylaxis (Grade 2C). We recommend against Doppler (or duplex) ultrasonography screening before hospital discharge (Grade 1B). For patients with isolated lower-extremity injuries requiring leg immobilization, we suggest no thromboprophylaxis (Grade 2B). For patients undergoing knee arthroscopy without a history of VTE, we suggest no thromboprophylaxis (Grade 2B).
CONCLUSIONS: Optimal strategies for thromboprophylaxis after major orthopedic surgery include pharmacologic and mechanical approaches.

PMID: 22315265 [PubMed - in process]

Antithrombotic Therapy for VTE Disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines.

This article addresses the treatment of VTE disease.
METHODS: We generated strong (Grade 1) and weak (Grade 2) recommendations based on high-quality (Grade A), moderate-quality (Grade B), and low-quality (Grade C) evidence.
RESULTS: For acute DVT or pulmonary embolism (PE), we recommend initial parenteral anticoagulant therapy (Grade 1B) or anticoagulation with rivaroxaban. We suggest low-molecular-weight heparin (LMWH) or fondaparinux over IV unfractionated heparin (Grade 2C) or subcutaneous unfractionated heparin (Grade 2B). We suggest thrombolytic therapy for PE with hypotension (Grade 2C). For proximal DVT or PE, we recommend treatment of 3 months over shorter periods (Grade 1B). For a first proximal DVT or PE that is provoked by surgery or by a nonsurgical transient risk factor, we recommend 3 months of therapy (Grade 1B; Grade 2B if provoked by a nonsurgical risk factor and low or moderate bleeding risk); that is unprovoked, we suggest extended therapy if bleeding risk is low or moderate (Grade 2B) and recommend 3 months of therapy if bleeding risk is high (Grade 1B); and that is associated with active cancer, we recommend extended therapy (Grade 1B; Grade 2B if high bleeding risk) and suggest LMWH over vitamin K antagonists (Grade 2B). We suggest vitamin K antagonists or LMWH over dabigatran or rivaroxaban (Grade 2B). We suggest compression stockings to prevent the postthrombotic syndrome (Grade 2B). For extensive superficial vein thrombosis, we suggest prophylactic-dose fondaparinux or LMWH over no anticoagulation (Grade 2B), and suggest fondaparinux over LMWH (Grade 2C).
CONCLUSION: Strong recommendations apply to most patients, whereas weak recommendations are sensitive to differences among patients, including their preferences.

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