G. Geroulakos

Diagnosis and Anticoagulant Treatment

2012;97(1):95-100. 64. Brill-Edwards P, Ginsberg JS, Gent M, et al. Safety of withholding heparin in pregnant women with a history of venous thromboembolism. Recurrence of clot in this pregnancy study group. N Engl J Med. 2000;343(20):1439-1444. 65. De Stefano V, Martinelli I, Rossi E, et al. The risk of recurrent venous thromboembolism in pregnancy and puerperium without antithrombotic prophylaxis. Br J Haematol. 2006;135(3):386-391. 66. White RH, Chan WS, Zhou H, Ginsberg JS. Recurrent venous thromboembolism after pregnancy-associated versus unprovoked thromboembolism. Thromb Haemost. 2008;100(2):246-252. 67. Pabinger I, Schneider B. Thrombotic risk in hereditary antithrombin III, protein C, or protein S deficiency. A cooperative, retrospective study. Gesellschaft fur Thromboseund Hamostaseforschung (GTH) Study Group on Natural Inhibitors. Arterioscler Thromb Vasc Biol. 1996;16(6):742-748. 68. Conard J, Horellou MH, Van Dreden P, Lecompte T, Samama M. Thrombosis and pregnancy in congenital deficiencies in AT III, protein C or protein S: study of 78 women. Thromb Haemost. 1990;63(2):319-320. 69. McColl MD, Ramsay JE, Tait RC, et al. Risk factors for pregnancy associated venous thromboembolism. Thromb Haemost. 1997;78(4):1183-1188. 70. Robertson L, Wu O, Langhorne P, et al. Thrombophilia in pregnancy: a systematic review. Br J Haematol. 2006;132(2):171-196. 71. Serour GI, Aboulghar M, Mansour R, Sattar MA, Amin Y, Aboulghar H. Complications of medically assisted conception in 3,500 cycles. Fertil Steril. 1998;70(4):638-642. 72. Mara M, Koryntova D, Rezabek K, et al. Thromboembolic complications in patients undergoing in vitro fertilization: retrospective clinical study. Ceska Gynekol. 2004;69(4):312-316. 73. Chan WS, Dixon ME. The ‘‘ART’’ of thromboembolism: a review of assisted reproductive technology and thromboembolic complications. Thromb Res. 2008;121(6):713-726. 74. Di Nisio M, Rutjes AW, Ferrante N, Tiboni GM, Cuccurullo F, Porreca E. Thrombophilia and outcomes of assisted reproduction technologies: a systematic review and meta-analysis. Blood. 2011;118(10):2670-2678. 75. Nelson-Piercy C, Powrie R, Borg JY, et al. Tinzaparin use in pregnancy: an international, retrospective study of the safety and efficacy profile. Eur J Obstet Gynecol Reprod Biol. 2011;159(2): 293-299. 76. Byrd LM, Shiach CR, Hay CR, Johnston TA. Osteopenic fractures in pregnancy: is low molecular weight heparin (LMWH) implicated? J Obstet Gynaecol. 2008;28(5):539-542. 77. Hellgren M, Tengborn L, Abildgaard U. Pregnancy in women with congenital antithrombin III deficiency: experience of treatment with heparin and antithrombin. Gynecol Obstet Invest. 1982;14(2):127-141. 78. Tiede A, Tait RC, Shaffer DW, et al. Antithrombin alfa in hereditary antithrombin deficient patients: a phase 3 study of prophylactic intravenous administration in high risk situations. Thromb Haemost. 2008;99(3):616-622. 79. Pernod G, Biron-Andreani C, Morange PE, et al. Recommendations on testing for thrombophilia in venous thromboembolic disease: a French consensus guideline. J Mal Vasc. 2009;34(3): 156-203. 80. Baglin T, Gray E, Greaves M, et al. Clinical guidelines for testing for heritable thrombophilia. Br J Haematol. 2010;149(2): 209-220. 81. Kearon C. Influence of hereditary or acquired thrombophilias on the treatment of venous thromboembolism. Curr Opin Hematol. 2012;19(5):363-370. 82. Jenkins PV, Rawley O, Smith OP, O’Donnell JS. Elevated factor VIII levels and risk of venous thrombosis. Br J Haematol. 2008; 157(6):653-663.

Prevention of postthrombotic syndrome.

bosis: a clinical outcome study. Thromb Haemost. 2001; 86(5):1170-1175. 101. Lindhoff-Last E, Kreutzenbeck HJ, Magnani HN. Treatment of 51 pregnancies with danaparoid because of heparin intolerance. Thromb Haemost. 2005;93(1):63-69. 102. Tardy B, Tardy-Poncet B, Viallon A, Piot M, Mazet E. Fatal danaparoid-sodium induced thrombocytopenia and arterial thrombosis. Thromb Haemost. 1998;80(3):530. 103. Farner B, Eichler P, Kroll H, Greinacher A. A comparison of danaparoid and lepirudin in heparin-induced thrombocytopenia. Thromb Haemost. 2001;85(6):950-957. 104. Kodityal S, Manhas AH, Udden M, Rice L. Danaparoid for heparin-induced thrombocytopenia: an analysis of treatment failures. Eur J Haematol. 2001;71:109-113. 105. Haas S, Walenga JM, Jeske WP, Fareed J. Heparin-induced thrombocytopenia: clinical considerations of alternative anticoagulation with various glycosaminoglycans and thrombin inhibitors. Clin Appl Thromb Hemost. 1999;5(1):52-59. 106. Lobo B, Finch C, Howard A, Minhas S. Fondaparinux for the treatment of patients with acute heparin-induced thrombocytopenia. Thromb Haemost. 2008;99(1):208-214. 107. Grouzi E, Kyriakou E, Panagou I, Spiliotopoulou I. Fondaparinux for the treatment of acute heparin-induced thrombocytopenia: a single-center experience. Clin Appl Thromb Hemost. 2010;16(6):663-667. 108. Warkentin TE, Pai M, Sheppard JI, Schulman S, Spyropoulos AC, Eikelboom JW. Fondaparinux treatment of acute heparininduced thrombocytopenia confirmed by the serotonin-release assay: a 30-month, 16-patient case series. J Thromb Haemost. 2011;9(12):2389-2396. 109. Hook K, Abrams CS. Treatment options in heparin-induced thrombocytopenia. Curr Opin Hematol. 2010;17(5):424-431. 110. Greinacher A, Alban S, Drummel V, Franz G, Mueller-Eckhardt C. Characterization of the structural requirements for a carbohydrate-based anticoagulant with a reduced risk of inducing the immunological type of heparin-associated thrombocytopenia. Thromb Haemost. 1995;74(4):886-892. 111. Walenga JM, Koza MJ, Lewis BE, Pifarre R. Relative heparininduced thrombocytopenic potential of low molecular weight heparins and new antithrombotic agents. Clin Appl Thromb Hemost. 1996;2(suppl 1):S21-S27. 112. Warkentin TE, Elavathil LJ, Hayward CP, Johnston MA, Russett JI, Kelton JG. The pathogenesis of venous limb gangrene associated with heparin-induced thrombocytopenia. Ann Intern Med. 1997;127(9):804-812. 113. Srinivasan AF, Rice L, Bartholomew JR, et al. Warfarininduced skin necrosis and venous limb gangrene in the setting of heparin-induced thrombocytopenia. Arch Intern Med. 2004; 164(1):66-70. 114. Hursting MJ, Lewis BE, MacFarlane DE. Transitioning from argatroban to warfarin therapy in patients with heparininduced thrombocytopenia. Clin Appl Thromb Hemost. 2005; 11(3):279-287. 115. Bartholomew JR, Hursting MJ. Transitioning from argatroban to warfarin in heparin-induced thrombocytopenia: an analysis of outcomes in patients with elevated international normalized ratio (INR). J Thromb Thrombolysis. 2005;19(3):183-188. 116. Walenga JM, Drenth AF, Mayuga M. Transition from argatroban to oral anticoagulation with phenprocoumon or acenocoumarol: effect on coagulation factor testing. Clin Appl Thromb Hemost. 2008;14(3):325-331.

Effect of diabetes mellitus on the clinical outcome of lower limb arterial bypass surgery: A propensity score analysis.

Objectives Diabetic patients who undergo lower limb arterial bypass surgery are considered to have a worse clinical outcome compared to non-diabetics. The aim of the study was to test this hypothesis after applying propensity score matching analysis. Patients and methods A total of 113 consecutive lower limb bypass procedures (55 diabetic and 58 non-diabetic) were evaluated regarding their clinical outcome. Endpoints of the study included amputation-free survival, limb salvage, patency and patients’ survival up to 36 months post-procedure. After propensity score matching analysis, two new groups, diabetic and non-diabetic, of 31 limbs in each one were created, both equivalent regarding all baseline characteristics. Results Between the propensity score matching groups, the amputation-free survival was 68.8% in the non-diabetic and 37.7% in the diabetic group at 36 months (p = 0.004). Similarly, the survival was 88.6% and 57.6%, respectively, in the two groups at the same time point (p = 0.01). On the contrary, no difference was found in patency (58.3% vs. 56%) and in limb salvage rate (74.1% vs. 60.8%). Conclusions Lower limbs arterial bypass surgery has similar results regarding patency and limb salvage rate in diabetic and non-diabetic patients. On the contrary, mortality is worse in diabetic patients, this affecting negatively their amputation-free survival.

Endovascular stent grafting for ascending aorta diseases

Objective Conventional open surgery encompassing cardiopulmonary bypass has been traditionally used for the treatment of ascending aorta diseases. However, more than one in five of these patients will be finally considered unfit for open repair. We conducted a systematic review and meta‐analysis to investigate the role of thoracic endovascular aortic repair (TEVAR) for aortic diseases limited to the ascending aorta. Methods The current meta‐analysis was conducted using the Preferred Reporting Items for Systematic Reviews and Meta‐Analyses guidelines. We investigated patients’ baseline characteristics along with early (30 days/in‐hospital stay) and late (beyond 30 days/in‐hospital stay) outcomes after TEVAR limited to the ascending aorta and not involving the arch vessels. Separate analyses for case reports and case series were conducted, and pooled proportions with 95% confidence intervals (CIs) of outcome rates were calculated. Results Approximately 67% of the patients had a prior cardiac operation. TEVAR was performed mainly for acute or chronic Stanford type A dissection (49%) or pseudoaneurysm (28%). The device was usually delivered through the femoral artery (67%), and rapid ventricular pacing was used in nearly half of the patients. Technical success of the method was 95.5% (95% CI, 87.8‐99.8). Among the early outcomes, conversion to open repair was 0.7% (95% CI, 0.1‐4.8), whereas mortality was 2.9% (95% CI, 0.02‐8.6). We estimated a pooled rate of 1.8% (95% CI, 0.1‐7.0) for neurologic events (stroke or transient ischemic attack) and 0.8% (95% CI, 0.1‐5.6) for myocardial infarction. Late endoleak was recorded in 16.4% (95% CI, 8.2‐26.0), and 4.4% (95% CI, 0.1‐12.4) of the population died in the postoperative period. Finally, reoperation was recorded in 8.9% (95% CI, 3.1‐16.4) of the study sample. Conclusions TEVAR in the ascending aorta seems to be safe and feasible for selected patients with various aortic diseases, although larger studies are required.

Cost-Effectiveness of Prevention and Treatment of VTE

factors associated with retrobulbar/peribulbar block: a prospective study in 1383 patients. Br J Anaesth. 2000;85(5):708-711. 19. Hirschman DR, Morby LJ, Hirschman DR, Morby LJ. A study of the safety of continued anticoagulation for cataract surgery patients. Nursing Forum. 2006;41(1):30-37. 20. Hylek EM, Regan S, Go AS, Hughes RA, Singer DE, Skates SJ. Clinical predictors of prolonged delay in return of the international normalized ratio to within the therapeutic range after excessive anticoagulation with warfarin. Ann Intern Med. 2001;135(6):393-400. 21. O’Donnell MJ, Kearon C, Johnson J, et al. Preoperative anticoagulant activity after bridging low-molecular-weight heparin for temporary interruption of warfarin. Ann Intern Med. 2007; 146(3):184-187. 22. Woods KDJ, Kathirgamanathan K, Yi Q, Crowther MA. Lowdose oral vitamin K to normalize the international normalized ratio prior to surgery in patients who require temporary interruption of warfarin. J Thromb Thrombolys. 2007;24(2):93-97. 23. Gerotziafas GT, Dupont C, Spyropoulos AC, et al. Differential inhibition of thrombin generation by vitamin K antagonists alone and associated with low-molecular-weight heparin. Thromb Haemost. 2009;102(1):42-48. 24. Dunn AS, Spyropoulos AC, Turpie AG, Turpie AGG. Bridging therapy in patients on long-term oral anticoagulants who require surgery: the prospective peri-operative enoxaparin cohort trial (PROSPECT). J Thromb Haemost. 2007;5(11):2211-2218. 25. Bath PM, Lindenstrom E, Boysen G, et al. Tinzaparin in acute ischaemic stroke (TAIST): a randomised aspirin-controlled trial. Lancet. 2001;358(9283):702-710. 26. Spyropoulos AC. Bridging of oral anticoagulation therapy for invasive procedures. Curr Hematol Rep. 2005;4(5):405-413. 27. Spyropoulos AC, Frost FJ, Hurley JS, Roberts M. Costs and clinical outcomes associated with low-molecular-weight heparin vs unfractionated heparin for perioperative bridging in patients receiving long-term oral anticoagulant therapy. Chest. 2004; 125(5):1642-1650. 28. Spyropoulos AC, Turpie AG, Dunn AS, et al. Perioperative bridging therapy with unfractionated heparin or low-molecularweight heparin in patients with mechanical prosthetic heart valves on long-term oral anticoagulants (from the REGIMEN Registry). Am J Cardiol. 2008;102(7):883-889. 29. Douketis JD, Johnson JA, Turpie AG. Low-molecular-weight heparin as bridging anticoagulation during interruption of warfarin: assessment of a standardized periprocedural anticoagulation regimen. Arch Intern Med. 2004;164(12):1319-1326. 30. Jaffer AK, Brotman DJ, Bash LD, Mahmood SK, Lott B, White RH. Variations in perioperative warfarin management: outcomes and practice patterns at nine hospitals. Am J Med. 123(2):141-150. 31. Hammerstingl C, Tripp C, Schmidt H, et al. Periprocedural bridging therapy with low-molecular-weight heparin in chronically anticoagulated patients with prosthetic mechanical heart valves: experience in 116 patients from the prospective BRAVE registry. J Heart Valve Disease. 2007;16(3):285-292. 32. Pengo V, Cucchini U, Denas G, et al. Standardized lowmolecular-weight heparin bridging regimen in outpatients on oral anticoagulants undergoing invasive procedure or surgery: an inception cohort management study. Circulation. 2009; 119(22):2920-2927. 33. Katholi RE, Nolan SP, McGuire LB. The management of anticoagulation during noncardiac operations in patients with prosthetic heart valves. A prospective study. Am Heart J. 1978;96(2):163-165. 34. Spyropoulos AC, Turpie AG, Dunn AS, et al. Clinical outcomes with unfractionated heparin or low-molecular-weight heparin as bridging therapy in patients on long-term oral anticoagulants: the REGIMEN registry. J Thromb Haemost. 2006; 4(6):1246-1252. 35. Garcia DA, Regan S, Henault LE, et al. Risk of thromboembolism with short-term interruption of warfarin therapy [see comment]. Arch Intern Med. 2008;168(1):63-69. 36. Malato AAR, Cigna V, Sciacca M, Abbene I, Saccullo G, Lo Cocco L, Siragusa S. Perioperative bridging therapy with low molecular weight heparin in patients requiring interruption of long-term oral anticoagulant therapy. Haematologica. 2006;91:10. 37. Hammerstingl C, Omran H. Bridging of oral anticoagulation with low-molecular-weight heparin: experience in 373 patients with renal insufficiency undergoing invasive procedures. Thromb Haemost. 2009;101(6):1085-1090. 38. Jaffer AK, Ahmed M, Brotman DJ, et al. Low-molecular-weightheparins as periprocedural anticoagulation for patients on longterm warfarin therapy: a standardized bridging therapy protocol. J Thromb Thrombolysis. 2005;20(1):11-16. 39. Spyropoulos AC. Bridging therapy and oral anticoagulation: current and future prospects. Curr Opin Hematol. 2010;17(5):444-449. 40. van Ryn J, Stangier J, Haertter S, et al. Dabigatran etexilate–a novel, reversible, oral direct thrombin inhibitor: interpretation of coagulation assays and reversal of anticoagulant activity. Thromb Haemost. 2010;103(6):1116-1127. 41. Douketis JD. Pharmacologic properties of the new oral anticoagulants: a clinician-oriented review with a focus on perioperative management. Curr Pharm Des. 2010;16(31):3436-3441.

General, vascular, bariatric, and plastic surgical patients.

International consensus statement. Guidelines according to scientific evidence. Int Angiol. 2005;24:1-26. 24. Scurr JH, Coleridge-Smith PD, Hasty JH. Deep venous thrombosis: a continuing problem. BMJ. 1988;297(6640):28. 25. White RH, Gettner S, Newman JM, Trauner KB, Romano PS. Predictors of rehospitalization for symptomatic venous thromboembolism after total hip arthroplasty. N Engl J Med. 2000; 343:1758-1764. 26. Eikelboom JW, Quinlan DJ, Douketis JD. Extended-duration prophylaxis against venous thromboembolism after total hip or knee replacement: a meta-analysis of the randomised trials. Lancet. 2001;358(9275):9-15. 27. Vaitkus PT, Leizorovicz A, Cohen AT, Turpie AG, Olsson CG, Goldhaber SZ. Mortality rates and risk factors for asymptomatic deep vein thrombosis in medical patients. Thromb Haemost. 2005;93(1):76-79. 28. Kucher N, Koo S, Quiroz R, et al. Electronic alerts to prevent venous thromboembolism among hospitalized patients. N Engl J Med. 2005;352(10):969-977. 29. Cohen AT, Agnelli G, Anderson FA, et al. Venous thromboembolism (VTE) in Europe. The number of VTE events and associated morbidity and mortality. Thromb Haemost. 2007;98(4):756-764. 30. Kucher N, Spirk D, Kalka C, et al. Clinical predictors of prophylaxis use prior to the onset of acute venous thromboembolism in hospitalized patients swiss venous thromboembolism registry (SWIVTER). J Thromb Haemost. 2008;6(12):2082-2087. 31. Cohen AT, Tapson VF, Bergmann JF, et al. Venous thromboembolism risk and prophylaxis in the acute hospital care setting (ENDORSE study): a multinational cross-sectional study. Lancet. 2008;371(9610):387-394. 32. Kucher N, Spirk D, Baumgartner I, et al. Lack of prophylaxis before the onset of acute venous thromboembolism among hospitalized cancer patients: the swiss venous thromboembolism registry (SWIVTER). Ann Oncol. 2010;21(5):931-935. 33. Anderson FA, Jr, Goldhaber SZ, Tapson VF, et al. Improving practices in US hospitals to prevent Venous Thromboembolism: lessons from ENDORSE. Am J Med. 2010;123(12):1099-1106 e8. 34. Vaughan-Shaw PG, Cannon C. Venous thromboembolism prevention in medical patients: a framework for improving practice. Phlebology. 2011;26(2):62-68. 35. Kucher N, Puck M, Blaser J, Bucklar G, Eschmann E, Luscher TF. Physician compliance with advanced electronic alerts for preventing venous thromboembolism among hospitalized medical patients. J Thromb Haemost. 2009;7:1291-1296.

Combined modalities in surgical patients.

Despite contemporary developments in pharmacology and biomedical engineering, venous thromboembolism (VTE) is not fully preventable and thus still remains a serious complication of trauma, surgery, and medical conditions. Current and previous guidelines recommend risk stratification to tailor implementation of prophylactic methods so that combined modalities are recommended based on supportive evidence in high-risk patients, although cost and potential adverse events make them less effective for low-risk groups. The reason for the increased efficacy of combined modalities is based on the multifactorial etiology of VTE as first described by Rudolph Virchow in the 19th century. Physical methods reduce venous stasis while pharmacological methods affect hypercoagulopathy. The fact that combined modalities are more effective than single modalities was first shown by Borow in 1983 followed by several studies supporting this concept. Although elastic stockings are effective in reducing further VTE rates achieved by perioperative antithrombotic prophylactic pharmacotherapy, as indicated in several places in this document, most modern studies have evaluated the role of the combination of intermittent pneumatic compression (IPC) with pharmacological methods, and this will be the focus of this section. A recent Cochrane review evaluated the efficacy of combined modalities (IPC) and pharmacological prophylaxis: treatment group) against single modalities alone (control group) to prevent pulmonary embolism (PE) and deep vein thrombosis (DVT) in patients at high risk of VTE. A total of 11 studies that included 7431 patients were identified, of which 6 were randomized-controlled trials (RCTs). The studies evaluated orthopedic patients (n 1⁄4 6), urology patients (n 1⁄4 2), and general surgery, cardiothoracic, and gynecology patients (n 1⁄4 3). Compared to compression alone, combined modalities significantly reduced the incidence of both symptomatic PE (from about 3% to 1%; odds ratio [OR] 0.39; 95% confidence interval [CI] 0.25-0.63) and DVT (from about 4% to 1%; OR 0.43; 95% CI 0.24-0.76). Compared to pharmacological prophylaxis alone, combined modalities significantly reduced the incidence of DVT (from 4.21% to 0.65%; OR 0.16; 95% CI 0.07-0.34). The studies were underpowered with regard to PE. The comparison of compression plus pharmacological prophylaxis versus compression plus aspirin showed a nonsignificant reduction in PE and DVT in favor of the former group. Repeat analysis restricted to the RCT confirmed the above findings. The additive role of mechanical and pharmacological modalities suggests that venous stasis and hypercoagulopathy are independent pathogenetic risk factors. The IPC reduces venous stasis by producing active flow enhancement and also increases tissue factor pathway inhibitor plasma levels. The results of the above meta-analyses endorse a recommendation that high-risk patients should receive multimodal prophylaxis. Although most patients who used combined modalities in the studies reviewed were considered to be at high risk of developing VTE, future studies on this topic should use the most recent and validated criteria to define the high-risk patient.

The Role of Neurosonology in the Diagnosis and Management of Patients with Carotid Artery Disease: A Review: Ultrasound in Carotid Artery Disease

Carotid artery disease (CAD) is a common cause of ischemic stroke with high rates of recurrence. Carotid endarterectomy (CEA) or carotid artery stenting (CAS) are highly recommended for the secondary prevention of symptomatic CAD during the first 14 days following the index event of transient ischemic attack or minor stroke. CEA or CAS may also be offered in selected cases with severe asymptomatic stenosis. Herein, we review the utility of neurosonology in the diagnosis and pre‐/peri‐interventional assessment of CAD patients who undergo carotid revascularization procedures. Carotid ultrasound may provide invaluable information on plaque echogenicity, ulceration, risk of thrombosis, and rupture. Transcranial Doppler or transcranial color‐coded sonography may further assist by mapping collateral circulation, evaluating the impairment of vasomotor reactivity, detecting microembolization, or reperfusion hemorrhage in real time. Neurosonology examinations are indispensable bedside tools assisting in the diagnosis, risk stratification, peri‐interventional monitoring, and follow‐up of patients with CAD.

Safety and efficacy of polyurethane vascular grafts for early hemodialysis access

Background: Arteriovenous grafts made of polyurethane (PU) have the advantage of early cannulation obviating the placement of a central vein catheter in patients with an acute need for long‐term hemodialysis. The aim of the present study was to evaluate the safety, efficacy and complication rate of PU vascular grafts for dialysis access in patients in whom early cannulation was performed. Methods: Between January 2007 and December 2015, 125 straight brachial‐axillary grafts were placed in patients with an acute thrombosis of a previous arteriovenous access. Sixty‐four were PU and 61 were polytetrafluoroethylene (PTFE) grafts. Patency and complications rates were compared between the two groups. Results: The median interval from implantation to cannulation was 1 day in the PU group vs 28 days in the PTFE group. Cumulative infection rate at 5 years was 13% and 8% in the PU and the PTFE groups, respectively (P = .6). None of the patients in the PU group developed a pseudoaneurysm necessitating intervention, compared with one patient in the PTFE group. Primary and secondary patency rates did not differ significantly between the two groups. The cumulative median primary patency was 23 months in the PU group vs 26 months in the PTFE group. Median secondary patency was 42 vs 33 months, respectively. Diabetes mellitus was the only factor adversely affecting graft patency in both groups. Conclusions: PU grafts offer the advantage of early cannulation with infection, pseudoaneurysm formation and patency rates similar to those of the PTFE grafts.

Inflammatory response following stent grafting for acute aortic syndrome

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