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• W2056540498 abstract "Antiphospholipid syndrome is a diagnosis with the clinical manifestations of thromboses in the presence of an antiphospholipid antibody. A 25-year-old man with a history of deep venous thrombosis, pulmonary emboli, and myocardial infarction, and receiving long-term anticoagulation with warfarin, all due to primary antiphospholipid syndrome, presented with blue toe syndrome from a primary superficial femoral artery thrombus. He was anticoagulated with fondaparinux in addition to dipyridamole and aspirin perioperatively. The area of thrombus was resected and reconstructed using a cephalic vein interposition graft. This report reviews antiphospholipid syndrome and identifies potential questions and problems relating to a rare clinical presentation. Antiphospholipid syndrome is a diagnosis with the clinical manifestations of thromboses in the presence of an antiphospholipid antibody. A 25-year-old man with a history of deep venous thrombosis, pulmonary emboli, and myocardial infarction, and receiving long-term anticoagulation with warfarin, all due to primary antiphospholipid syndrome, presented with blue toe syndrome from a primary superficial femoral artery thrombus. He was anticoagulated with fondaparinux in addition to dipyridamole and aspirin perioperatively. The area of thrombus was resected and reconstructed using a cephalic vein interposition graft. This report reviews antiphospholipid syndrome and identifies potential questions and problems relating to a rare clinical presentation. The association between antiphospholipid syndrome (APS) and hypercoagulability has been well described. Its definite diagnosis is made by the presence of (1) at least one type of antiphospholipid antibody and (2) the clinical manifestations of venous and arterial thromboses, recurrent fetal loss, or thrombocytopenia.1Miyakis S. Lockshin M.D. Atsumi T. Branch D.W. Brey R.L. Cervera R. et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost. 2006; 4: 295-306Crossref PubMed Scopus (4569) Google Scholar Although venous thromboses predominate, lower extremity arterial thromboses or thromboembolism, or both, are distinctly uncommon. In this report, we present a patient diagnosed with primary APS who had blue toe syndrome from a superficial femoral artery thrombotic source. A 25-year-old man, who did not smoke, presented to our vascular clinic with a 6-week history of painful left toe ulcers. His history included APS and heparin-induced thrombocytopenia (HIT), both diagnosed at another institution 8 years earlier after he had sustained a pulmonary embolism from bilateral lower extremity deep vein thrombosis (DVT). An inferior vena cava filter (IVCF) placement was deemed necessary at that time. There was no mention of failed anticoagulation therapy. Since then, postphlebitic syndrome with bilateral venous stasis ulcers had developed. He was also diagnosed with a myocardial infarction 1-year prior at another institution after complaining of chest pains and with elevated troponin levels. He was managed conservatively, with maintenance of anticoagulation with warfarin and aspirin. Records documented that his cardiac event was likely related to hypercoagulability. Review of his history showed that a definite diagnosis of APS was due to his documented thrombotic events and the presence of anticardiolipin immunoglobulin G (IgG) antibodies of 149 U glycopeptidolipid (reference range, ≥80 interpreted “high positive”). This was his second positive test result for anticardiolipin IgG antibody in several years. The results of the rest of his hypercoagulable workup, including factor V Leiden and prothrombin gene mutations, were normal. Levels of antithrombin III, protein C, and protein S levels were essentially not interpretable because all were drawn during an acute thrombotic event. Owing to his high risk of thrombosis if he were to stop taking warfarin, these levels were not repeated. His current medications included warfarin, aspirin, hydrochlorothiazide, and simvastatin. The physical examination noted bilateral lower extremity edema and anterior tibial ulcers relating to venous stasis (Fig 1, Left). The first and fifth toes on his left foot had distal ulcerations, and the third and fourth toes showed tender, flat, punctate bluish discolored lesions (Fig 1, Right). His pulse examination result was normal. Recent laboratory values showed normal results for complete blood cell count and chemistry profile. Coagulation studies showed an elevated prothrombin time, with an international normalized ratio (INR) of 2.5 and a partial thromboplastin time that was twice the control level. A cardiac echocardiogram showed distal hypokinesis of the left ventricle consistent with a previous myocardial infarction. There were no findings to suggest a cardiac thrombus. Computed tomography (CT) angiography of the chest, abdomen, and pelvis was unremarkable for arterial lesions but confirmed the presence of an IVCF and caval thrombosis distal to the filter. Left leg arterial duplex ultrasound imaging revealed velocities >400 cm/s at the midsuperficial femoral artery (SFA) level. These findings were used to establish a diagnosis of left blue toe syndrome from a likely SFA lesion, and surgical intervention was recommended. Five days before surgery, warfarin was stopped and fondaparinux injections, dipyridamole, and aspirin were started. Heparin-associated antibody detection by enzyme-linked immunosorbent assay was re-sent and results were negative. Intraoperatively, a left lower extremity angiogram demonstrated a 3-cm filling defect in the left mid-SFA (Fig 2). Surgical exposure of this area, after a single dose of heparin (5000 U), revealed gross periarterial inflammation and fibrosis. Its lumen showed intimal ulceration with a well-organized thrombus (Fig 3, Left). Resection and reconstruction using an end-to-end left cephalic vein interposition graft was then performed (Fig 3, Right). Histopathologic evaluation had shown an organized thrombus with recanalization and without evidence of atherosclerosis or vasculitis in the affected vessel wall (Fig 4).Fig 3Left, Intraoperative photograph shows the lumen of the left superficial femoral artery at its distal third demonstrating organized thrombus and periarterial fibrosis. No periarterial calcification or intimal thickening was evident upon surgical manipulation. Right, The photograph shows the final appearance of the cephalic vein interposition graft.View Large Image Figure ViewerDownload Hi-res image Download (PPT)Fig 4Histopathologic section of arterial vessel wall shows thrombus without evidence for atherosclerosis. Hemotoxylin and eosin staining, ×40 original magnification.View Large Image Figure ViewerDownload Hi-res image Download (PPT) Warfarin was restarted on the first postoperative day while maintaining fondaparinux, aspirin, and dipyridamole. The patient's platelet count remained normal throughout his hospital course. Before he was discharged on postoperative day 4, a repeat left thigh arterial duplex ultrasound scan revealed velocities of 158 cm/s, reflecting a patent graft. He was seen at 2 weeks, 1 month, and 3 months, in routine postoperative clinic evaluation with a patent graft and healed toe ulcers. Warfarin, dipyridamole, and aspirin therapy will be continued indefinitely. The patient was enrolled in a periodic graft surveillance program. The diagnosis of APS is based on the presence of antiphospholipid antibodies and the clinical manifestations of arterial or venous thrombosis, recurrent fetal loss, or thrombocytopenia.1Miyakis S. Lockshin M.D. Atsumi T. Branch D.W. Brey R.L. Cervera R. et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost. 2006; 4: 295-306Crossref PubMed Scopus (4569) Google Scholar The major antiphospholipid antibodies associated with APS include lupus anticoagulants, anticardiolipin antibodies, and antibodies to β2 glycoprotein-I.1Miyakis S. Lockshin M.D. Atsumi T. Branch D.W. Brey R.L. Cervera R. et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost. 2006; 4: 295-306Crossref PubMed Scopus (4569) Google Scholar, 2Asherson R.A. Khamashta M.A. Ordi-Ros J. Derksen R.H. Machin S.J. Barquinero J. et al.The “primary” antiphospholipid syndrome: major clinical and serological features.Medicine (Baltimore). 1989; 68: 366-374Crossref PubMed Scopus (955) Google Scholar, 3Brey R.L. Abbott R.D. Curb J.D. Sharp D.S. Ross G.W. Stallworth C.L. et al.beta(2)-Glycoprotein 1-dependent anticardiolipin antibodies and risk of ischemic stroke and myocardial infarction: the Honolulu heart program.Stroke. 2001; 32: 1701-1706Crossref PubMed Scopus (210) Google Scholar, 4Levine J.S. Branch D.W. Rauch J. The antiphospholipid syndrome.N Engl J Med. 2002; 346: 752-763Crossref PubMed Scopus (1273) Google Scholar, 5Insko E.K. Haskal Z.J. Antiphospholipid syndrome: patterns of life threatening and severe recurrent vascular complications.Radiology. 1997; 202: 319-326PubMed Google Scholar, 6Reber G. Tincani A. Sanmarco M. de Moerloose P. Boffa M.C. Proposals for the measurement of anti-beta2-glycoprotein I antibodies Standardization group of the European Forum on Antiphospholipid Antibodies.J Thromb Haemost. 2004; 2: 1860-1862Crossref PubMed Scopus (134) Google Scholar, 7Tincani A. Allegri F. Sanmarco M. Cinquini M. Taglietti M. Balsetrieri G. et al.Anticardiolipin antibody assay: a methodological analysis for a better consensus in routine determinations–a cooperative project of the European Antiphospholipid Forum.Thromb Haemost. 2001; 86: 575-583PubMed Google Scholar In a large series of 1000 APS patients, 15.2% had both venous and arterial thrombosis, with most the arterial vessels being cerebral.8Cervera R. Piette J.C. Font J. Khamashta M.A. Shoenfeld Y. Camps M.T. et al.Antiphospholipid syndrome: clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients.Arthritis Rheum. 2002; 46: 1019-1027Crossref PubMed Scopus (1497) Google Scholar In the Euro-Phospholipid Project, 4.3% of patients with APS cumulatively presented with arterial lower extremity thrombosis.8Cervera R. Piette J.C. Font J. Khamashta M.A. Shoenfeld Y. Camps M.T. et al.Antiphospholipid syndrome: clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients.Arthritis Rheum. 2002; 46: 1019-1027Crossref PubMed Scopus (1497) Google Scholar This study, however, did not differentiate atherosclerosis from thromboembolic events in APS patients. Therefore, the true incidence of primary arterial thrombosis affecting peripheral extremities in APS is unknown. Generally, the recommended first-line therapy for thrombosis includes the initiation of unfractionated or low-molecular-weight (LMW) heparin, with a transition to oral warfarin therapy.1Miyakis S. Lockshin M.D. Atsumi T. Branch D.W. Brey R.L. Cervera R. et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost. 2006; 4: 295-306Crossref PubMed Scopus (4569) Google Scholar, 9Crowther M.A. Ginsberg J.S. Julian J. Math M. Denburg J. Hirsh J. et al.A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.N Engl J Med. 2003; 349: 1133-1138Crossref PubMed Scopus (738) Google Scholar Strong clinical evidence supports this approach for the treatment of APS-associated venous thrombosis, yet there is weakness of data on primary or recurrent arterial events.10Lim W. Crowther M.A. Eikelboom J.W. Management of antiphospholipid antibody syndrome: a systematic review.JAMA. 2006; 295: 1050-1057Crossref PubMed Scopus (368) Google Scholar In contrast with cerebral ischemia in APS patients,11Sacco R.L. Adams R. Albers G. Alberts M.J. Benavente O. Furie K. et al.Guidelines for prevention of stroke in patients with ischemic stroke or transient ischemic attack: a statement for healthcare professionals from the American Heart Association/American Stroke Association Council on Stroke: co-sponsored by the Council on Cardiovascular Radiology and Intervention.Stroke. 2006; 37: 577-617Crossref PubMed Scopus (504) Google Scholar no specific clinical trials have been designed to evaluate the optimal therapy of noncerebral arterial thrombosis.1Miyakis S. Lockshin M.D. Atsumi T. Branch D.W. Brey R.L. Cervera R. et al.International consensus statement on an update of the classification criteria for definite antiphospholipid syndrome (APS).J Thromb Haemost. 2006; 4: 295-306Crossref PubMed Scopus (4569) Google Scholar, 10Lim W. Crowther M.A. Eikelboom J.W. Management of antiphospholipid antibody syndrome: a systematic review.JAMA. 2006; 295: 1050-1057Crossref PubMed Scopus (368) Google Scholar Furthermore, there is uncertainty with the optimal treatment for recurrent thromboembolic events, as in the case of our patient. This has been reported as high as 7% despite warfarin therapy.9Crowther M.A. Ginsberg J.S. Julian J. Math M. Denburg J. Hirsh J. et al.A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.N Engl J Med. 2003; 349: 1133-1138Crossref PubMed Scopus (738) Google Scholar Thrombocytopenia has been associated with APS. It is important clinically to differentiate patients with HIT and thrombocytopenia associated with APS. HIT patients with APS are a separate challenge that requires modifications in therapy. This can include other antithrombotic regimens such as synthetic hirudins, argatroban, and fondaparinux, which normally do not cross-react with HIT antibodies.12Holton S.G. Knox S.K. Tefferi A. Use of fondaparinux in a patient with antiphospholipid antibody syndrome and heparin-associated thrombocytopenia.J Thromb Haemost. 2006; 4: 1632-1634Crossref PubMed Scopus (19) Google Scholar, 13Parody R. Olive A. Souto J.C. Fontcuberta J. Fondaparinux (ARIXTRA) as an alternative anti-thrombotic prophylaxis when there is hypersensitivity to low molecular weight and unfractionated heparins.Haematologica. 2003; 88: ECR32PubMed Google Scholar, 14Kovacs M.J. Successful treatment of heparin induced thrombocytopenia (HIT) with fondaparinux.Thromb Haemost. 2005; 93: 999-1000PubMed Google Scholar Our patient presented a challenge of all three proportions. He presented acutely with an isolated peripheral arterial thrombotic lesion of unclear etiology, his thrombotic episode occurred while he was receiving warfarin therapy and aspirin, and he carried a diagnosis of HIT, which we needed to confirm. Once an embolic source was ruled unlikely, we can only hypothesize that the femoral lesion was a result of a local or a transient systemic inflammatory process related to his disease that led to endothelial dysfunction, complement and platelet activation, and ultimately, thrombus formation.15Mackworth-Young C.G. Antiphospholipid syndrome: multiple mechanisms.Clin Exp Immunol. 2004; 136: 393-401Crossref PubMed Scopus (92) Google Scholar, 16Giannakopoulos B. Passam F. Rahgozar S. Krilis S. Current concepts on the pathogenesis of the antiphospholipid syndrome.Blood. 2007; 109: 422-430Crossref PubMed Scopus (188) Google Scholar, 17Alexanderson E. Cruz P. Vargas A. Meave A. Ricalde A. Talayero J.A. et al.Endothelial dysfunction in patients with antiphospholipid syndrome assessed with positron emission tomography.J Nucl Cardiol. 2007; 14: 566-572Crossref PubMed Scopus (12) Google Scholar, 18Jy W. Tiede M. Bidot C.J. Horstman L.L. Jimenez J.J. Chirinos J. et al.Platelet activation rather than endothelial injury identifies risk of thrombosis in subjects positive for antiphospholipid antibodies.Thromb Res. 2007; 121: 319-325Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar This lesion subsequently caused distal arterial embolism culminating as blue toe syndrome and toe ulcerations. Thrombosis due to premature or accelerated atherosclerosis in setting of traditional risk factors (smoking, diabetes, hypertension, and hypercholesterolemia) have been documented in APS patients.19Christodoulou C. Sangle S. D'Cruz D.P. Vasculopathy and arterial stenotic lesions in the antiphospholipid syndrome.Rheum. 2007; 46: 907-910Crossref PubMed Scopus (28) Google Scholar, 20Shoenfeld Y. Gerli R. Doria A. Matsuura E. Cerinic M.M. Ronda N. et al.Accelerated atherosclerosis in autoimmune rheumatic diseases.Circ. 2005; 112: 3337-3347Crossref PubMed Scopus (449) Google Scholar, 21Vlachoyiannopoulos P.G. Samarkos M. Peripheral vascular disease in antiphospholipid syndrome.Thromb Res. 2004; 114: 509-519Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar Despite this view of vasculopathy in APS, our patient's histopathologic evaluation did not show evidence of atherosclerosis to support this concept. A recent randomized control trial, Antiphospholipid Antibody Acetylsalicylic Acid (APLASA),22Erkan D. Harrison M.J. Levy R. Peterson M. Petri M. Sammaritano L. et al.Aspirin for primary thrombosis prevention in the antiphospholipid syndrome: a randomized, double-blind, placebo-controlled trial in asymptomatic antiphospholipid antibody-positive individuals.Arthritis Rheum. 2007; 56: 2382-2391Crossref PubMed Scopus (286) Google Scholar showed that asymptomatic patients with antiphospholipid antibodies generally are not recommended aspirin to prevent thrombosis. In contrast, antiphospholipid antibody–positive patients with documented thromboses are recommended heparinization and managed long term with oral warfarin therapy to a targeted INR between 2 and 3.23Crowther M.A. Ginsberg J.S. Julian J. Denburg J. Hirsh J. Douketis J. et al.A comparison of two intensities of warfarin for the prevention of recurrent thrombosis in patients with the antiphospholipid antibody syndrome.N Engl J Med. 2003; 349: 1133-1138Crossref PubMed Scopus (432) Google Scholar, 24Finazzi G. Marchioli R. Brancaccio V. Schinoco P. Wisloff F. Musial J. et al.A randomized clinical trial of high-intensity warfarin vs. conventional antithrombotic therapy for the prevention of recurrent thrombosis in patients with the antiphospholipid syndrome (WAPS).J Thromb Haemost. 2005; 5: 848-853Crossref Scopus (438) Google Scholar The addition of an antiplatelet agent such as aspirin decreases platelet activity and may benefit APS patients with cardiac manifestations.25Zavaleta N.E. Montes R.M. Soto M.E. Vanzzini N.A. Amigo M.C. Primary antiphospholipid syndrome: a 5-year transesophageal echocardiographic followup study.J Rheumatol. 2004; 31: 2402-2407PubMed Google Scholar Operating on a patient with known primary APS without perioperative anticoagulation has been associated with a very high risk for graft thrombosis.26Nitecki S. Brenner B. Hoffman A. Lanir N. Schramek A. Torem S. Lower limb ischaemia in primary antiphospholipid syndrome.Eur J Vasc Surg. 1993; 7: 414-419Abstract Full Text PDF PubMed Scopus (23) Google Scholar Therefore, a strict perioperative anticoagulation regimen is paramount. We re-sent a heparin-associated antibody detection panel and proceeded with our surgical intervention by initiating fondaparinux in combination with aspirin and dipyridamole for additional antiplatelet activity. With a negative documentation for HIT, we are hopeful that this drastically opens this patient's options for potential future anticoagulation strategies. This can include adding LMW heparin to therapeutic warfarin if a rethrombosis were to occur.10Lim W. Crowther M.A. Eikelboom J.W. Management of antiphospholipid antibody syndrome: a systematic review.JAMA. 2006; 295: 1050-1057Crossref PubMed Scopus (368) Google Scholar To further aid in reducing the risk of graft failure, an autogenous conduit was our choice. The cephalic vein was selected because of the diseased leg veins from chronic venous hypertension and reflux as a result of caval and lower extremity venous thrombosis. The role for surgical intervention in primary APS of the lower extremity arteries is unclear. Asherson et al27Asherson R.A. Cervera R. Shoenfeld Y. Peripheral vascular occlusions leading to gangrene and amputations in antiphospholipid antibody positive patients.Ann N Y Acad Sci. 2007; 1108: 515-529Crossref PubMed Scopus (16) Google Scholar reported a collective experience of seven patients with primary APS involving the lower extremities where the outcomes were amputations. However, this report did not mention if perioperative anticoagulation was ever used or if previous limb salvage procedures were undertaken. The Table reports selected primary APS patients with lower extremity arterial thromboembolic manifestations.28Shortell C.K. Ouriel K. Green R.M. Condemi J.J. DeWeese J.A. Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis.J Vasc Surg. 1992; 15: 158-166Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar, 29Jicha D.L. Caty M.G. Lillehei C.W. Primary antiphospholipid syndrome in a child with lower extremity arterial thrombosis.J Ped Surg. 1994; 29: 1519-1520Abstract Full Text PDF PubMed Scopus (8) Google Scholar These interventions were associated with early failure rates thought to be largely due to the absence of perioperative anticoagulation. This observation was documented by Ahn et al,30Ahn S.S. Kalunian K. Rosove M. Moore W.S. Postoperative thrombotic complications in patients with the lupus anticoagulant: Increased risk after vascular procedures.J Vasc Surg. 1988; 7: 749-756PubMed Scopus (51) Google Scholar who noticed the rate of thrombosis correlated highly with lack of perioperative anticoagulants or antiplatelet agents in vascular procedures in patients with lupus anticoagulants.TableLower extremity arterial manifestations in primary antiphospholipid syndromeFirst author (year)Age/sexSymptomsSite on angiographyTreatmentPost-op Anticoagulation with warfarinOutcomeShortell (1992)28Shortell C.K. Ouriel K. Green R.M. Condemi J.J. DeWeese J.A. Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis.J Vasc Surg. 1992; 15: 158-166Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar48/FToe gangreneNot mentionedLumbar sympathectomyNoneTemporary improvement65/MToe gangreneFem-popFem-pop bypass graftNoneOccluded 2 monFem-pop graft revisionNoneOccluded 12 mon41/FLE gangreneFem-popFemoral endarterectomyNoneOccluded 6 mon, BKAIliofemoral bypassNoneOccluded 5 mon52/FBlue toesAortoiliacAortobifemoral bypassNoneThrombosed 24 hABF thrombectomyNonePatent at 1 mon27/MSevere claudicationBilateral poplitealBilateral fem-pop bypassNot mentionedThrombosedRevision fem-popPatent at 6 monNitecki (1993)26Nitecki S. Brenner B. Hoffman A. Lanir N. Schramek A. Torem S. Lower limb ischaemia in primary antiphospholipid syndrome.Eur J Vasc Surg. 1993; 7: 414-419Abstract Full Text PDF PubMed Scopus (23) Google Scholar19/FClaudication, ulcerNot mentionedConservative-pentoxifyllineNoneUlcer improved38/FClaudication, ulcerNot mentionedConservative-pentoxifyllineNoneUlcer healed38/MClaudication/gangreneNot mentionedFem-pop bypassNoneThrombosed 2 dJicha (1994)29Jicha D.L. Caty M.G. Lillehei C.W. Primary antiphospholipid syndrome in a child with lower extremity arterial thrombosis.J Ped Surg. 1994; 29: 1519-1520Abstract Full Text PDF PubMed Scopus (8) Google Scholar12/FToe necrosisCFA, SFA, ATAConservative-heparinWarfarinNo evidence recurrentThrombotic events; duration not mentionedABF, Aortobifemoral; ATA, anterior tibial artery; BKA, below knee amputation; CFA, common femoral artery; Fem-pop, femoropopliteal; LE, lower extremity; SFA, superficial femoral artery. Open table in a new tab ABF, Aortobifemoral; ATA, anterior tibial artery; BKA, below knee amputation; CFA, common femoral artery; Fem-pop, femoropopliteal; LE, lower extremity; SFA, superficial femoral artery. Other studies of lower extremity bypass operations have been reported in patients with antiphospholipid antibodies. Lee et al31Lee R.W. Taylor Jr, L.M. Landry G.J. Goodnight S.H. Moneta G.L. Edwards J.M. et al.Prospective comparison of infrainguinal bypass grafting in patients with and without antiphospholipid antibodies.J Vasc Surg. 1996; 24: 524-531Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar reported no differences in graft patency, limb salvage, and patient survival rates for patients with or without antiphospholipid antibodies undergoing elective infrainguinal bypass grafting. Lam et al32Lam E.Y. Taylor Jr, L.M. Landry G.J. Porter J.M. Moneta G.L. Relationship between antiphospholipid antibodies and progression of lower extremity arterial occlusive disease after lower extremity bypass operations.J Vasc Surg. 2001; 33: 976-982Abstract Full Text Full Text PDF PubMed Scopus (34) Google Scholar showed that patients with antiphospholipid antibodies who underwent lower extremity bypass operations will likely have progression of atherosclerosis. However, these articles did not report whether these patients with positive antibodies had primary or secondary antiphospholipid syndrome.21Vlachoyiannopoulos P.G. Samarkos M. Peripheral vascular disease in antiphospholipid syndrome.Thromb Res. 2004; 114: 509-519Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar We cannot find any scientific evidence in the form of clinical trials for optimal medical or surgical therapy, or both, for APS patients who present with nonatherosclerotic thromboembolic events in lower extremity arteries. In our opinion, if an operation is unavoidable, perioperative and long-term anticoagulation is essential. We recognize that sometimes it is difficult to differentiate an embolus from primary thrombosis, especially in absence of classic findings of atherosclerotic disease and cardiac arrhythmia. Our conclusion for APS thrombosis was supported by our in situ evaluation of the grossly abnormal vessel and the pathologist's final description and conclusion. The femoral thrombus was adherent to the vessel wall and recanalization had occurred to suggest it was chronic. Our negative cardiac source workup and angiographic imaging further suggests primary thrombosis. The occluded IVCF also makes it unlikely for a lower extremity DVT paradoxic embolic event to have occurred. To our knowledge, our report represents a rare case of distal embolization caused by isolated SFA thrombosis in a patient diagnosed with primary APS. Antiphospholipid syndrome is a coagulation disorder that often leads to thrombosis. Primary peripheral arterial thrombosis is rare in APS. Patients can present with severe acute limb ischemia or in a subtler manner with microemboli and blue toe syndrome. With an aggressive anticoagulation regimen, arterial reconstruction seems to be safe and feasible. Studies are needed to establish optimal anticoagulation regimens for recurrent thromboses while patients are receiving warfarin therapy. Furthermore, studies are needed to define optimal medical and surgical therapy for primary thrombosis of peripheral arterial vessels associated with APS." @default.
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• W2056540498 title "Superficial femoral artery thrombosis as a cause for distal embolism in primary antiphospholipid syndrome" @default.
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