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• W1976260077 abstract "In 1977, Macfarlane [1Macfarlane R.G. Introduction.Br Med Bull. 1977; 33: 183-5Crossref Scopus (20) Google Scholar] proposed that ‘thrombosis is hemostasis in the wrong place’, and since then pathological studies, clinical studies, and meta‐analyses of randomized trials of antiplatelet, anticoagulant and thrombolytic drugs have supported this hypothesis by showing that platelet‐fibrin hemostatic plugs are the pathophysiological basis for both arterial and venous thrombosis. However, medical textbooks, and guidelines for prescribing drugs, continue to consider arterial and venous thrombosis as separate diseases, with different pathology, pathophysiology, epidemiology and treatments. For example, in the current British National Formulary (March 2006) [2British Medical Association and the Royal Pharmaceutical Society of Great BritainBritish National Formulary. BMJ Publishing Group and RPS Publishing, 2006: 119-28Google Scholar], Section 2.8 (Anticoagulants) starts: ‘The main use of anticoagulants is to prevent thrombus formation or extension of an existing thrombosis in the slower‐moving venous side of the circulation, where the thrombus consists of a fibrin web enmeshed with platelets and red cells… Anticoagulants are of less use in preventing thrombus formation in arteries, for in faster flowing vessels thrombi are composed mainly of platelets with little fibrin.’ This statement ignores the strong evidence base for fibrin‐rich thrombi in acute coronary syndromes, and the efficacy of anticoagulants in primary prevention of coronary heart disease (CHD) and in treatment of acute coronary syndromes [3Harrington R.A. Becker R.C. Ezekowitz M. Meade T.W. O'Connor C.M. Vorchheimer D.A. Guyatt G.H. Antithrombotic therapy for coronary artery disease.Chest. 2004; 126: 513s-548sAbstract Full Text Full Text PDF PubMed Scopus (213) Google Scholar] or in secondary prevention of arterial events [4Hirsh J. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines.Chest. 2004; 126: 1s-703sPubMed Google Scholar]. Likewise, Section 2.9 (Antiplatelet drugs) starts: ‘Antiplatelet drugs decrease platelet aggregation and may inhibit thrombus formation in the arterial circulation, where anticoagulants have little effect.’ This section ignores the evidence for platelet activation and platelet rich thrombi in the initial stages of deep vein thrombosis (DVT) [5Hume M. Sevitt S Thomas DP Venous Thrombosis and Pulmonary Embolism. Harvard University Press, 1970: 25-53Google Scholar], and the proven efficacy of aspirin in prevention of venous thromboembolism (VTE), for example following orthopedic surgery [6Pulmonary Embolism Prevention [PEP] Trial Collaborative GroupPrevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: Pulmonary Embolism Prevention [PEP] Trial.Lancet. 2000; 355: 1295-302Abstract Full Text Full Text PDF PubMed Scopus (935) Google Scholar], or in prevention of venous as well as arterial events in persons with clinically‐evident arterial disease [7Antithrombotic Trialists’ CollaborationCollaborative meta‐analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high‐risk patients.BMJ. 2002; 324: 71-86Crossref PubMed Google Scholar]. Now the epidemiologists are entering the debate on the associations between arterial disease and venous thrombosis: why has it taken them so long? For 50 years, cardiovascular epidemiology has concentrated on CHD, neglecting stroke, peripheral arterial disease (PAD), and VTE, each of which causes substantial morbidity and mortality. In aging populations, CHD now accounts for a minority of clinical cardiovascular events [8Rothwell P.M. Coull A.J. Silver L.E. Fairhead J.F. Giles M.F. Lovelock C.E. Redgrave J.N.E. Bull L.M. Welch S.J.V. Cuthbertson F.C. Binney L.E. Crutnikov S.A. Anslow P. Banning A.P. Mantz D. Mehta Z. for the Oxford Vascular StudyPopulation‐based study of event rate, incidence, case fatality, and mortality for all acute vascular events in all arterial territories (Oxford Vascular Study).Lancet. 2005; 366: 1773-83Abstract Full Text Full Text PDF PubMed Scopus (782) Google Scholar], and at last there is increasing interest in the epidemiology of VTE [9Rosendaal F.R. Venous thrombosis: a multicausal disease.Lancet. 1999; 353: 1167-73Abstract Full Text Full Text PDF PubMed Scopus (1349) Google Scholar, 10Heit J.A. Venous thromboembolism: disease burden, outcomes and risk factors.J Thromb Haemost. 2005; 3: 1611-8Abstract Full Text Full Text PDF PubMed Scopus (352) Google Scholar] as well as stroke and PAD. As a consequence, there are increasing numbers of reports on the association between arterial disease (or its risk factors) and VTE, including some ‘positive’ [11Ageno W. Prandoni P. Romualdi E. Shirarduzzi A. Dentali F. Pesavento R. Crowther M. Venco A. The metabolic syndrome and the risk of venous thrombosis. A case control study.J Thromb Haemost. 2006; 4: 1914-8Abstract Full Text Full Text PDF PubMed Scopus (143) Google Scholar, 12Squizzato A. Romualdi E. Ageno W. Why should statins prevent venous thromboembolism (VTE)? A systematic literature search and a call for action.J Thromb Haemost. 2006; 4: 1925-7Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar, 13Eliasson A. Bergqvist D. Björck M. Acosta S. Sternby N.H. Ögren M. Prevalence and risk of venous thrombembolism in patients with verified arterial thrombosis. A population study based on 23 796 consecutive autopsies.J Thromb Haemost. 2006; 4: 1897-1902Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, 14Prandoni P. Ghirarduzzi A. Prins M.H. Pengo V. Davidson B.L. Sorensen H. Pesavento R. Iotti M. Casiglia E. Iliceto S. Pagnan A. Lensing A.W.A. Venous thromboembolism and the risk of subsequent symptomatic atherosclerosis.J Thromb Haemost. 2006; 4: 1891-6Abstract Full Text Full Text PDF PubMed Scopus (145) Google Scholar] and some ‘negative’ [15Reich L.M. Folsom A.R. Key N.S. Boland L.L. Heckbert S.R. Rosamond W.D. Cushman M. Prospective study of subclinical atherosclerosis and venous thromboembolism.J Thromb Haemost. 2006; 4: 1909-13Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar, 16Van Der Hagen P.B. Folsom A.R. Jenny N.S. Heckbert S.R. O'Meara E.S. Reich L.M. Rosendaal F.R. Cushman M. Subclinical atherosclerosis and the risk of future venous thrombosis in the Cardiovascular Health Study.J Thromb Haemost. 2006; 4: 1903-8Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar] reports in this issue. To make sense of such ‘conflicting’ reports, and to interpret the clinical significance of these findings, it is important to consider the associations of VTE with three stages of the development of arterial disease: risk factors, subclinical disease, and clinical disease. Conversely, we need to consider the risk of arterial events (as well as recurrent VTE) in patients with established VTE, when advising on long‐term antithrombotic prophylaxis. Arterial disease and VTE share several common risk factors, including age, obesity, estrogens (pregnancy, combined oral contraceptives, oral hormone replacement therapy), acute infections, and genetic factors including non‐O ABO blood group and certain thrombophilias [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar]. One potential common pathophysiological substrate for these associations is activation of hemostasis [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar] and this hypothesis is supported by the efficacy of antiplatelet and anticoagulant drugs in prophylaxis of both arterial disease and VTE [3Harrington R.A. Becker R.C. Ezekowitz M. Meade T.W. O'Connor C.M. Vorchheimer D.A. Guyatt G.H. Antithrombotic therapy for coronary artery disease.Chest. 2004; 126: 513s-548sAbstract Full Text Full Text PDF PubMed Scopus (213) Google Scholar, 4Hirsh J. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy: Evidence Based Guidelines.Chest. 2004; 126: 1s-703sPubMed Google Scholar, 6Pulmonary Embolism Prevention [PEP] Trial Collaborative GroupPrevention of pulmonary embolism and deep vein thrombosis with low dose aspirin: Pulmonary Embolism Prevention [PEP] Trial.Lancet. 2000; 355: 1295-302Abstract Full Text Full Text PDF PubMed Scopus (935) Google Scholar, 7Antithrombotic Trialists’ CollaborationCollaborative meta‐analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high‐risk patients.BMJ. 2002; 324: 71-86Crossref PubMed Google Scholar]. Ageno et al. [11Ageno W. Prandoni P. Romualdi E. Shirarduzzi A. Dentali F. Pesavento R. Crowther M. Venco A. The metabolic syndrome and the risk of venous thrombosis. A case control study.J Thromb Haemost. 2006; 4: 1914-8Abstract Full Text Full Text PDF PubMed Scopus (143) Google Scholar] report a case–control study of the associations of the metabolic syndrome with idiopathic DVT, secondary DVT, and controls. They observed an association of metabolic syndrome with idiopathic DVT (but not secondary DVT), despite similar body mass index (BMI) in these groups. They acknowledge the continuing controversy on the definition of the metabolic syndrome, and on whether its association with CHD is greater than that of its individual components. The authors report that waist circumference, serum triglycerides [and low‐density lipoprotein (LDL) cholesterol on univariate analysis only] showed associations with DVT, and discuss the possibility that prothrombotic effects of abdominal adipocytes and dyslipidemia [e.g. increased factor (F) VII and plasminogen activation inhibitor type 1 (PAI‐1)] might promote venous, as well as arterial, thrombosis. However, meta‐analyses of studies of plasma levels and functional genetic polymorphisms for FVII and PAI‐1 do not show clearly significant independent associations with CHD or VTE [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar]. Further studies (and meta‐analyses of such studies) are required to establish, with confidence, the associations (independent of BMI, high‐density lipoprotein cholesterol, and each other) of waist circumference and serum triglyceride with both arterial events and VTE. LDL cholesterol is an established independent risk factor for CHD, and the Cholesterol Trialists’ Collaboration has established that reduction in LDL cholesterol by statins is associated with proportional reductions in risks of CHD, stroke, and cardiovascular mortality [18Cholesterol Trialists’ CollaborationEfficacy and safety of cholesterol‐lowering treatment: prospective meta‐analysis of data from 90 056 participants in 14 randomised trials of statins.Lancet. 2005; 366: 1267-78Abstract Full Text Full Text PDF PubMed Scopus (5736) Google Scholar]. Squizzato et al. [12Squizzato A. Romualdi E. Ageno W. Why should statins prevent venous thromboembolism (VTE)? A systematic literature search and a call for action.J Thromb Haemost. 2006; 4: 1925-7Abstract Full Text Full Text PDF PubMed Scopus (28) Google Scholar] report that observational studies suggest an association of statin use with reduced risk of VTE, and suggest that statins might have antithrombotic effects. However, their hypothesis that statins might reduce the risk of VTE requires evaluation in randomized controlled trials and meta‐analyses of these [18Cholesterol Trialists’ CollaborationEfficacy and safety of cholesterol‐lowering treatment: prospective meta‐analysis of data from 90 056 participants in 14 randomised trials of statins.Lancet. 2005; 366: 1267-78Abstract Full Text Full Text PDF PubMed Scopus (5736) Google Scholar]. In the PROSPER study of older patients (at highest risk of VTE) [19Prosper Study GroupPravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial.Lancet. 2002; 360: 1623-30Abstract Full Text Full Text PDF PubMed Scopus (2977) Google Scholar] and the statin effect is currently under study. How should these reports influence clinical practice? Not at all, at present. Obesity is already established as a risk factor for arterial disease, VTE and many other diseases, and all obese patients should be encouraged to lose weight, whether or not they have arterial disease, VTE, other obesity‐related disorders, or none of these. Worldwide, evidence‐based clinical practice guidelines now agree that statins should be considered as part of cardiovascular prevention in all persons at increased risk (all those with clinical evidence of arterial disease, and those with > 20% risk of CHD or stroke over the next 10 years). Prescription of cheap, generic statins will facilitate implementation of such guidance and lead to clinical benefit worldwide. Whether or not patients with VTE, who do not fulfill the above criteria, will benefit from statin therapy requires further evidence from meta‐analyses of randomized trials. Subclinical evidence of arterial disease may be obtained from electrocardiography (ECG), coronary artery calcification on computed tomography (CT), or magnetic resonance imaging (MRI) for CHD; the ankle brachial pressure index (ABPI) for PAD; or carotid arterial ultrasound [intima‐medial thickness (IMT), plaque, or stenosis]. Recent reports from the Atherosclerosis Risk in Communities (ARIC) study (carotid IMT) [15Reich L.M. Folsom A.R. Key N.S. Boland L.L. Heckbert S.R. Rosamond W.D. Cushman M. Prospective study of subclinical atherosclerosis and venous thromboembolism.J Thromb Haemost. 2006; 4: 1909-13Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar], and the Cardiovascular Health Study (CHS) (carotid IMT and plaque, ABPI; ECG) [16Van Der Hagen P.B. Folsom A.R. Jenny N.S. Heckbert S.R. O'Meara E.S. Reich L.M. Rosendaal F.R. Cushman M. Subclinical atherosclerosis and the risk of future venous thrombosis in the Cardiovascular Health Study.J Thromb Haemost. 2006; 4: 1903-8Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar] show no association of subclinical arterial disease with incident VTE on multivariate analyses including cardiovascular risk factors. These results from two large, prospective studies of incident VTE are in contrast to the previous report of Prandoni et al. [20Prandoni P. Bilova F. Marchiori A. Bernardi E. Petrobelli F. Lensing A.W.A. Prins M.H. Girolami A. An association between atherosclerosis and venous thrombosis.N Engl J Med. 2003; 348: 1435-41Crossref PubMed Scopus (539) Google Scholar] in a case–control study that patients with previous, idiopathic VTE had a higher risk of carotid plaques; possibly due to the well‐established risk of confounding bias in such case–control studies. Confounding may, in part, occur from mutual risk factors for arterial disease and VTE, as discussed above. How should these reports influence clinical practice? Not at all, at present. Screening for subclinical arterial disease has not been established as a cost‐effective addition to prediction and primary prevention of cardiovascular disease from conventional risk scores (which are usually based on age, sex, smoking habit, diabetes, blood pressure, and the ratio of total to HDL cholesterol). Likewise, there is no evidence to support such screening in patients with established clinical VTE. Patients with clinical arterial disease, at least in the acute phase, are at increased risk of VTE. As discussed above, patients with ‘chronic’ clinical arterial disease frequently have established risk factors for VTE (e.g. age, obesity and possibly other components of the metabolic syndrome, and genetic factors including non‐O ABO blood groups and certain thrombophilias). In particular, patients with PAD have a high risk of VTE, especially when immobilized, for example with critical limb ischemia (CLI), or when undergoing surgery for CLI or repair of abdominal aortic aneurysm [21Andreani D. Bell P. Bollinger A. Breddin K. Cumberland D. Dormandy J. Fagrell B. Krone W. Lowe G. Natali J. Stock G. Verstraete M. Viver Manresa E. European Working Group on Critical Leg Ischaemia Organising CommitteeSecond European Consensus document on chronic critical leg ischaemia.Circulation. 1991; 84: 1-26PubMed Google Scholar]. Reduced arterial blood flow to the lower limb may promote venous stasis [21Andreani D. Bell P. Bollinger A. Breddin K. Cumberland D. Dormandy J. Fagrell B. Krone W. Lowe G. Natali J. Stock G. Verstraete M. Viver Manresa E. European Working Group on Critical Leg Ischaemia Organising CommitteeSecond European Consensus document on chronic critical leg ischaemia.Circulation. 1991; 84: 1-26PubMed Google Scholar]. All such patients should receive antithrombotic prophylaxis [21Andreani D. Bell P. Bollinger A. Breddin K. Cumberland D. Dormandy J. Fagrell B. Krone W. Lowe G. Natali J. Stock G. Verstraete M. Viver Manresa E. European Working Group on Critical Leg Ischaemia Organising CommitteeSecond European Consensus document on chronic critical leg ischaemia.Circulation. 1991; 84: 1-26PubMed Google Scholar]. VTE was a common complication of acute myocardial infarction (AMI) in the era before thrombolysis or percutaneous coronary intervention (PCI) became established treatments in evolving AMI, and is now less common since the introduction of routine thrombolysis/PCI, antiplatelet therapy (aspirin/clopidogrel/GP IIb/IIIa inhibitors) anticoagulant therapy (heparins, fondaparinux), and early mobilization and hospital discharge [3Harrington R.A. Becker R.C. Ezekowitz M. Meade T.W. O'Connor C.M. Vorchheimer D.A. Guyatt G.H. Antithrombotic therapy for coronary artery disease.Chest. 2004; 126: 513s-548sAbstract Full Text Full Text PDF PubMed Scopus (213) Google Scholar]. VTE following acute stroke may be reduced by heparins in selected cases, or graduated compression stockings [22Albers G.W. Amarenco P. Easton J.D. Sacco R.L. Teal P. Antithrombotic and thrombolytic therapy for ischemic stroke.Chest. 2004; 126: 483s-512sAbstract Full Text Full Text PDF PubMed Scopus (477) Google Scholar]. Eliasson et al. [13Eliasson A. Bergqvist D. Björck M. Acosta S. Sternby N.H. Ögren M. Prevalence and risk of venous thrombembolism in patients with verified arterial thrombosis. A population study based on 23 796 consecutive autopsies.J Thromb Haemost. 2006; 4: 1897-1902Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar] report a large autopsy study of the risk of VTE and arterial thrombosis. Patients with cervico‐cranial thrombosis (at risk of stroke) or PAD had an increased risk of VTE, whereas coronary thrombosis showed a negative association with risk of VTE (possibly as a competing cause of death). This study supports the routine use of antithrombotic therapy in patients with clinical stroke or PAD, as prophylaxis of both recurrent arterial thrombi and VTE. This is usually aspirin in the chronic phase [7Antithrombotic Trialists’ CollaborationCollaborative meta‐analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high‐risk patients.BMJ. 2002; 324: 71-86Crossref PubMed Google Scholar], and additional measures in the acute phase as outlined in the previous paragraph. Prandoni et al. [14Prandoni P. Ghirarduzzi A. Prins M.H. Pengo V. Davidson B.L. Sorensen H. Pesavento R. Iotti M. Casiglia E. Iliceto S. Pagnan A. Lensing A.W.A. Venous thromboembolism and the risk of subsequent symptomatic atherosclerosis.J Thromb Haemost. 2006; 4: 1891-6Abstract Full Text Full Text PDF PubMed Scopus (145) Google Scholar] report a prospective study of symptomatic arterial events following a first episode of VTE. Those with idiopathic VTE had a 60% higher risk of arterial events than those with VTE secondary to known risk factors for VTE, after adjusting for age and other risk factors for arterial events (sex, smoking habit, hyperlipidemia, hypertension, obesity, diabetes, and previous symptomatic arterial disease). The authors suggest that this association may result from arterial events and idiopathic VTE sharing common risk factors, which might include a prothrombotic state. In support of this hypothesis, epidemiological studies have shown that the two most common genetic thrombophilias (the FV Leiden mutation and the prothrombin G20210A mutation) are associated with risk of CHD as well as VTE [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar, 23Ye Z. Liu E.H.C. Higgins J.P.T. Keavney B.D. Lowe G.D.O. Collins R. Danesh J. Seven haemostatic gene polymorphisms in coronary disease: meta‐analysis of 66 155 cases and 91 307 controls.Lancet. 2006; 367: 651-8Abstract Full Text Full Text PDF PubMed Scopus (353) Google Scholar], as is their common phenotype, resistance to activated protein C [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar, 24Smith A. Patterson C. Yarnell J. Rumley A. Ben‐Shlomo Y. Lowe G. Which hemostatic markers add to the predictive value of conventional risk factors for coronary heart disease and ischemic stroke? The Caerphilly Study.Circulation. 2005; 112: 3080-7Crossref PubMed Scopus (206) Google Scholar]. Epidemiological studies have also shown that fibrin D‐dimer, a marker of cross‐linked fibrin turnover, is also associated with risk of arterial as well as venous thrombotic events [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar, 25Lowe G.D.O. Fibrin D‐dimer and risk of cardiovascular events.Semin Vasc Med. 2005; 5: 387-98Crossref PubMed Scopus (53) Google Scholar]. How should these reports influence clinical practice? Patients with VTE should be evaluated for risk of all cardiovascular events when considering long‐term antithrombotic prophylaxis. Thrombophilia screening is not clinically useful in prediction of either arterial or venous thrombotic events, and D‐dimer is still under evaluation for such purposes [17Lowe G.D.O. Can haematological tests predict cardiovascular risk? The 2005 Kettle Lecture.Br J Haematol. 2006; 133: 232-50Crossref PubMed Scopus (76) Google Scholar, 25Lowe G.D.O. Fibrin D‐dimer and risk of cardiovascular events.Semin Vasc Med. 2005; 5: 387-98Crossref PubMed Scopus (53) Google Scholar]. When oral anticoagulants are discontinued following an episode of VTE, aspirin should be considered for those with a risk of CHD or stroke above 2% per year, for prophylaxis of recurrent VTE as well as arterial events [7Antithrombotic Trialists’ CollaborationCollaborative meta‐analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high‐risk patients.BMJ. 2002; 324: 71-86Crossref PubMed Google Scholar, 26Antithrombotic Therapy. A National Guideline. Scottish Intercollegiate Guidelines Network (SIGN), 1999http://www.sign.ac.ukGoogle Scholar]. Further studies of risk of arterial, as well as venous, events following a first episode of VTE should be performed; randomized trials of antiplatelet agents after discontinuation of oral anticoagulants following VTE are currently in progress [27Hovens M.M.C. Snoep J.D. Tamsma J.T. Huisman M.V. Aspirin in the prevention and treatment of venous thromboembolism.J Thromb Haemost. 2006; 4: 1470-5Abstract Full Text Full Text PDF PubMed Scopus (70) Google Scholar]. The authors state that they have no conflict of interest." @default.
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• W1976260077 title "Arterial disease and venous thrombosis: are they related, and if so, what should we do about it?" @default.
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