<\/a><\/p>\n
<\/p>\n
To the Editor:<\/em> In his review of the management of venous thromboembolism(Dec. 12 issue),1<\/span><\/sup><\/a> Ginsberg failed to mention the role of echocardiographyin the diagnosis of this disorder. Despite the importance ofventilation\u2013perfusion lung scanning, it has its limitations.It usually necessitates the transfer of the patient, who maybe acutely dyspneic, to the radiology department and occasionallyto a different hospital. On the other hand, echocardiography,whether transthoracic or transesophageal, is widely available,carries a minimal risk or none, and can help in making the diagnosisat the bedside. In the absence of chronic pulmonary disease,echocardiographic features that suggest pulmonary embolism includea dilated hypokinetic right ventricle and the presence of tricuspidregurgitation with increased velocity, suggesting an elevationof the pulmonary arterial systolic pressure. The absence ofleft ventricular dysfunction helps rule out the cardiac diseaseas a cause of acute dyspnea. Visualization of a right atrialthrombus confirms the diagnosis.2<\/span><\/sup><\/a><\/p>\nBedside echocardiography is a practical diagnostic procedurethat in some patients eliminates the need for further studies.<\/p>\nBassem S. Ibrahim, M.R.C.P.\nNational Heart Institute<\/em>\nCairo, Egypt<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGinsberg JS. Management of venous thromboembolism. N Engl J Med 1996;335:1816-1828.[Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Kuyk M, Mols P, Englert M. Right atrial thrombus leading to pulmonary embolism. Br Heart J 1984;51:462-464.[Abstract]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We think Ginsberg failed to emphasize the importanceof recurrent embolism. All patients with pulmonary embolismare at risk for further embolism, and therefore, diagnosingpulmonary embolism is not enough. Instead, every patient shouldbe evaluated for residual large thrombi, from the poplitealvein to the vena cava, by Doppler ultrasonography or venography.Patients with large residual thrombi may die from recurrentembolism, whereas patients without thrombi will not. Whetherthrombolytic therapy prevents recurrent embolism is unknown.Vena caval filters are effective in preventing pulmonary embolism.1<\/span><\/sup><\/a>Placement of a vena caval filter may be the pivotal step toprevent death \u2014 by preventing further embolism in patientswith pulmonary embolism who have residual venous thrombi.<\/p>\nChristoph Pechlaner, M.D.\nThomas Buratti, M.D.\nMichael Joannidis,M.D.\nInnsbruck University Hospital<\/em>\nA-6020 Innsbruck, Austria<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
Bedside echocardiography is a practical diagnostic procedurethat in some patients eliminates the need for further studies.<\/p>\n
Bassem S. Ibrahim, M.R.C.P.\nNational Heart Institute<\/em>\nCairo, Egypt<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGinsberg JS. Management of venous thromboembolism. N Engl J Med 1996;335:1816-1828.[Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Kuyk M, Mols P, Englert M. Right atrial thrombus leading to pulmonary embolism. Br Heart J 1984;51:462-464.[Abstract]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We think Ginsberg failed to emphasize the importanceof recurrent embolism. All patients with pulmonary embolismare at risk for further embolism, and therefore, diagnosingpulmonary embolism is not enough. Instead, every patient shouldbe evaluated for residual large thrombi, from the poplitealvein to the vena cava, by Doppler ultrasonography or venography.Patients with large residual thrombi may die from recurrentembolism, whereas patients without thrombi will not. Whetherthrombolytic therapy prevents recurrent embolism is unknown.Vena caval filters are effective in preventing pulmonary embolism.1<\/span><\/sup><\/a>Placement of a vena caval filter may be the pivotal step toprevent death \u2014 by preventing further embolism in patientswith pulmonary embolism who have residual venous thrombi.<\/p>\nChristoph Pechlaner, M.D.\nThomas Buratti, M.D.\nMichael Joannidis,M.D.\nInnsbruck University Hospital<\/em>\nA-6020 Innsbruck, Austria<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
References<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGinsberg JS. Management of venous thromboembolism. N Engl J Med 1996;335:1816-1828.[Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Kuyk M, Mols P, Englert M. Right atrial thrombus leading to pulmonary embolism. Br Heart J 1984;51:462-464.[Abstract]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We think Ginsberg failed to emphasize the importanceof recurrent embolism. All patients with pulmonary embolismare at risk for further embolism, and therefore, diagnosingpulmonary embolism is not enough. Instead, every patient shouldbe evaluated for residual large thrombi, from the poplitealvein to the vena cava, by Doppler ultrasonography or venography.Patients with large residual thrombi may die from recurrentembolism, whereas patients without thrombi will not. Whetherthrombolytic therapy prevents recurrent embolism is unknown.Vena caval filters are effective in preventing pulmonary embolism.1<\/span><\/sup><\/a>Placement of a vena caval filter may be the pivotal step toprevent death \u2014 by preventing further embolism in patientswith pulmonary embolism who have residual venous thrombi.<\/p>\nChristoph Pechlaner, M.D.\nThomas Buratti, M.D.\nMichael Joannidis,M.D.\nInnsbruck University Hospital<\/em>\nA-6020 Innsbruck, Austria<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
<\/a><\/p>\n\nGinsberg JS. Management of venous thromboembolism. N Engl J Med 1996;335:1816-1828.[Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Kuyk M, Mols P, Englert M. Right atrial thrombus leading to pulmonary embolism. Br Heart J 1984;51:462-464.[Abstract]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We think Ginsberg failed to emphasize the importanceof recurrent embolism. All patients with pulmonary embolismare at risk for further embolism, and therefore, diagnosingpulmonary embolism is not enough. Instead, every patient shouldbe evaluated for residual large thrombi, from the poplitealvein to the vena cava, by Doppler ultrasonography or venography.Patients with large residual thrombi may die from recurrentembolism, whereas patients without thrombi will not. Whetherthrombolytic therapy prevents recurrent embolism is unknown.Vena caval filters are effective in preventing pulmonary embolism.1<\/span><\/sup><\/a>Placement of a vena caval filter may be the pivotal step toprevent death \u2014 by preventing further embolism in patientswith pulmonary embolism who have residual venous thrombi.<\/p>\nChristoph Pechlaner, M.D.\nThomas Buratti, M.D.\nMichael Joannidis,M.D.\nInnsbruck University Hospital<\/em>\nA-6020 Innsbruck, Austria<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
To the Editor:<\/em> We think Ginsberg failed to emphasize the importanceof recurrent embolism. All patients with pulmonary embolismare at risk for further embolism, and therefore, diagnosingpulmonary embolism is not enough. Instead, every patient shouldbe evaluated for residual large thrombi, from the poplitealvein to the vena cava, by Doppler ultrasonography or venography.Patients with large residual thrombi may die from recurrentembolism, whereas patients without thrombi will not. Whetherthrombolytic therapy prevents recurrent embolism is unknown.Vena caval filters are effective in preventing pulmonary embolism.1<\/span><\/sup><\/a>Placement of a vena caval filter may be the pivotal step toprevent death \u2014 by preventing further embolism in patientswith pulmonary embolism who have residual venous thrombi.<\/p>\nChristoph Pechlaner, M.D.\nThomas Buratti, M.D.\nMichael Joannidis,M.D.\nInnsbruck University Hospital<\/em>\nA-6020 Innsbruck, Austria<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
Christoph Pechlaner, M.D.\nThomas Buratti, M.D.\nMichael Joannidis,M.D.\nInnsbruck University Hospital<\/em>\nA-6020 Innsbruck, Austria<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
References<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
<\/a><\/p>\n\nGreenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996;9:50-58.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nTo the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
To the Editor:<\/em> We agree with Ginsberg that the duration of anticoagulanttherapy in patients who have venous thromboembolism should bedetermined by balancing the risks of continuing therapy againstthe risk of recurrent thrombosis and the complications of therapy.He points out that there are no data to assist us in makingdecisions about the use of anticoagulation therapy in asymptomaticcarriers of a thrombophilic defect (i.e., anticoagulation treatmentrestricted to high-risk situations vs. life-long prophylaxis)or in these same patients after a first thrombotic event (i.e.,treatment for three to six months vs. life-long treatment).However, there is evidence that overall mortality in familieswith antithrombin deficiency and protein C deficiency does notdiffer from that in the general population.1<\/span><\/sup><\/a>,<\/sup>2<\/span><\/sup><\/a> The mortalityrates in these families were calculated back into the previouscentury, before thrombophilia was recognized and before anticoagulationtherapy existed. These results also hold true for the most severetype of thrombophilia, type I antithrombin deficiency.3<\/span><\/sup><\/a><\/p>\nAlthough these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
Although these results are general and cannot guide managementin the case of patients with recurrent thrombosis or familiesthat appear to be extremely prone to thrombosis, they are reassuringand do not support the use of prophylactic anticoagulation solelyon the basis of the presence of the biochemical defect, especiallyin the light of the known risks of the therapy (a 1 to 3 percentrisk of major hemorrhage per year and a 0.3 to 0.6 percent riskof fatal hemorrhage per year).4<\/span><\/sup><\/a>,<\/sup>5<\/span><\/sup><\/a><\/p>\nOn the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\nFrits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
On the basis of these retrospective data, we believe that asymptomaticpatients with heritable thrombophilia should not receive anticoagulantagents except in situations in which the risk of thrombosisis increased \u2014 for example, after surgery and during immobilization.<\/p>\n
Frits R. Rosendaal, M.D.\nFelix J.M. van der Meer, M.D.\nJan P.Vandenbroucke, M.D.\nUniversity Hospital Leiden<\/em>\nNL-2300 RC Leiden,the Netherlands<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
References<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
<\/a><\/p>\n\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a> <\/a><\/li>\nAllaart CF, Rosendaal FR, Noteboom WMP, Vandenbroucke JP, Briet E. Survival in families with hereditary protein C deficiency, 1820 to 1993. BMJ 1995;311:910-913.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan Boven HH, Olds RJ, Thein S-L, et al. Hereditary antithrombin deficiency: heterogeneity of the molecular basis and mortality in Dutch families. Blood 1994;84:4209-4213.[Abstract\/Full\u00a0Text]<\/span><\/a> <\/a><\/li>\nvan der Meer FJM, Rosendaal FR, Vandenbroucke JP, Briet E. Assessment of a bleeding risk index in two cohorts of patients treated with oral anticoagulants. Thromb Haemost 1996;76:12-16.[Medline]<\/span><\/a> <\/a><\/li>\nPalareti G, Leali N, Coccheri S, et al. Bleeding complications of oral anticoagulant treatment: an inception-cohort, prospective collaborative study (ISCOAT). Lancet 1996;348:423-428.[CrossRef]<\/span><\/a>[Medline]<\/span><\/a><\/li>\n<\/ol>\n\nDr. Ginsberg replies:<\/p>\nTo the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
Dr. Ginsberg replies:<\/p>\n
To the Editor:<\/em> Ibrahim suggests that echocardiography is a practicalprocedure that eliminates the need for further studies in somepatients with suspected pulmonary embolism. In a patient withsuspected pulmonary embolism and a clear-cut right atrial thrombus,a diagnosis of pulmonary embolism can be made. However, thefrequency of this finding is probably very low, since the sourceof pulmonary embolism in most patients is leg-vein thrombosis.1<\/span><\/sup><\/a>Although in the absence of chronic pulmonary disease, a dilated,hypokinetic right ventricle with or without tricuspid insufficiencymay be diagnostic of pulmonary embolism, the accuracy of thisfinding has not been established. Overall, the clinical utilityof echocardiography in the evaluation of patients with suspectedpulmonary embolism is not known. Furthermore, clinicians shouldnot be distracted from performing tests that have a clear-cututility in diagnosing pulmonary embolism, such as lung scanning,venous ultrasonography, or pulmonary angiography.<\/p>\nPechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\nI agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
Pechlaner and colleagues suggest that all patients with establishedpulmonary embolism should undergo extensive evaluation to determinethe presence (and extent) of deep-vein thrombosis, with theplacement of a vena caval filter if large residual thrombi arepresent. Such an approach is costly and associated with sideeffects (of venography, cavography, and insertion of the filter)and in view of the clear-cut efficacy of anticoagulant therapy,cannot be justified. Although some experts recommend insertionof a filter in patients with free-floating thrombi, the necessityfor this measure (above and beyond anticoagulant therapy) hasnever been demonstrated.<\/p>\n
I agree with Rosendaal and colleagues that routine anticoagulanttherapy is not indicated in asymptomatic patients with thrombophilia,2<\/span><\/sup><\/a>but the data are retrospective, and a small but clinically importantincrease in mortality in these patients cannot be ruled out.Furthermore, although mortality is the most important complicationof venous thromboembolism, there is substantial associated morbidity(the post-thrombotic syndrome and chronic thromboembolic pulmonaryhypertension), which may be reduced by long-term anticoagulanttherapy.<\/p>\nJeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
Jeffrey S. Ginsberg, M.D.\nMcMaster University<\/em>\nHamilton, ON L8N3Z5, Canada<\/em><\/p>\nReferences<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
References<\/strong><\/span><\/p>\n <\/p>\n<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
<\/a><\/p>\n\nHull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983;98:891-899.[Medline]<\/span><\/a> <\/a><\/li>\nRosendaal FR, Heijboer H, Briet E, et al. Mortality in hereditary antithrombin-III deficiency: 1830 to 1989. Lancet 1991;337:260-262.[Medline]<\/span><\/a><\/li>\n<\/ol>\n\n <\/p>\n <\/p>\n\n\n\n<\/td>\n\n\n\n\n\n\n<\/td>\n<\/tr>\n\n\n\n\n\n<\/td>\n<\/tr>\n\n<\/td>\nAdd to Personal Archive<\/a><\/strong><\/span><\/td>\n<\/tr>\n\n<\/span><\/td>\n
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