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24 Januari 2009 Peripheral Vascular Disease  A non-invasive perspective AZHARI  GANI
 
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[object Object],[object Object],[object Object],[object Object],[object Object],Schroll M, J Chr Dis 1981 Sukhija R, Am J Cardiol 2003
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[object Object],[object Object],Vesey J, Health Care Strategic Mx 2003
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Meluzin et al Eur J Echo 2003
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[object Object],[object Object],[object Object],Neumeyer M, Hershey Med Dept
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1 Cohen AT. Presented at the 5th Annual Congress of the European Federation of Internal Medicine; 2005. 2 Eurostat statistics on health and safety 2001.  Available from: http://epp.eurostat.cec.eu.int. ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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GRIP- VTE  SURVEY
1 Geerts WH, et al. Chest. 2004;126:338S-400S.  2 Leizorovicz A, et al.  Circulation. 2004;110(24 Suppl 1):IV13-9.   (%) 17 20 50 50 0 10 20 30 40 50 60 Internal medicine General surgery Acute ischemic stroke Orthopedic surgery Prevalence of VTE is High ,[object Object]
[object Object],[object Object],[object Object],70% Medical 30% Surgical Inpatient VTE, %  Adapted from: Diebold J, Lohrs U.  Pathol Res Pract . 1991;187:260-266. 5,039 Hospitalized Patients
VTE  mostly Undiagnosed Less than half of all cases  of  fatal PE  are detected  prior to death  1 Approximately 80% of DVT  are clinically silent  2,3 1. Goldhaber SZ, et al.  American Journal of Medicine  1982;73:822-826. 2. Lethen H, et al.  American Journal of Cardiology  1997;80:1066-1069. 3. Sandler DA, et al.  J. Royal Soc. Med.  1989; 82:203-205. 20  % 80  %
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],The Acute  i ll ness  Hospitalized medical Patients frequency of VTE  “   in the absence of prophylaxis “
MECHANISME VTE  IN HEART FAILURE
Venous stasis (I mmobilization)  Vascular lesion  (surgical, trauma, inflammation) Hypercoagulability. (Deficiency of Protein C, Protein S, AT III) Rudolf Ludwig Karl Virchow  (1821-1902) "Father of Pathology”   Thrombogenesis
Chest  2002;122;1440-1456
Lopez, J. A. et al. Hematology 2004;2004:439-456 Model for venous thrombosis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Venous thrombosis: Stasis leads to the development of a thrombus composed of red cells and fibrin Slow, turbulent blood flow in valve cusps result in areas of local stasis Prandoni P,  et al.   Haematologica  1997;  82 :423–428.
Venous thrombosis: Deep vein thrombosis Thrombus growth results in proximal progression along the vein Pulmonary embolism Damage to veins (PTS) Prandoni P,  et al.   Haematologica  1997;  82 :423–428.
 
Adapted from Sevitt S. The structure and growth of valve-pocket thrombi in femoral veins. J Clin Pathol. 1974;27:517-28
[object Object],[object Object],[object Object],[object Object],MANY PHYSICIANS UNREGCONIZED VTE
P U L M O N A R Y  E M B O L I S M S A S Y M P T O M A T I C 80-90% 10-20% V T E C  H  F V T E S Y M P T O M A T I C
Practice guidelines ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],*LDUH: UFH 5,000 U SC BID or TID 1. Albers GW, et al. Chest. 2008;133:71-109 2. Nicolaides AN.  Int Angiol,  2001; 20: 1-37
PRIME 1   86%   UFH 5000 IU tid   Enoxaparin 40 mg od THE-PRINCE 2   19%   UFH 5000 IU tid   Enoxaparin 40 mg od Hillbom, et al 3   43%   UFH 5000 IU tid   Enoxaparin 40 mg od 1.4 0.2 Trial  RRR Thromboprophylaxis Patients with VTE (%) 10.4 8.4 34.7 19.7 1 Lechler E,  et al.  Haemostasis.   1996;26 Suppl  2:49-56. 2 Kleber FX, et al.  Am Heart J.  2003;145:614-21. 3 Hillbom M, et al.  Acta Neurol Scand.  2002;106:84-92. P  < 0.001 for equivalence P  = 0.015 for equivalence P  = 0.044 LMWH vs UFH tid = three times daily.
Safety end point Aes = adverse event; ALAT=Alanine aminotransferase; ASAT= aspartate aminotransferase *>5 cm diameter at injection site  
CONSENSUS RECOMMENDATIONS IN  ACUTE HEART FAILURE Consensus body Subcutaneous UFH LMWH + Recommendation grade** ACCP Consensus Statement 5 Recommendation 1 A International Union of Angiology* Subcutaneous UFH High dose LMWH + A * Recommendations are for medical patients with disease-related and/or additional  patient-related risk factors + Enoxaparin (40 mg once-daily) is the only low molecular weight heparin licensed  for the prevention of venous thromboembolism in hospitalised, acutely ill patients  with heart failure NYHA Class III/IV **Grade of recommendation based on scientifically sound clinical trials in which the  results are clear cut
VTE risk and ACCP prophylaxis use in medical patients with 6 key diagnoses Medical patients (%) Bergmann J-F, et al. XXIII  World Congress of the I UA. June 2008;Athens, Greece.
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Pad slide

  • 1. 24 Januari 2009 Peripheral Vascular Disease A non-invasive perspective AZHARI GANI
  • 2.  
  • 3.
  • 4.
  • 5.
  • 6.
  • 7.
  • 8.
  • 9.
  • 10.
  • 11.
  • 12.  
  • 13.
  • 14. Meluzin et al Eur J Echo 2003
  • 15.
  • 16.  
  • 17.  
  • 18.  
  • 19.  
  • 20.  
  • 21.
  • 22.
  • 23.
  • 24.
  • 25.
  • 26. GRIP- VTE SURVEY
  • 27.
  • 28.
  • 29. VTE mostly Undiagnosed Less than half of all cases of fatal PE are detected prior to death 1 Approximately 80% of DVT are clinically silent 2,3 1. Goldhaber SZ, et al. American Journal of Medicine 1982;73:822-826. 2. Lethen H, et al. American Journal of Cardiology 1997;80:1066-1069. 3. Sandler DA, et al. J. Royal Soc. Med. 1989; 82:203-205. 20 % 80 %
  • 30.
  • 31. MECHANISME VTE IN HEART FAILURE
  • 32. Venous stasis (I mmobilization) Vascular lesion (surgical, trauma, inflammation) Hypercoagulability. (Deficiency of Protein C, Protein S, AT III) Rudolf Ludwig Karl Virchow (1821-1902) &quot;Father of Pathology” Thrombogenesis
  • 34.
  • 35. Venous thrombosis: Stasis leads to the development of a thrombus composed of red cells and fibrin Slow, turbulent blood flow in valve cusps result in areas of local stasis Prandoni P, et al. Haematologica 1997; 82 :423–428.
  • 36. Venous thrombosis: Deep vein thrombosis Thrombus growth results in proximal progression along the vein Pulmonary embolism Damage to veins (PTS) Prandoni P, et al. Haematologica 1997; 82 :423–428.
  • 37.  
  • 38. Adapted from Sevitt S. The structure and growth of valve-pocket thrombi in femoral veins. J Clin Pathol. 1974;27:517-28
  • 39.
  • 40. P U L M O N A R Y E M B O L I S M S A S Y M P T O M A T I C 80-90% 10-20% V T E C H F V T E S Y M P T O M A T I C
  • 41.
  • 42. PRIME 1 86% UFH 5000 IU tid Enoxaparin 40 mg od THE-PRINCE 2 19% UFH 5000 IU tid Enoxaparin 40 mg od Hillbom, et al 3 43% UFH 5000 IU tid Enoxaparin 40 mg od 1.4 0.2 Trial RRR Thromboprophylaxis Patients with VTE (%) 10.4 8.4 34.7 19.7 1 Lechler E, et al. Haemostasis. 1996;26 Suppl 2:49-56. 2 Kleber FX, et al. Am Heart J. 2003;145:614-21. 3 Hillbom M, et al. Acta Neurol Scand. 2002;106:84-92. P < 0.001 for equivalence P = 0.015 for equivalence P = 0.044 LMWH vs UFH tid = three times daily.
  • 43. Safety end point Aes = adverse event; ALAT=Alanine aminotransferase; ASAT= aspartate aminotransferase *>5 cm diameter at injection site  
  • 44. CONSENSUS RECOMMENDATIONS IN ACUTE HEART FAILURE Consensus body Subcutaneous UFH LMWH + Recommendation grade** ACCP Consensus Statement 5 Recommendation 1 A International Union of Angiology* Subcutaneous UFH High dose LMWH + A * Recommendations are for medical patients with disease-related and/or additional patient-related risk factors + Enoxaparin (40 mg once-daily) is the only low molecular weight heparin licensed for the prevention of venous thromboembolism in hospitalised, acutely ill patients with heart failure NYHA Class III/IV **Grade of recommendation based on scientifically sound clinical trials in which the results are clear cut
  • 45. VTE risk and ACCP prophylaxis use in medical patients with 6 key diagnoses Medical patients (%) Bergmann J-F, et al. XXIII World Congress of the I UA. June 2008;Athens, Greece.
  • 46.

Notes de l'éditeur

  1. The Worcester DVT Study, conducted at 16 short-stay hospitals in Worcester, Massachusetts, examined the incidence and fatality rates of VTE in hospitalized patients. In this study, there were a total of 615 recognized episodes of VTE, yielding an annual incidence of 107 per 100,000. The authors note that extrapolating these data to the United States as a whole would yield approximately 260,000 total cases per year. 1 The International Cooperative Pulmonary Embolism Registry (ICOPER) analyzed prospective cohort data to determine mortality and recurrence rates for pulmonary embolism (PE). 2 The investigators found that even though one third of the patients in the registry were receiving prophylaxis, PE still occurred with a high mortality rate. The rate of occurrence of PE may be higher than reported because many cases are diagnosed only upon autopsy and because some studies that report prevalence of DVT do not include patients in long-term care facilities, where the rates may be even higher. Because of these events, fatal PE may be one of the most common preventable causes of death among hospitalized patients. 3 Postthrombotic syndrome (PTS) is a chronic condition consisting of leg pain, edema, venous ectasia, and skin induration and ulceration that often occurs after an episode of DVT. 4 In a prospective, long-term follow-up of DVT patients, symptomatic DVT was a risk factor for recurrence, which may persist for many years. 5 PTS was found to occur in nearly one third of the patient population and to be strongly associated with recurrent ipsilateral DVT. From this evaluation, it was suggested that the time course of thromboprophylaxis in DVT patients should be extended. Reasons for underutilizing thromboprophylaxis include the belief that it is not necessary due to the lowered incidence of VTE over the past decades, concerns about bleeding complications, and misconceptions about the magnitude of the problem due to the often silent nature of VTE. 6 References 1. Anderson FA et al. A population-based perspective of the hospital incidence and case-fatality rates of deep vein thrombosis and pulmonary embolism. Arch Intern Med . 1991;151:933-938. 2. Goldhaber SZ et al. Acute pulmonary embolism: clinical outcomes in the International Cooperative Pulmonary Embolism Registry (ICOPER) . Lancet . 1999;353:1386-1389. 3. Clagett GP et al. Prevention of venous thromboembolism. Chest . 1995;108(suppl):312S-334S. 4. Kahn SR et al. Effect of postthrombotic syndrome on health-related quality of life after deep venous thrombosis. Arch Int Med . 2002;162:1144-1148. 5. Prandoni P et al. The clinical course of deep-vein thrombosis. Prospective long-term follow-up of 528 symptomatic patients. Haematologica . 1997;82:423-428. 6. Geerts WH et al. Prevention of venous thromboembolism. Chest . 2001;119(suppl):132S-175S.
  2. There is a very strong association between pulmonary embolism (PE) and deep vein thrombosis (DVT) in the legs: • 90% of pulmonary emboli are the result of DVT 1 • DVT is the most common concomitant disorder found objectively in more than half of all PE patients. 2 A recent study showed that 82% of patients with acute PE had detectable DVT at the time PE was diagnosed 3 • Asymptomatic PE occurs in more than 50% of patients with symptomatic proximal DVT, in more than 35% of patients with asymptomatic proximal DVT and in around 7–8% of patients with asymptomatic distal DVT 4 • Many of the known risk factors for venous thromboembolic disease (VTE) – recent surgery, immobility, cancer, trauma and hypercoagulability – are also often found in patients with PE. 5,6 1–2% of patients with DVT die as a result of acute PE. 7 PE accounts for a significant proportion of all deaths. In the USA, for example, 600,000 people develop PE each year and 60,000 die as a result. 8 75% of these deaths occur during the initial hospital admission: detection of VTE at an earlier stage would allow more deaths to be prevented. 1 Perrier A, et al. Arch. Int. Med. 1996; 156 :531–536. 2 Pesavento R, et al . Minerva Cardioangiol. 1997; 45 : 369–375. 3 Girard P, et al. Chest 1999; 116 :903–908. 4 Partsch H, et al. J. Vasc. Surg. 1996; 24 :774–782. 5 Goldhaber SZ, et al. Lancet 1999; 353 :1386–1389. 6 Stein PD, et al. Chest 1999: 116 :909–913. 7 Hirsch J. et al. Circulation 1996; 93 :2212–2245. 8 Rosendaal FR. Lancet 1999; 353 :1167–1173
  3. Both the American College of Chest Physicians (ACCP) guidelines and an International Consensus Statement recommend the use of thromboprophylaxis for general medical patients with risk factors for VTE. The International Consensus Group specifies that low-molecular-weight heparin (LMWH) is preferred for patients with chronic respiratory disease or CHF. References: Geerts WH, Heit JA, Clagett GP, et al. Prevention of venous thromboembolism. Chest . 2001;119:132S – 175S. Nicolaides AN. Prevention of venous thromboembolism. International Consensus Statement. Guidelines compiled in accordance with the scientific evidence. Int Angiol . 2001;20:1 – 37.