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Inflamatia in TVPInflamatia in TVP
Alexandru Andritoiu, MD
Sp. Militar Craiova
Tromboza venoasa profunda (TVP)Tromboza venoasa profunda (TVP)
• Provocata
• Neprovocata
• Proximala
• Distala
COMPLICATII
EP
Deces
Recurenta TVP/EP
Sindrom post-trombotic
Ulcer venos
Vene profunde
Flux sanguin
normal
TVP Embol
Kahn S. Blood 2009; 114: 4624-4631. Kahn S. Blood review 2002. 16: 155-165.
TVP vs TromboflebitaTVP vs Tromboflebita
Flebitele
Tromboflebita superficialaTromboflebita superficiala
• trombus endovenos +
inflamatie adiacenta in vv
superficiale
TVPTVP
• trombus in vv profunde
• adesea nu asociaza
inflamatie (manifesta
clinic)
Tromboflebita superficialaTromboflebita superficiala
• Varice hidrostatice
• Semne cutanate inflamatorii
• Tratament cu AINS (topice)
Boala trombo-embolicaBoala trombo-embolica
Boala trombo-embolica
• TVP
• EP • Morbiditate
• Mortalitate
• Impact economic
Subiecte propuseSubiecte propuse
1) Mecanismele inflamatorii in TVP acuta
2) Bolile inflamatorii si riscul TVP
3) Cum putem combate inflamatia in TVP?
4) Inflamatia si rezolutia trombusului
5) Sdr. post-trombotic si inflamatia
??
1) Mecanismele inflamatorii in TVP acuta
2) Bolile inflamatorii si riscul TVP
3) Cum putem combate inflamatia in TVP?
4) Inflamatia si rezolutia trombusului
5) Sdr. post-trombotic si inflamatia
Prakash Saha et al. Arterioscler Thromb Vasc Biol. 2011;31:506-512
(1) Activation of the endothelium (EC; red cell) generates intravascular danger signals, which guide
leukocytes to areas of inflammation and induces TF production. (2) Upregulation of adhesion
molecules on endothelium mediate PMN recruitment, and TF generates thrombin, activating platelet
(Plt) deposition and converting fibrinogen to cross-linked fibrin (Fb) that entraps the main RBC
mass.
Inflamatia si trombogeneza venoasa
Arterioscler Thromb Vasc Biol. 2011;31:506-512
TVP acutaTVP acuta
• PMN (+++)
• Rol in remodelarea peretelui venos
Cascada aderarii leucocitareCascada aderarii leucocitare
in raspunsul inflamatorin raspunsul inflamator
D. Neil Granger and Elena Senchenkovaş 2010 by Morgan & Claypool Life Sciences.
ImmediatImmediat dupa injuriadupa injuria endotelialendoteliala, celulelea, celulele endotelialendotelialee sisi plaplachetele suntchetele sunt
activateactivate,, declansanddeclansand expresiexpresiaa moleculemoleculelor de adeziune celularalor de adeziune celulara
Thomas W. Wakefield et al. Arterioscler Thromb Vasc Biol. 2008;28:387-391
Rolul microparticulelorRolul microparticulelor
Thomas W. Wakefield et al. Arterioscler Thromb Vasc Biol. 2008;28:387-391
Levels of P-selectin have been found to be elevated
in DVT patients, and are decreased with heparin
treatment
Biomarker levels of soluble P-selectin, and D-dimer
in an algorithm to diagnose DVT:
Sensitivity 73%
Specificity 81%
TVP idiopatica este in relatie cu raspunsulTVP idiopatica este in relatie cu raspunsul
inflamator sistemic si cresterea nivelelor serice aleinflamator sistemic si cresterea nivelelor serice ale
markerilor circulatori ai disfunctiei endotelialemarkerilor circulatori ai disfunctiei endoteliale
• 49 pts. TVP primara
• Markeri de inflamatie:
• high sensitive C-reactive protein (hs CRP),
• IL-6, IL-8,TNF-a,
• Markeri ai disfunctiei endoteliale
• von Willebrand factor (vWF)
• P-selectin
• vascular adhesion molecule (VCAM-1)
Jezovnik M. K. , Poredos P. International Angiology 2010;29: (3):226-31
CONCLUSION: Patients with idiopathic venous thrombosis have increased levels of circulating markers of
inflammation and blood markers of endothelial dysfunction. Higher levels of both groups of markers indicate that
patients in the stable phase of the disease have an increased systemic inflammatory response. The
interrelationship between inflammatory markers and markers of endothelial dysfunction favour the hypothesis that
inflammation could be involved in the etiopathogenesis of idiopathic venous thrombosis.
J Vasc Surgery 2002;35:701-706
Clinical Chemistry 2015:61:2:3013-316
Predictori ai TVP
• FR
• IL-6
• IL-8
• CRP
Whether these markers may be useful in
the diagnosis of VTE is as yet uncertain
International Journal of General Medicine 2015:8 37–40
Relatia dintre volumul trombusului siRelatia dintre volumul trombusului si
testele inflamatoriitestele inflamatorii
• TVP v. poplitee
• TVP vv musculare
gambiere
• Markeri inflam (+)
• Risc scazut de SPT
• TVP ileo-femurala
• TVP femuro-poplitee
• Markeri inflam (+++)
• Risc major de SPT
Markerii inflamatori,Markerii inflamatori,
D-dimerii si riscul de TVPD-dimerii si riscul de TVP
recurentarecurenta
Concluzii:
• Nivelele crescute de CRP si D-dimeri
cresc riscul recurentei TVP, in timp ce
nivelele crescute de citokine
proinflamatorii, NU!
• Pts cu nivele crescute simultat de CRP si
D-dimeri au cel mai mare risc de
recutenta a TVP.
Roshani S, et al. Leiden Thrombophilia Study LETS (2012)
????
1) Mecanismele inflamatorii in TVP acuta
2) Bolile inflamatorii si riscul TVP
3) Cum putem combate inflamatia in TVP?
4) Inflamatia si rezolutia trombusului
5) Sdr. post-trombotic si inflamatia
TVP si bolile inflamatorii croniceTVP si bolile inflamatorii cronice
• Boli de sistem (colagenoze): PR, LES
• Neoplazii
• IBD (RCUH, b. Chron)
• Sepsis
• Boala Behçet
• Vasculite autoimune
• Arterita Takayasu
• Sdr. antifosfolipidic
• TAO
Pts cu IBD au un risc de TVP de 2-3 x mai mare decat populatia generala
Cercul vicios inflamatie-coagulareCercul vicios inflamatie-coagulare
??????
1) Mecanismele inflamatorii in TVP acuta
2) Bolile inflamatorii si riscul TVP
3) Cum putem combate inflamatia in TVP?
4) Inflamatia si rezolutia trombusului
5) Sdr. post-trombotic si inflamatia
Putem combate inflamatiaPutem combate inflamatia
din TVP ?din TVP ?
• heparine
• statine
• sulodexid
• IL-10 (in studiu)
• AINS (doar in tromboflebita superficiala)
• inhiba activarea si aderarea celulelor
inflamatorii (leucocite)
• reduce productia de citokine
• inhiba degradarea mastocitelor si
eliberarea de histamina
• protejeaza celulele endoteliale de
actiunea citotoxica
• inhiba prod de heparinaza de catre
plachete
• previne aderarea neutrofilelor la cel.
endoteliale
• Astm bronsic
• SCA
• CABPG
• Chir. Cataractei
• IBD
,,considering heparins as the main stay treatment of ACS, its effects are more
pronounced as anticoagulating than as an anti-inflammatory agent in this
pathological condition”.
Adv Pharmacol Sci. 2015
• Mastocitele tisulare sunt singura sursa
de heparina endogena care poate fi
implicata in controlul raspunsului
inflamator.
• Heparina inhiba influxul neutrofilelor la
locul inflamatiei, cat si adeziunea
leucocitelor in venulele post-capilare.
Lipidele circulante in exces:
• Efect protrombotic
• Cresc productia de trombina
• Activare plachetara
• Disfunctie endoteliala
Statinele reduc riscul de TVP independent de nivelul colesterolului seric
Rosuvastatin – 43%Rosuvastatin – 43%
• In studiul JUPITER (Justification for
the Use of Statins in Prevention: an
Intervention Trial Evaluating
Rosuvastatin), rosuvastatin 20 mg a
redus rata cazurilor noi de TEV cu
43% la o populatie sanatoasa cu
markeri de inflamatie cronica
sistemica documentata prin cresterea
concentratiei de CRP (2 mg/dL).
Kones R. Drug Design, Development and Therapy 2010
Molecula CRP
Rodriguez A et al. Thromb Thrombolysis. 2012 May ; 33(4): 371–382
Mecanisme propuse in reducerea riscului de TVP la pts
tratati cu statine:
• scaderea PAI-1
• cresterea expresiei tPA,
• scaderea agregarii plachetare,
• cresterea expresiei trombomodulinei
Efectul concret al Rosuvastatinei nu se cunoaste!
Pe langa efectul anti-trombotic/anti-inflamator, statinele
nu au risc de sangerare-posibila terapie asociata in TVP
Statinele reduc riscul de TVPStatinele reduc riscul de TVP
PLOS ONE | DOI:10.1371/journal.pone.0116621 February 13, 2015
Mannello F, Medda V, Ligi D, Raffetto JD (2013) Glycosaminoglycan sulodexide inhibition of mmp-9 gelatinase secretion and
activity: possible pharmacological role against collagen degradation in vascular chronic diseases. Curr Vasc Pharmacol
2013;11:354-365
Mannello F. Modulation of matrix metalloproteinases and cytokines by glycosaminoglycan sulodexide in macrophage-like cells:
possible role and treatment in chronic venous diseases. XVII World Meeting of the International Union of Phlebology.
SDX-proprietati anti-inflamatoriiSDX-proprietati anti-inflamatorii
SDX-PEV SDX p.o.
+/- or TRIFLUSAL
• IL-10 prezenta in
exces in peretele
venos ca raspuns la
tromboza venoasa
• adm. de IL-10 a
scazut volumul
trombusului
Journal of Imunology, 1998;161:1471-1476
Circulation. 2001;103:1718-1720
????????
1) Mecanismele inflamatorii in TVP acuta
2) Bolile inflamatorii si riscul TVP
3) Cum putem combate inflamatia in TVP?
4) Inflamatia si rezolutia trombusului
5) Sdr. post-trombotic si inflamatia
Rezolutia trombusuluiRezolutia trombusului
Pattern-uri diferite:
• periferic
• central (tunelizare)
• tip cavernos
(multilocular)
• Predomina macrofagele
• IL-8 rol chemotactic
• MMPs 2 si 9
• Urokinase activity (+++)
• VEGF (+++)
• IL-1alfa
• IL-2
• Lf-niciun rol!
Procesul de baza: NEOVASCULARIZATIE PERIADVENTICIALA HIPOXIC-INDUSA
The dynamics of recanalization are
characterized by distal-to-proximal
extension and in the first 6 months are
significantly influenced by thrombosis
etiology
Puskas A. Int Angiol 2007(26);1:53-63
• Organizarea si recanalizarea trombusului este
rezultatul unui proces “outside-in”outside-in” cu celulelecu celulele
inflamatorii patrunzand in interiorulinflamatorii patrunzand in interiorul
trombusului via peretele venostrombusului via peretele venos.
• Hipoxia relativa din interiorul trombusului
poate repreyenta un stimul ptr formarea de
vase de neoformatie deyvoltate din peretele
venos inspre trombus, care, impreuna cu
retractia trombusului, conduce la
recanalizarea venei si reaparitia fluxului
sanguin venos.
Arterioscler Thromb Vasc Biol. 2010;30:2443-2451
Rolul leucocitelor in rezolutia trombusului
Prakash Saha et al. Arterioscler Thromb Vasc Biol. 2011;31:506-512
VEGF expression in the naturally resolving mouse thrombusVEGF expression in the naturally resolving mouse thrombus
Colin Edward Evans et al. Arterioscler Thromb Vasc Biol. 2010;30:2443-2451
Etapa imediata post-tromboza se caracterizeaza prin tromboliza
fiziologica dependenta de prezenta leucocitelor (NTR) care lucreaza
intr-un mediu proinflamator generat de citokine
Thomas W. Wakefield et al. Arterioscler Thromb Vasc Biol. 2008;28:387-391
• Statinele au proprietatti anti-inflamatorii, pro-
angiogenice and pro-fibrinolitice care pot influenta
favorabil recanalizarea si organizarea trombusului.
• Atorvastatina amplifica rata recanalizarii si inhiba
inflamatia de la nivelul peretelui venos, cat si fibroza.
Int J Surg 2012;(10):8:S4
??????????
1) Mecanismele inflamatorii in TVP acuta
2) Bolile inflamatorii si riscul TVP
3) Cum putem combate inflamatia in TVP?
4) Inflamatia si rezolutia trombusului
5) Sdr. post-trombotic si inflamatia
Factorii majori de prognostic ai SPT:
• tromboza reziduala
• reflux in v. femurala si popitee
Estimate la 3 luni dupa TVP acuta
Journal of Thrombosis and Haemostasis, 11: 795–805
Sindromul post-tromboticSindromul post-trombotic
Colectia Dr. A. Andritoiu
Case-Report 1Case-Report 1
TVP ilio-femuralaTVP ilio-femurala
S. Mirel, 42 aniS. Mirel, 42 ani
• TVP idiopatica stg.
• Ileo-Fem-Pop
• CT
• VSH 71 mm/h
• CRP 7.7 mg/dL
• Fibrinogen 622 mg/dL
• Leuc 10.200/mmc
• Fara semne de
inflamatie locala
Case-Report 2Case-Report 2
TVP v. popliteeTVP v. poplitee
N. Simona, 32 ani
• TVP acuta
(idiopatica)-10 z
• V poplitee stg.
• CDUS
• VSH 30 mm/h
• Fibrinogen 202 mg/dL
• CRP 1.1 mg/dL
• Leuc 8.300/mmc
In care caz riscul aparitiei SPTIn care caz riscul aparitiei SPT
este mai mare?este mai mare?
Raspuns corect: Cazul 1Raspuns corect: Cazul 1
Argumente:
• Localizare proximala
• Volum mare al trombusului
• TV idiopatica
• Raspuns slab la AVK (trombus masiv la INR 4.4)
• Probe inflamatorii (+++)
J Thromb Haemost 2015; 13: 398–408.
Inflammation in deep vein thrombosis and the
development of post-thrombotic syndrome:
A prospective study
110 pts TVP (evaluati la 12 luni pr SPT)
IL-6
CRP
• Rezultatele acestui studiu sugereaza ca
inflamatia ar putea juca un rol in
clearance-ul incomplet al trombusului,
persistenta obstructiei venoase si aparitia
dupa 1 an a SPT.
Klappe E et al. J of Thrombosis and Haemostasis 2009;7(4):582-587
BMC Cardiovascular Disorders 2007
• Primul studiu prospectiv care a evaluat
rolul predictiv al unor biomarkeri in
aparitia SPT
Triada lui Virchow…Triada lui Virchow…
nu-i apartine lui Virchow!nu-i apartine lui Virchow!
1821-1902
The elements comprising Virchow's triad were
neither proposed by Virchow, nor did he ever
suggest a triad to describe the pathogenesis of
venous thrombosis

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Inflamatia in TVP

  • 1. Inflamatia in TVPInflamatia in TVP Alexandru Andritoiu, MD Sp. Militar Craiova
  • 2. Tromboza venoasa profunda (TVP)Tromboza venoasa profunda (TVP) • Provocata • Neprovocata • Proximala • Distala COMPLICATII EP Deces Recurenta TVP/EP Sindrom post-trombotic Ulcer venos Vene profunde Flux sanguin normal TVP Embol Kahn S. Blood 2009; 114: 4624-4631. Kahn S. Blood review 2002. 16: 155-165.
  • 3. TVP vs TromboflebitaTVP vs Tromboflebita Flebitele Tromboflebita superficialaTromboflebita superficiala • trombus endovenos + inflamatie adiacenta in vv superficiale TVPTVP • trombus in vv profunde • adesea nu asociaza inflamatie (manifesta clinic)
  • 4. Tromboflebita superficialaTromboflebita superficiala • Varice hidrostatice • Semne cutanate inflamatorii • Tratament cu AINS (topice)
  • 5. Boala trombo-embolicaBoala trombo-embolica Boala trombo-embolica • TVP • EP • Morbiditate • Mortalitate • Impact economic
  • 6. Subiecte propuseSubiecte propuse 1) Mecanismele inflamatorii in TVP acuta 2) Bolile inflamatorii si riscul TVP 3) Cum putem combate inflamatia in TVP? 4) Inflamatia si rezolutia trombusului 5) Sdr. post-trombotic si inflamatia
  • 7. ?? 1) Mecanismele inflamatorii in TVP acuta 2) Bolile inflamatorii si riscul TVP 3) Cum putem combate inflamatia in TVP? 4) Inflamatia si rezolutia trombusului 5) Sdr. post-trombotic si inflamatia
  • 8. Prakash Saha et al. Arterioscler Thromb Vasc Biol. 2011;31:506-512 (1) Activation of the endothelium (EC; red cell) generates intravascular danger signals, which guide leukocytes to areas of inflammation and induces TF production. (2) Upregulation of adhesion molecules on endothelium mediate PMN recruitment, and TF generates thrombin, activating platelet (Plt) deposition and converting fibrinogen to cross-linked fibrin (Fb) that entraps the main RBC mass. Inflamatia si trombogeneza venoasa
  • 9. Arterioscler Thromb Vasc Biol. 2011;31:506-512 TVP acutaTVP acuta • PMN (+++) • Rol in remodelarea peretelui venos
  • 10. Cascada aderarii leucocitareCascada aderarii leucocitare in raspunsul inflamatorin raspunsul inflamator D. Neil Granger and Elena Senchenkovaş 2010 by Morgan & Claypool Life Sciences.
  • 11. ImmediatImmediat dupa injuriadupa injuria endotelialendoteliala, celulelea, celulele endotelialendotelialee sisi plaplachetele suntchetele sunt activateactivate,, declansanddeclansand expresiexpresiaa moleculemoleculelor de adeziune celularalor de adeziune celulara Thomas W. Wakefield et al. Arterioscler Thromb Vasc Biol. 2008;28:387-391
  • 12. Rolul microparticulelorRolul microparticulelor Thomas W. Wakefield et al. Arterioscler Thromb Vasc Biol. 2008;28:387-391
  • 13. Levels of P-selectin have been found to be elevated in DVT patients, and are decreased with heparin treatment Biomarker levels of soluble P-selectin, and D-dimer in an algorithm to diagnose DVT: Sensitivity 73% Specificity 81%
  • 14. TVP idiopatica este in relatie cu raspunsulTVP idiopatica este in relatie cu raspunsul inflamator sistemic si cresterea nivelelor serice aleinflamator sistemic si cresterea nivelelor serice ale markerilor circulatori ai disfunctiei endotelialemarkerilor circulatori ai disfunctiei endoteliale • 49 pts. TVP primara • Markeri de inflamatie: • high sensitive C-reactive protein (hs CRP), • IL-6, IL-8,TNF-a, • Markeri ai disfunctiei endoteliale • von Willebrand factor (vWF) • P-selectin • vascular adhesion molecule (VCAM-1) Jezovnik M. K. , Poredos P. International Angiology 2010;29: (3):226-31 CONCLUSION: Patients with idiopathic venous thrombosis have increased levels of circulating markers of inflammation and blood markers of endothelial dysfunction. Higher levels of both groups of markers indicate that patients in the stable phase of the disease have an increased systemic inflammatory response. The interrelationship between inflammatory markers and markers of endothelial dysfunction favour the hypothesis that inflammation could be involved in the etiopathogenesis of idiopathic venous thrombosis.
  • 15. J Vasc Surgery 2002;35:701-706
  • 16. Clinical Chemistry 2015:61:2:3013-316 Predictori ai TVP • FR • IL-6 • IL-8 • CRP
  • 17. Whether these markers may be useful in the diagnosis of VTE is as yet uncertain
  • 18. International Journal of General Medicine 2015:8 37–40
  • 19. Relatia dintre volumul trombusului siRelatia dintre volumul trombusului si testele inflamatoriitestele inflamatorii • TVP v. poplitee • TVP vv musculare gambiere • Markeri inflam (+) • Risc scazut de SPT • TVP ileo-femurala • TVP femuro-poplitee • Markeri inflam (+++) • Risc major de SPT
  • 20. Markerii inflamatori,Markerii inflamatori, D-dimerii si riscul de TVPD-dimerii si riscul de TVP recurentarecurenta Concluzii: • Nivelele crescute de CRP si D-dimeri cresc riscul recurentei TVP, in timp ce nivelele crescute de citokine proinflamatorii, NU! • Pts cu nivele crescute simultat de CRP si D-dimeri au cel mai mare risc de recutenta a TVP. Roshani S, et al. Leiden Thrombophilia Study LETS (2012)
  • 21. ???? 1) Mecanismele inflamatorii in TVP acuta 2) Bolile inflamatorii si riscul TVP 3) Cum putem combate inflamatia in TVP? 4) Inflamatia si rezolutia trombusului 5) Sdr. post-trombotic si inflamatia
  • 22. TVP si bolile inflamatorii croniceTVP si bolile inflamatorii cronice • Boli de sistem (colagenoze): PR, LES • Neoplazii • IBD (RCUH, b. Chron) • Sepsis • Boala Behçet • Vasculite autoimune • Arterita Takayasu • Sdr. antifosfolipidic • TAO
  • 23. Pts cu IBD au un risc de TVP de 2-3 x mai mare decat populatia generala
  • 24. Cercul vicios inflamatie-coagulareCercul vicios inflamatie-coagulare
  • 25. ?????? 1) Mecanismele inflamatorii in TVP acuta 2) Bolile inflamatorii si riscul TVP 3) Cum putem combate inflamatia in TVP? 4) Inflamatia si rezolutia trombusului 5) Sdr. post-trombotic si inflamatia
  • 26. Putem combate inflamatiaPutem combate inflamatia din TVP ?din TVP ? • heparine • statine • sulodexid • IL-10 (in studiu) • AINS (doar in tromboflebita superficiala)
  • 27. • inhiba activarea si aderarea celulelor inflamatorii (leucocite) • reduce productia de citokine • inhiba degradarea mastocitelor si eliberarea de histamina • protejeaza celulele endoteliale de actiunea citotoxica • inhiba prod de heparinaza de catre plachete • previne aderarea neutrofilelor la cel. endoteliale
  • 28. • Astm bronsic • SCA • CABPG • Chir. Cataractei • IBD ,,considering heparins as the main stay treatment of ACS, its effects are more pronounced as anticoagulating than as an anti-inflammatory agent in this pathological condition”. Adv Pharmacol Sci. 2015
  • 29. • Mastocitele tisulare sunt singura sursa de heparina endogena care poate fi implicata in controlul raspunsului inflamator. • Heparina inhiba influxul neutrofilelor la locul inflamatiei, cat si adeziunea leucocitelor in venulele post-capilare.
  • 30. Lipidele circulante in exces: • Efect protrombotic • Cresc productia de trombina • Activare plachetara • Disfunctie endoteliala Statinele reduc riscul de TVP independent de nivelul colesterolului seric
  • 31. Rosuvastatin – 43%Rosuvastatin – 43% • In studiul JUPITER (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin), rosuvastatin 20 mg a redus rata cazurilor noi de TEV cu 43% la o populatie sanatoasa cu markeri de inflamatie cronica sistemica documentata prin cresterea concentratiei de CRP (2 mg/dL).
  • 32. Kones R. Drug Design, Development and Therapy 2010 Molecula CRP
  • 33. Rodriguez A et al. Thromb Thrombolysis. 2012 May ; 33(4): 371–382 Mecanisme propuse in reducerea riscului de TVP la pts tratati cu statine: • scaderea PAI-1 • cresterea expresiei tPA, • scaderea agregarii plachetare, • cresterea expresiei trombomodulinei Efectul concret al Rosuvastatinei nu se cunoaste! Pe langa efectul anti-trombotic/anti-inflamator, statinele nu au risc de sangerare-posibila terapie asociata in TVP
  • 34. Statinele reduc riscul de TVPStatinele reduc riscul de TVP
  • 35. PLOS ONE | DOI:10.1371/journal.pone.0116621 February 13, 2015
  • 36. Mannello F, Medda V, Ligi D, Raffetto JD (2013) Glycosaminoglycan sulodexide inhibition of mmp-9 gelatinase secretion and activity: possible pharmacological role against collagen degradation in vascular chronic diseases. Curr Vasc Pharmacol 2013;11:354-365 Mannello F. Modulation of matrix metalloproteinases and cytokines by glycosaminoglycan sulodexide in macrophage-like cells: possible role and treatment in chronic venous diseases. XVII World Meeting of the International Union of Phlebology. SDX-proprietati anti-inflamatoriiSDX-proprietati anti-inflamatorii
  • 37. SDX-PEV SDX p.o. +/- or TRIFLUSAL
  • 38. • IL-10 prezenta in exces in peretele venos ca raspuns la tromboza venoasa • adm. de IL-10 a scazut volumul trombusului Journal of Imunology, 1998;161:1471-1476
  • 40. ???????? 1) Mecanismele inflamatorii in TVP acuta 2) Bolile inflamatorii si riscul TVP 3) Cum putem combate inflamatia in TVP? 4) Inflamatia si rezolutia trombusului 5) Sdr. post-trombotic si inflamatia
  • 41. Rezolutia trombusuluiRezolutia trombusului Pattern-uri diferite: • periferic • central (tunelizare) • tip cavernos (multilocular) • Predomina macrofagele • IL-8 rol chemotactic • MMPs 2 si 9 • Urokinase activity (+++) • VEGF (+++) • IL-1alfa • IL-2 • Lf-niciun rol! Procesul de baza: NEOVASCULARIZATIE PERIADVENTICIALA HIPOXIC-INDUSA The dynamics of recanalization are characterized by distal-to-proximal extension and in the first 6 months are significantly influenced by thrombosis etiology Puskas A. Int Angiol 2007(26);1:53-63
  • 42. • Organizarea si recanalizarea trombusului este rezultatul unui proces “outside-in”outside-in” cu celulelecu celulele inflamatorii patrunzand in interiorulinflamatorii patrunzand in interiorul trombusului via peretele venostrombusului via peretele venos. • Hipoxia relativa din interiorul trombusului poate repreyenta un stimul ptr formarea de vase de neoformatie deyvoltate din peretele venos inspre trombus, care, impreuna cu retractia trombusului, conduce la recanalizarea venei si reaparitia fluxului sanguin venos. Arterioscler Thromb Vasc Biol. 2010;30:2443-2451
  • 43. Rolul leucocitelor in rezolutia trombusului Prakash Saha et al. Arterioscler Thromb Vasc Biol. 2011;31:506-512
  • 44. VEGF expression in the naturally resolving mouse thrombusVEGF expression in the naturally resolving mouse thrombus Colin Edward Evans et al. Arterioscler Thromb Vasc Biol. 2010;30:2443-2451
  • 45. Etapa imediata post-tromboza se caracterizeaza prin tromboliza fiziologica dependenta de prezenta leucocitelor (NTR) care lucreaza intr-un mediu proinflamator generat de citokine Thomas W. Wakefield et al. Arterioscler Thromb Vasc Biol. 2008;28:387-391
  • 46. • Statinele au proprietatti anti-inflamatorii, pro- angiogenice and pro-fibrinolitice care pot influenta favorabil recanalizarea si organizarea trombusului. • Atorvastatina amplifica rata recanalizarii si inhiba inflamatia de la nivelul peretelui venos, cat si fibroza. Int J Surg 2012;(10):8:S4
  • 47. ?????????? 1) Mecanismele inflamatorii in TVP acuta 2) Bolile inflamatorii si riscul TVP 3) Cum putem combate inflamatia in TVP? 4) Inflamatia si rezolutia trombusului 5) Sdr. post-trombotic si inflamatia
  • 48. Factorii majori de prognostic ai SPT: • tromboza reziduala • reflux in v. femurala si popitee Estimate la 3 luni dupa TVP acuta Journal of Thrombosis and Haemostasis, 11: 795–805
  • 50. Case-Report 1Case-Report 1 TVP ilio-femuralaTVP ilio-femurala S. Mirel, 42 aniS. Mirel, 42 ani • TVP idiopatica stg. • Ileo-Fem-Pop • CT • VSH 71 mm/h • CRP 7.7 mg/dL • Fibrinogen 622 mg/dL • Leuc 10.200/mmc • Fara semne de inflamatie locala
  • 51. Case-Report 2Case-Report 2 TVP v. popliteeTVP v. poplitee N. Simona, 32 ani • TVP acuta (idiopatica)-10 z • V poplitee stg. • CDUS • VSH 30 mm/h • Fibrinogen 202 mg/dL • CRP 1.1 mg/dL • Leuc 8.300/mmc
  • 52. In care caz riscul aparitiei SPTIn care caz riscul aparitiei SPT este mai mare?este mai mare? Raspuns corect: Cazul 1Raspuns corect: Cazul 1 Argumente: • Localizare proximala • Volum mare al trombusului • TV idiopatica • Raspuns slab la AVK (trombus masiv la INR 4.4) • Probe inflamatorii (+++)
  • 53. J Thromb Haemost 2015; 13: 398–408.
  • 54. Inflammation in deep vein thrombosis and the development of post-thrombotic syndrome: A prospective study 110 pts TVP (evaluati la 12 luni pr SPT) IL-6 CRP • Rezultatele acestui studiu sugereaza ca inflamatia ar putea juca un rol in clearance-ul incomplet al trombusului, persistenta obstructiei venoase si aparitia dupa 1 an a SPT. Klappe E et al. J of Thrombosis and Haemostasis 2009;7(4):582-587
  • 55. BMC Cardiovascular Disorders 2007 • Primul studiu prospectiv care a evaluat rolul predictiv al unor biomarkeri in aparitia SPT
  • 56.
  • 57.
  • 58. Triada lui Virchow…Triada lui Virchow… nu-i apartine lui Virchow!nu-i apartine lui Virchow! 1821-1902 The elements comprising Virchow's triad were neither proposed by Virchow, nor did he ever suggest a triad to describe the pathogenesis of venous thrombosis

Editor's Notes

  1. Inflammation in venous thrombogenesis. i, Activation of the endothelium (EC; red cell) generates intravascular danger signals, which guide leukocytes to areas of inflammation and induces TF production. ii, Upregulation of adhesion molecules on endothelium mediate PMN recruitment, and TF generates thrombin, activating platelet (Plt) deposition and converting fibrinogen to cross-linked fibrin (Fb) that entraps the main RBC mass. ICAM indicates intercellular adhesion molecule. iii, PMN accumulation in the subendothelial layer and subsequent exposure of collagen (Col) causes platelet aggregation and further PMN sequestration, establishing a nidus for thrombus formation. PMN apoptosis in response to inflammatory stimuli releases neutrophil extracellular traps (NETs; blue strands) that provide a scaffold for further RBC capture. iv, Reactive oxygen species (ROS), released from the vessel wall and leukocytes, oxidize hemoglobin (Hb) to methemoglobin (MetHb; blue RBC). As trapped RBCs lyse, Fe3+ contained in MetHb is released and induces further RBC lysis. This leads to a positive feedback loop with increased areas of endothelial dysfunction, resulting in thrombus propagation.
  2. Figure 1. Immediately after endothelial cell injury, endothelial cells and platelets are activated promoting the expression of cell adhesion molecules. This vascular response promotes leukocyte rolling and tethering onto the endothelium that initiates an inflammatory event which can lead to thrombosis. (Modified from Myers DD et al, Front Biosci 2005;10:2752.)‏
  3. Figure 2. Proposed mechanism of the role of microparticles. (1) With stimulation, selectins are upregulated and bind to PSGL-1 on leukocytes and platelets; (2) Microparticles which are procoagulant are produced, especially from monocytes but also from platelets and endothelial cells; (3) These microparticles then are concentrated back into the area of thrombosis; (4) This then leads to thrombus amplification. (Modified from Myers DD et al, Front Biosci 2005;10:2753.)‏
  4. Putative functions of leukocytes in venous thrombus resolution. Leukocytes accumulate in the venous thrombus during its resolution. PMNs predominate in the early stages of resolution, with mononuclear phagocytes (Mϕ) predominating later. The origin of these cells appears to be from the BM; however, the contribution of tissue-resident macrophages or cells derived from the splenic reservoir remains unknown. Leukocytes signal through a TLR9 mechanism and may be stimulated by fibrin(ogen) and its degradation products. They are speculated to have a number of functions that are important for thrombus resolution.
  5. Figure 3. VEGF expression in the naturally resolving mouse thrombus. A, VEGF was elevated at days 3 and 7 compared with days 1 and 14 after thrombus induction. *P<0.001 versus days 1 and 14. B and C, Positive correlation between HIF1α and VEGF expression at day 3 (B) (R=0.81, n=10, P<0.005) and day 7 (C) (R=0.85, n=13, P<0.0005).
  6. Figure 3. Early time postthrombosis is characterized by thrombolysis that is leukocyte dependent, primarily neutrophils, and driven by a proinflammatory cytokine mileau. This transitions overtime to a monocyte predominant thrombus environment, with plasmin- and MMP-mediated thrombus breakdown. Coincident with the thrombus changes are early collagenolytic (and likely elastinolysis) changes, followed by later vein wall fibrosis. (Reproduced with permission from Henke PK, Vascular 2007; 15:369.)‏