Skip to main content
Erschienen in: Current Infectious Disease Reports 11/2014

01.11.2014 | Cardiovascular Infections (D Levine, Section Editor)

The Role of Hemostasis in Infective Endocarditis

verfasst von: Emanuele Durante-Mangoni, Rosa Molaro, Domenico Iossa

Erschienen in: Current Infectious Disease Reports | Ausgabe 11/2014

Einloggen, um Zugang zu erhalten

Abstract

Infective endocarditis (IE) is a thromboinflammatory disease of the endocardium, with pathophysiology mostly the result of the interplay between microorganisms and modifiers of the hemostasis system. In this setting, the evidence gathered so far warrants a more systematic appraisal. In this review article, experimental and clinical data on the role of hemostasis in IE are summarized. Starting from the current pathogenetic model of IE, we discuss the dual role of platelets in this condition, the microbial interaction with the hemostasis system, also describing nonspecific hemostasis changes during sepsis. We finally propose our hypothesis of thrombophilia as a possible trigger of IE, highlighting the challenges that the study of hemostasis in IE presents. The role of hemostasis in IE appears to be an exciting field of research. The activity of the hemostasis system is highly relevant in terms of susceptibility, progression, and treatment of IE. Pharmacologic modulation of hemostasis before and after IE onset is possible and represents still a largely unexplored area of study.
Literatur
1.
Zurück zum Zitat Thiene G, Basso C. Pathology and pathogenesis of infective endocarditis in native heart valves. Cardiovasc Pathol. 2006;15(5):256–63.PubMedCrossRef Thiene G, Basso C. Pathology and pathogenesis of infective endocarditis in native heart valves. Cardiovasc Pathol. 2006;15(5):256–63.PubMedCrossRef
3.
Zurück zum Zitat Moreillon P, Que YA, Bayer AS. Pathogenesis of streptococcal and staphylococcal endocarditis. Infect Dis Clin North Am. 2002;16:297–318.PubMedCrossRef Moreillon P, Que YA, Bayer AS. Pathogenesis of streptococcal and staphylococcal endocarditis. Infect Dis Clin North Am. 2002;16:297–318.PubMedCrossRef
4.
Zurück zum Zitat Widmer E, Que YA, Entenza JM, et al. New concepts in the pathophysiology of infective endocarditis. Curr Infect Dis Rep. 2006;8:271–9.PubMedCrossRef Widmer E, Que YA, Entenza JM, et al. New concepts in the pathophysiology of infective endocarditis. Curr Infect Dis Rep. 2006;8:271–9.PubMedCrossRef
5.
Zurück zum Zitat Bombeli T, Mueller M, Haeberli A. Anticoagulant properties of the vascular endothelium. Thromb Haemost. 1997;77:408–23.PubMed Bombeli T, Mueller M, Haeberli A. Anticoagulant properties of the vascular endothelium. Thromb Haemost. 1997;77:408–23.PubMed
7.
Zurück zum Zitat Ford I, Douglas CW. The role of platelets in infective endocarditis. Platelets. 1997;8(5):285–94.PubMedCrossRef Ford I, Douglas CW. The role of platelets in infective endocarditis. Platelets. 1997;8(5):285–94.PubMedCrossRef
8.
Zurück zum Zitat Kiefer TL, Bashore TM. Infective endocarditis: a comprehensive overview. Rev Cardiovasc Med. 2012;13(2/3):e105–20.PubMed Kiefer TL, Bashore TM. Infective endocarditis: a comprehensive overview. Rev Cardiovasc Med. 2012;13(2/3):e105–20.PubMed
9.
Zurück zum Zitat Rohmann S, Erbel R, Gorge G, et al. Prediction of rapid versus prolonged healing of infective endocarditis by monitoring vegetation size. J Am Soc Echocardiogr. 1991;4:465–74.PubMedCrossRef Rohmann S, Erbel R, Gorge G, et al. Prediction of rapid versus prolonged healing of infective endocarditis by monitoring vegetation size. J Am Soc Echocardiogr. 1991;4:465–74.PubMedCrossRef
10.
Zurück zum Zitat Rohmann S, Erbel R, Gorge G, et al. Clinical relevance of vegetation localization by transesophageal echocardiography in infective endocarditis. Eur Heart J. 1992;13:446–52.PubMed Rohmann S, Erbel R, Gorge G, et al. Clinical relevance of vegetation localization by transesophageal echocardiography in infective endocarditis. Eur Heart J. 1992;13:446–52.PubMed
11.
Zurück zum Zitat Sakariasse KS, Holme PA, et al. Shear-induced platelet activation and platelet microparticle formation in native human blood. Thromb Res. 1998;92:S33–43.CrossRef Sakariasse KS, Holme PA, et al. Shear-induced platelet activation and platelet microparticle formation in native human blood. Thromb Res. 1998;92:S33–43.CrossRef
12.
Zurück zum Zitat Girdhar G, Bluestein D. Biological effects of dynamic shear stress in cardiovascular pathologies and devices. Expert Rev Med Devic. 2008;5(2):167–81.CrossRef Girdhar G, Bluestein D. Biological effects of dynamic shear stress in cardiovascular pathologies and devices. Expert Rev Med Devic. 2008;5(2):167–81.CrossRef
13.•
Zurück zum Zitat Vanassche T, Peetermans WE, Herrgods MC, Herijgers P, Verhamme P. Anti-thrombotic therapy in infective endocarditis. Expert Rev Cardiovasc Ther. 2011;9(9):1203–19. This review comprehensively summarizes the current evidence on the pharmacologic modulation of the hemostasis system in infective endocarditis.PubMedCrossRef Vanassche T, Peetermans WE, Herrgods MC, Herijgers P, Verhamme P. Anti-thrombotic therapy in infective endocarditis. Expert Rev Cardiovasc Ther. 2011;9(9):1203–19. This review comprehensively summarizes the current evidence on the pharmacologic modulation of the hemostasis system in infective endocarditis.PubMedCrossRef
14.
Zurück zum Zitat Patti JM, Allen BL, MecGavin MJ, Hook M. MSCRAMM-mediated adherence of microorganism to host tissues. Annu Rev Microbiol. 1994;48:585–617.PubMedCrossRef Patti JM, Allen BL, MecGavin MJ, Hook M. MSCRAMM-mediated adherence of microorganism to host tissues. Annu Rev Microbiol. 1994;48:585–617.PubMedCrossRef
15.
Zurück zum Zitat François P, Vaudaux P, Lew PD. Role of plasma and extracellular matrix proteins in the physiopathology of foreign body infections. Ann Vasc Surg. 1998;12(1):34–40.PubMedCrossRef François P, Vaudaux P, Lew PD. Role of plasma and extracellular matrix proteins in the physiopathology of foreign body infections. Ann Vasc Surg. 1998;12(1):34–40.PubMedCrossRef
16.
Zurück zum Zitat Johnson CM, Bowie EJ. Pigs with von Willebrand disease may be resistant to experimental infective endocarditis. J Lab Clin Med. 1992;120(4):553–8.PubMed Johnson CM, Bowie EJ. Pigs with von Willebrand disease may be resistant to experimental infective endocarditis. J Lab Clin Med. 1992;120(4):553–8.PubMed
17.
Zurück zum Zitat Sullam PM, Bayer AS, Foss WM, Cheung AL. Diminished platelet binding in vitro by Staphylococcus aureus is associated with reduced virulence in a rabbit model of infective endocarditis. Infect Immun. 1996;64(12):4915–21.PubMedPubMedCentral Sullam PM, Bayer AS, Foss WM, Cheung AL. Diminished platelet binding in vitro by Staphylococcus aureus is associated with reduced virulence in a rabbit model of infective endocarditis. Infect Immun. 1996;64(12):4915–21.PubMedPubMedCentral
18.
Zurück zum Zitat Yeaman MR. The role of platelets in antimicrobial host defense. Clin Infect Dis. 1997;25(5):951–68.PubMedCrossRef Yeaman MR. The role of platelets in antimicrobial host defense. Clin Infect Dis. 1997;25(5):951–68.PubMedCrossRef
19.
Zurück zum Zitat Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management of infective endocarditis and its complication. Circulation. 1998;98:2936–28.PubMedCrossRef Bayer AS, Bolger AF, Taubert KA, et al. Diagnosis and management of infective endocarditis and its complication. Circulation. 1998;98:2936–28.PubMedCrossRef
20.
Zurück zum Zitat Yeaman MR, Norman DC, Bayer AS. Platelet microbicidal protein enhances antibiotic-induced killing of and postantibiotic effect in Staphylococcus aureus. Antimicrob Agents Chemother. 1992;36(8):1665–70.PubMedCrossRefPubMedCentral Yeaman MR, Norman DC, Bayer AS. Platelet microbicidal protein enhances antibiotic-induced killing of and postantibiotic effect in Staphylococcus aureus. Antimicrob Agents Chemother. 1992;36(8):1665–70.PubMedCrossRefPubMedCentral
21.
Zurück zum Zitat Yeaman MR, Norman DC, Bayer AS. Staphylococcus aureus susceptibility to thrombin-induced platelet microbicidal protein is independent of platelet adherence and aggregation in vitro. Infect Immun. 1992;60(6):2368–74.PubMedPubMedCentral Yeaman MR, Norman DC, Bayer AS. Staphylococcus aureus susceptibility to thrombin-induced platelet microbicidal protein is independent of platelet adherence and aggregation in vitro. Infect Immun. 1992;60(6):2368–74.PubMedPubMedCentral
22.
Zurück zum Zitat Yeaman MR, Sullam PM, Dazin PF, Bayer AS. Platelet microbicidal protein alone and in combination with antibiotics reduces Staphylococcus aureus adherence to platelets in vitro. Infect Immun. 1994;62(8):3416–23.PubMedPubMedCentral Yeaman MR, Sullam PM, Dazin PF, Bayer AS. Platelet microbicidal protein alone and in combination with antibiotics reduces Staphylococcus aureus adherence to platelets in vitro. Infect Immun. 1994;62(8):3416–23.PubMedPubMedCentral
23.
Zurück zum Zitat Yeaman MR, Tang YQ, Shen AJ, Bayer AS, Selsted ME. Purification and in vitro activities of rabbit platelet microbicidal proteins. Infect Immun. 1997;65(3):1023–31.PubMedPubMedCentral Yeaman MR, Tang YQ, Shen AJ, Bayer AS, Selsted ME. Purification and in vitro activities of rabbit platelet microbicidal proteins. Infect Immun. 1997;65(3):1023–31.PubMedPubMedCentral
25.•
Zurück zum Zitat Kupferwasser LI, Yeaman MR, Shapiro SM, Nast CC, Bayer AS. In vitro susceptibility to thrombin-induced platelet microbicidal protein is associated with reduced disease progression and complication rates in experimental Staphylococcus aureus endocarditis: microbiological, histopathologic, and echocardiographic analyses. Circulation. 2002;105(6):746–52. This study elegantly describes the antimicrobial effects of platelet-derived proteins.PubMedCrossRef Kupferwasser LI, Yeaman MR, Shapiro SM, Nast CC, Bayer AS. In vitro susceptibility to thrombin-induced platelet microbicidal protein is associated with reduced disease progression and complication rates in experimental Staphylococcus aureus endocarditis: microbiological, histopathologic, and echocardiographic analyses. Circulation. 2002;105(6):746–52. This study elegantly describes the antimicrobial effects of platelet-derived proteins.PubMedCrossRef
26.
Zurück zum Zitat Dankert J, Krijgsveld J, van Der Werff J, Joldersma W, Zaat SA. Platelet microbicidal activity is an important defense factor against viridans streptococcal endocarditis. J Infect Dis. 2001;184(5):597–605.PubMedCrossRef Dankert J, Krijgsveld J, van Der Werff J, Joldersma W, Zaat SA. Platelet microbicidal activity is an important defense factor against viridans streptococcal endocarditis. J Infect Dis. 2001;184(5):597–605.PubMedCrossRef
27.
Zurück zum Zitat Patti JM, Höök M. Microbial adhesins recognizing extracellular matrix macromolecules. Curr Opin Cell Biol. 1994;6(5):752–8.PubMedCrossRef Patti JM, Höök M. Microbial adhesins recognizing extracellular matrix macromolecules. Curr Opin Cell Biol. 1994;6(5):752–8.PubMedCrossRef
28.
29.
Zurück zum Zitat Flock JI, Fröman G, Jönsson K, Guss B, Signäs C, Nilsson B, et al. Cloning and expression of the gene for a fibronectin-binding protein from Staphylococcus aureus. EMBO J. 1987;6(8):2351–7.PubMedPubMedCentral Flock JI, Fröman G, Jönsson K, Guss B, Signäs C, Nilsson B, et al. Cloning and expression of the gene for a fibronectin-binding protein from Staphylococcus aureus. EMBO J. 1987;6(8):2351–7.PubMedPubMedCentral
30.
Zurück zum Zitat Fröman G, Switalski LM, Speziale P, Höök M. Isolation and characterization of a fibronectin receptor from Staphylococcus aureus. J Biol Chem. 1987;262(14):6564–71.PubMed Fröman G, Switalski LM, Speziale P, Höök M. Isolation and characterization of a fibronectin receptor from Staphylococcus aureus. J Biol Chem. 1987;262(14):6564–71.PubMed
31.
Zurück zum Zitat Signäs C, Raucci G, Jönsson K, Lindgren PE, Anantharamaiah GM, Höök M, et al. Nucleotide sequence of the gene for a fibronectin-binding protein from Staphylococcus aureus: use of this peptide sequence in the synthesis of biologically active peptides. Proc Natl Acad Sci U S A. 1989;86(2):699–703.PubMedCrossRefPubMedCentral Signäs C, Raucci G, Jönsson K, Lindgren PE, Anantharamaiah GM, Höök M, et al. Nucleotide sequence of the gene for a fibronectin-binding protein from Staphylococcus aureus: use of this peptide sequence in the synthesis of biologically active peptides. Proc Natl Acad Sci U S A. 1989;86(2):699–703.PubMedCrossRefPubMedCentral
32.
Zurück zum Zitat Jönsson K, Signäs C, Müller HP, Lindberg M. Two different genes encode fibronectin binding proteins in Staphylococcus aureus. The complete nucleotide sequence and characterization of the second gene. Eur J Biochem. 1991;202(3):1041–8.PubMedCrossRef Jönsson K, Signäs C, Müller HP, Lindberg M. Two different genes encode fibronectin binding proteins in Staphylococcus aureus. The complete nucleotide sequence and characterization of the second gene. Eur J Biochem. 1991;202(3):1041–8.PubMedCrossRef
33.
Zurück zum Zitat Peacock SJ, Foster TJ, Cameron BJ, Berendt AR. Bacterial fibronectin-binding proteins and endothelial cell surface fibronectin mediate adherence of Staphylococcus aureus to resting human endothelial cells. Microbiology. 1999;145(Pt 12):3477–86.PubMed Peacock SJ, Foster TJ, Cameron BJ, Berendt AR. Bacterial fibronectin-binding proteins and endothelial cell surface fibronectin mediate adherence of Staphylococcus aureus to resting human endothelial cells. Microbiology. 1999;145(Pt 12):3477–86.PubMed
34.
Zurück zum Zitat Que YA et al. Fibrinogen and fibronectin binding cooperate for valve infection and invasion in Staphylococcus aureus experimental endocarditis. J Exp Med. 2005;201:1627–35.PubMedCrossRefPubMedCentral Que YA et al. Fibrinogen and fibronectin binding cooperate for valve infection and invasion in Staphylococcus aureus experimental endocarditis. J Exp Med. 2005;201:1627–35.PubMedCrossRefPubMedCentral
35.
Zurück zum Zitat Sinha B, Francois PP, Nusse O, Foti M, Hartford OM, Vaudaux P, et al. Fibronectin-binding protein acts as Staphylococcus aureus invasin via fibronectin bridging to integrin alpha5beta1. Cell Microbiol. 1999;1(2):101–17.PubMedCrossRef Sinha B, Francois PP, Nusse O, Foti M, Hartford OM, Vaudaux P, et al. Fibronectin-binding protein acts as Staphylococcus aureus invasin via fibronectin bridging to integrin alpha5beta1. Cell Microbiol. 1999;1(2):101–17.PubMedCrossRef
36.
Zurück zum Zitat McDevitt D, Francois PP, Vaudaux P, Foster TJ. Molecular characterization of the clumping factor (fibrinogen receptor) of Staphylococcus aureus. Mol Microbiol. 1994;11(2):237–48.PubMedCrossRef McDevitt D, Francois PP, Vaudaux P, Foster TJ. Molecular characterization of the clumping factor (fibrinogen receptor) of Staphylococcus aureus. Mol Microbiol. 1994;11(2):237–48.PubMedCrossRef
37.
Zurück zum Zitat Wann ER, Gurusiddappa S, Hook M. The fibronectin-binding MSCRAMM FnbpA of Staphylococcus aureus is a bifunctional protein that also binds to fibrinogen. J Biol Chem. 2000;275(18):13863–71.PubMedCrossRef Wann ER, Gurusiddappa S, Hook M. The fibronectin-binding MSCRAMM FnbpA of Staphylococcus aureus is a bifunctional protein that also binds to fibrinogen. J Biol Chem. 2000;275(18):13863–71.PubMedCrossRef
38.
Zurück zum Zitat Downer R, Roche F, Park PW, Mecham RP, Foster TJ. The elastin-binding protein of Staphylococcus aureus (EbpS) is expressed at the cell surface as an integral membrane protein and not as a cell wall-associated protein. J Biol Chem. 2002;277(1):243–50.PubMedCrossRef Downer R, Roche F, Park PW, Mecham RP, Foster TJ. The elastin-binding protein of Staphylococcus aureus (EbpS) is expressed at the cell surface as an integral membrane protein and not as a cell wall-associated protein. J Biol Chem. 2002;277(1):243–50.PubMedCrossRef
39.
Zurück zum Zitat Roche FM, Downer R, Keane F, Speziale P, Park PW, Foster TJ. The N-terminal A domain of fibronectin-binding proteins A and B promotes adhesion of Staphylococcus aureus to elastin. J Biol Chem. 2004;279(37):38433–40.PubMedCrossRef Roche FM, Downer R, Keane F, Speziale P, Park PW, Foster TJ. The N-terminal A domain of fibronectin-binding proteins A and B promotes adhesion of Staphylococcus aureus to elastin. J Biol Chem. 2004;279(37):38433–40.PubMedCrossRef
40.
Zurück zum Zitat O’Brien LM, Walsh EJ, Massey RC, Peacock SJ, Foster TJ. Staphylococcus aureus clumping factor B (ClfB) promotes adherence to human type I cytokeratin 10: implications for nasal colonization. Cell Microbiol. 2002;4(11):759–70.PubMedCrossRef O’Brien LM, Walsh EJ, Massey RC, Peacock SJ, Foster TJ. Staphylococcus aureus clumping factor B (ClfB) promotes adherence to human type I cytokeratin 10: implications for nasal colonization. Cell Microbiol. 2002;4(11):759–70.PubMedCrossRef
41.
Zurück zum Zitat Que YA, François P, Haefliger JA, Entenza JM, Vaudaux P, Moreillon P. Reassessing the role of Staphylococcus aureus clumping factor and fibronectin-binding protein by expression in Lactococcus lactis. Infect Immun. 2001;69(10):6296–302.PubMedCrossRefPubMedCentral Que YA, François P, Haefliger JA, Entenza JM, Vaudaux P, Moreillon P. Reassessing the role of Staphylococcus aureus clumping factor and fibronectin-binding protein by expression in Lactococcus lactis. Infect Immun. 2001;69(10):6296–302.PubMedCrossRefPubMedCentral
42.
Zurück zum Zitat Fitzgerald JR, Loughman A, Keane F, Brennan M, Knobel M, Higgins J, et al. Fibronectin-binding proteins of Staphylococcus aureus mediate activation of human platelets via fibrinogen and fibronectin bridges to integrin GPIIb/IIIa and IgG binding to the FcgammaRIIa receptor. Mol Microbiol. 2006;59(1):212–30.PubMedCrossRef Fitzgerald JR, Loughman A, Keane F, Brennan M, Knobel M, Higgins J, et al. Fibronectin-binding proteins of Staphylococcus aureus mediate activation of human platelets via fibrinogen and fibronectin bridges to integrin GPIIb/IIIa and IgG binding to the FcgammaRIIa receptor. Mol Microbiol. 2006;59(1):212–30.PubMedCrossRef
43.
Zurück zum Zitat Loughman A, Fitzgerald JR, Brennan MP, Higgins J, Downer R, Cox D, et al. Roles for fibrinogen, immunoglobulin and complement in platelet activation promoted by Staphylococcus aureus clumping factor A. Mol Microbiol. 2005;57(3):804–18.PubMedCrossRef Loughman A, Fitzgerald JR, Brennan MP, Higgins J, Downer R, Cox D, et al. Roles for fibrinogen, immunoglobulin and complement in platelet activation promoted by Staphylococcus aureus clumping factor A. Mol Microbiol. 2005;57(3):804–18.PubMedCrossRef
44.
Zurück zum Zitat Vanassche T, Verhaegen J, Peetermans WE, Hoylaerts MF, Verhamme P. Dabigatran inhibits Staphylococcus aureus coagulase activity. J Clin Microbiol. 2010;48(11):4248–50.PubMedCrossRefPubMedCentral Vanassche T, Verhaegen J, Peetermans WE, Hoylaerts MF, Verhamme P. Dabigatran inhibits Staphylococcus aureus coagulase activity. J Clin Microbiol. 2010;48(11):4248–50.PubMedCrossRefPubMedCentral
45.
Zurück zum Zitat Schouten M, Wiersinga WJ, Levi M, van der Poll T. Inflammation, endothelium, and coagulation in sepsis. J Leukoc Biol. 2008;83:536–45.PubMedCrossRef Schouten M, Wiersinga WJ, Levi M, van der Poll T. Inflammation, endothelium, and coagulation in sepsis. J Leukoc Biol. 2008;83:536–45.PubMedCrossRef
46.
Zurück zum Zitat Opal SM, Esmon CT. Bench-to-bedside review: functional relationships between coagulation and the innate immune response and their respective roles in the pathogenesis of sepsis. Crit Care. 2003;7:23–38.PubMedCrossRefPubMedCentral Opal SM, Esmon CT. Bench-to-bedside review: functional relationships between coagulation and the innate immune response and their respective roles in the pathogenesis of sepsis. Crit Care. 2003;7:23–38.PubMedCrossRefPubMedCentral
47.
Zurück zum Zitat Henneke P, Golenbock DT. Innate immune recognition of lipopolysaccharide by endothelial cells. Crit Care Med. 2002;30:S207–13.PubMedCrossRef Henneke P, Golenbock DT. Innate immune recognition of lipopolysaccharide by endothelial cells. Crit Care Med. 2002;30:S207–13.PubMedCrossRef
48.
Zurück zum Zitat Zhang FX, Kirschning CJ, Mancinelli R, Xu XP, Jin YP, Faure E, et al. Bacterial lipopolysaccharide activates nuclear factor-κ B through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes. J Biol Chem. 1999;274:7611–4.PubMedCrossRef Zhang FX, Kirschning CJ, Mancinelli R, Xu XP, Jin YP, Faure E, et al. Bacterial lipopolysaccharide activates nuclear factor-κ B through interleukin-1 signaling mediators in cultured human dermal endothelial cells and mononuclear phagocytes. J Biol Chem. 1999;274:7611–4.PubMedCrossRef
49.
Zurück zum Zitat Akca S, Haji-Michael P, de Mendonca A, Suter P, Levi M, Vincent JL. Time course of platelet counts in critically ill patients. Crit Care Med. 2002;30:753–6.PubMedCrossRef Akca S, Haji-Michael P, de Mendonca A, Suter P, Levi M, Vincent JL. Time course of platelet counts in critically ill patients. Crit Care Med. 2002;30:753–6.PubMedCrossRef
50.
Zurück zum Zitat Zielinski T, Wachowicz B, Saluk-Juszczak J, Kaca W. Polysaccharide part of Proteus mirabilis lipopolysaccharide may be responsible for the stimulation of platelet adhesion to collagen. Platelets. 2002;13:419–24.PubMedCrossRef Zielinski T, Wachowicz B, Saluk-Juszczak J, Kaca W. Polysaccharide part of Proteus mirabilis lipopolysaccharide may be responsible for the stimulation of platelet adhesion to collagen. Platelets. 2002;13:419–24.PubMedCrossRef
51.
Zurück zum Zitat Zimmerman GA, McIntyre TM, Prescott SM, Stafforini DM. The platelet-activating factor signaling system and its regulators in syndromes of inflammation and thrombosis. Crit Care Med. 2002;30:S294–301.PubMedCrossRef Zimmerman GA, McIntyre TM, Prescott SM, Stafforini DM. The platelet-activating factor signaling system and its regulators in syndromes of inflammation and thrombosis. Crit Care Med. 2002;30:S294–301.PubMedCrossRef
52.
Zurück zum Zitat Hamilton KK, Sims PJ. Changes in cytosolic Ca2+ associated with von Willebrand factor release in human endothelial cells exposed to histamine. Study of microcarrier cell monolayers using the fluorescent probe indo-1. J Clin Investig. 1987;79:600–8.PubMedCrossRefPubMedCentral Hamilton KK, Sims PJ. Changes in cytosolic Ca2+ associated with von Willebrand factor release in human endothelial cells exposed to histamine. Study of microcarrier cell monolayers using the fluorescent probe indo-1. J Clin Investig. 1987;79:600–8.PubMedCrossRefPubMedCentral
53.
54.
Zurück zum Zitat Reinhart K, Bayer O, Brunkhorst F, Meisner M. Markers of endothelial damage in organ dysfunction and sepsis. Crit Care Med. 2002;30:S302–12.PubMedCrossRef Reinhart K, Bayer O, Brunkhorst F, Meisner M. Markers of endothelial damage in organ dysfunction and sepsis. Crit Care Med. 2002;30:S302–12.PubMedCrossRef
55.
Zurück zum Zitat Cermak J, Key NS, Bach RR, et al. C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor. Blood. 1993;82:513–20.PubMed Cermak J, Key NS, Bach RR, et al. C-reactive protein induces human peripheral blood monocytes to synthesize tissue factor. Blood. 1993;82:513–20.PubMed
56.
Zurück zum Zitat Durante Mangoni E, Adinolfi LE, Tripodi MF, Andreana A, Gambardella M, Ragone E, et al. Risk factors for ‘major’ embolic events in hospitalized patients with infective endocarditis. Am Heart J. 2003;146:55–61.CrossRef Durante Mangoni E, Adinolfi LE, Tripodi MF, Andreana A, Gambardella M, Ragone E, et al. Risk factors for ‘major’ embolic events in hospitalized patients with infective endocarditis. Am Heart J. 2003;146:55–61.CrossRef
57.•
Zurück zum Zitat Dickerman SA, Abrutyn E, Barsic B, et al. The relationship between the initiation of antimicrobial therapy and the incidence of stroke in infective endocarditis: an analysis from the ICE Prospective Cohort Study (ICE-PCS). Am Heart J. 2007;154:1086–94. Prospective study on a representative patient dataset showing the effect of antimicrobial treatment on inflammatory markers and embolic risk. PubMedCrossRef Dickerman SA, Abrutyn E, Barsic B, et al. The relationship between the initiation of antimicrobial therapy and the incidence of stroke in infective endocarditis: an analysis from the ICE Prospective Cohort Study (ICE-PCS). Am Heart J. 2007;154:1086–94. Prospective study on a representative patient dataset showing the effect of antimicrobial treatment on inflammatory markers and embolic risk. PubMedCrossRef
58.
Zurück zum Zitat Vigo C. Effect of C-reactive protein on platelet-activating factor induced platelet aggregation and membrane stabilization. J Biol Chem. 1985;260:3418–22.PubMed Vigo C. Effect of C-reactive protein on platelet-activating factor induced platelet aggregation and membrane stabilization. J Biol Chem. 1985;260:3418–22.PubMed
59.
Zurück zum Zitat Fiedel BA, Simpson RM, Gewurz H. Effects of C-reactive protein (CRP) on platelet function. Ann NY Acad Sci. 1982;389:263–73.PubMedCrossRef Fiedel BA, Simpson RM, Gewurz H. Effects of C-reactive protein (CRP) on platelet function. Ann NY Acad Sci. 1982;389:263–73.PubMedCrossRef
60.
Zurück zum Zitat Fiedel BA. Influence of tuftsin-like synthetic peptides derived from C-reactive protein (CRP) on platelet behaviour. Immunology. 1988;64:487–93.PubMedPubMedCentral Fiedel BA. Influence of tuftsin-like synthetic peptides derived from C-reactive protein (CRP) on platelet behaviour. Immunology. 1988;64:487–93.PubMedPubMedCentral
61.
Zurück zum Zitat Berckmans RJ, Nieuwland R, Boing AN, Romijn FP, Hack CE, Sturk A. Cell-derived microparticles circulate in healthy humans and support low grade thrombin generation. Thromb Haemost. 2001;85:639–46.PubMed Berckmans RJ, Nieuwland R, Boing AN, Romijn FP, Hack CE, Sturk A. Cell-derived microparticles circulate in healthy humans and support low grade thrombin generation. Thromb Haemost. 2001;85:639–46.PubMed
62.
Zurück zum Zitat Esmon CT. The interactions between inflammation and coagulation. Br J Haematol. 2005;131:417–30.PubMedCrossRef Esmon CT. The interactions between inflammation and coagulation. Br J Haematol. 2005;131:417–30.PubMedCrossRef
63.
Zurück zum Zitat Levi M, van der Poll T. Two-way interactions between inflammation and coagulation. Trends Cardiovasc Med. 2005;15:254–9.PubMedCrossRef Levi M, van der Poll T. Two-way interactions between inflammation and coagulation. Trends Cardiovasc Med. 2005;15:254–9.PubMedCrossRef
64.
Zurück zum Zitat Levi M, van der Poll T, Buller HR. Bidirectional relation between inflammation and coagulation. Circulation. 2004;109:2698–704.PubMedCrossRef Levi M, van der Poll T, Buller HR. Bidirectional relation between inflammation and coagulation. Circulation. 2004;109:2698–704.PubMedCrossRef
65.
Zurück zum Zitat Tleyjeh IM, Steckelberg JM, Murad HS, Anavekar NS, Ghomrawi HM, Mirzoyev Z, et al. Temporal trends in infective endocarditis: a population-based study in Olmsted County, Minnesota. JAMA. 2005;293(24):3022–8.PubMedCrossRef Tleyjeh IM, Steckelberg JM, Murad HS, Anavekar NS, Ghomrawi HM, Mirzoyev Z, et al. Temporal trends in infective endocarditis: a population-based study in Olmsted County, Minnesota. JAMA. 2005;293(24):3022–8.PubMedCrossRef
66.
Zurück zum Zitat Duval X, Delahaye F, Alla F, Tattevin P, Obadia JF, Le Moing V, et al. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. J Am Coll Cardiol. 2012;59(22):1968–76.PubMedCrossRef Duval X, Delahaye F, Alla F, Tattevin P, Obadia JF, Le Moing V, et al. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. J Am Coll Cardiol. 2012;59(22):1968–76.PubMedCrossRef
67.
Zurück zum Zitat Fedeli U, Schievano E, Buonfrate D, Pellizzer G, Spolaore P. Increasing incidence and mortality of infective endocarditis: a population-based study through a record-linkage system. BMC Infect Dis. 2011;11:48.PubMedCrossRefPubMedCentral Fedeli U, Schievano E, Buonfrate D, Pellizzer G, Spolaore P. Increasing incidence and mortality of infective endocarditis: a population-based study through a record-linkage system. BMC Infect Dis. 2011;11:48.PubMedCrossRefPubMedCentral
69.
Zurück zum Zitat Kupferwasser LI, Hafner G, Mohr-Kahaly S, Erbel R, Meyer J, Darius H. The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events. J Am Coll Cardiol. 1999;33:1365–71.PubMedCrossRef Kupferwasser LI, Hafner G, Mohr-Kahaly S, Erbel R, Meyer J, Darius H. The presence of infection-related antiphospholipid antibodies in infective endocarditis determines a major risk factor for embolic events. J Am Coll Cardiol. 1999;33:1365–71.PubMedCrossRef
70.
Zurück zum Zitat Lopez LR, Hurley BL, Durante-Mangoni E, Simpson DF, Tripodi MF, Guardascione M, et al. Oxidative modification of low-density lipoprotein (LDL) and oxLDL/b2GPI complexes in patients with infectious endocarditis: possible role in aortic valve disease. J Thromb Haemost. 2005;3(Suppl. 1):abstr. #1881. Lopez LR, Hurley BL, Durante-Mangoni E, Simpson DF, Tripodi MF, Guardascione M, et al. Oxidative modification of low-density lipoprotein (LDL) and oxLDL/b2GPI complexes in patients with infectious endocarditis: possible role in aortic valve disease. J Thromb Haemost. 2005;3(Suppl. 1):abstr. #1881.
71.
Zurück zum Zitat Ileri M, Alper A, Senen K, Durmaz T, Atak R, Hisar I, et al. Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events. Am J Cardiol. 2003;91:689–92.PubMedCrossRef Ileri M, Alper A, Senen K, Durmaz T, Atak R, Hisar I, et al. Effect of infective endocarditis on blood coagulation and platelet activation and comparison of patients with to those without embolic events. Am J Cardiol. 2003;91:689–92.PubMedCrossRef
72.
Zurück zum Zitat Buyukasýk NS, Ileri M, Alper A, Senen K, Atak R, Hisar I, et al. Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events. Clin Cardiol. 2004;27:154–8.PubMedCrossRef Buyukasýk NS, Ileri M, Alper A, Senen K, Atak R, Hisar I, et al. Increased blood coagulation and platelet activation in patients with infective endocarditis and embolic events. Clin Cardiol. 2004;27:154–8.PubMedCrossRef
73.
Zurück zum Zitat Mannucci PM. Venous thrombosis: the history of knowledge. Pathophysiol Haemost Thromb. 2002;32:209–12.PubMedCrossRef Mannucci PM. Venous thrombosis: the history of knowledge. Pathophysiol Haemost Thromb. 2002;32:209–12.PubMedCrossRef
75.
Zurück zum Zitat Strong JP, Richards ML. Cigarette smoking and atherosclerosis in autopsied men. Atherosclerosis. 1976;23:451–76.PubMedCrossRef Strong JP, Richards ML. Cigarette smoking and atherosclerosis in autopsied men. Atherosclerosis. 1976;23:451–76.PubMedCrossRef
76.
Zurück zum Zitat Di Micco P, D’Uva M. Editorial comment. To understand the two way clinical association between cancer and thrombophilia. Exp Oncol. 2003;25:243–4. Di Micco P, D’Uva M. Editorial comment. To understand the two way clinical association between cancer and thrombophilia. Exp Oncol. 2003;25:243–4.
77.
Zurück zum Zitat Lane DA, Mannucci PM, Bauer KA, Bertina RM, Bochkov NP, Boulyjenkov V, Chandy M, Dahlbäck B, Ginter EK, Miletich JP, Rosendaal FR, Seligsohn U. Inherited thrombophilia. Thromb Haemost. 1996; 76:651–62 (part I) & 824–34 (part II) Lane DA, Mannucci PM, Bauer KA, Bertina RM, Bochkov NP, Boulyjenkov V, Chandy M, Dahlbäck B, Ginter EK, Miletich JP, Rosendaal FR, Seligsohn U. Inherited thrombophilia. Thromb Haemost. 1996; 76:651–62 (part I) & 824–34 (part II)
78.
Zurück zum Zitat Vossen CY, Conard J, Fontcuberta J, et al. Familial thrombophilia and lifetime risk of venous thrombosis. J Thromb Haemost. 2004;2:1526–33.PubMedCrossRef Vossen CY, Conard J, Fontcuberta J, et al. Familial thrombophilia and lifetime risk of venous thrombosis. J Thromb Haemost. 2004;2:1526–33.PubMedCrossRef
79.
Zurück zum Zitat Seligsohn U, Lubetsky A. Genetic susceptibility to venous thrombosis. N Engl J Med. 2001;344:1222–31.PubMedCrossRef Seligsohn U, Lubetsky A. Genetic susceptibility to venous thrombosis. N Engl J Med. 2001;344:1222–31.PubMedCrossRef
80.
Zurück zum Zitat Green D. Genetic hypercoagulability: screening should be an informed choice. Blood. 2001;98:20.PubMedCrossRef Green D. Genetic hypercoagulability: screening should be an informed choice. Blood. 2001;98:20.PubMedCrossRef
81.
Zurück zum Zitat Mannucci PM. Genetic hypercoagulability: prevention suggests testing family members. Blood. 2010;98:21–2.CrossRef Mannucci PM. Genetic hypercoagulability: prevention suggests testing family members. Blood. 2010;98:21–2.CrossRef
82.
Zurück zum Zitat De Stefano V, Finazzi G, Mannucci PM. Inherited thrombophilia: pathogenesis, clinical syndromes, and management. Blood. 2006;87:3531. De Stefano V, Finazzi G, Mannucci PM. Inherited thrombophilia: pathogenesis, clinical syndromes, and management. Blood. 2006;87:3531.
83.
Zurück zum Zitat Martinelli I. Risk factors in venous thromboembolism. Thromb Haemost. 2001;86:395–403.PubMed Martinelli I. Risk factors in venous thromboembolism. Thromb Haemost. 2001;86:395–403.PubMed
84.
Zurück zum Zitat De Stefano V, Rossi E, Paciaroni K, et al. Screening for inherited thrombophilia: indications and therapeutic implications. Haematologica. 2002;87:1095–108.PubMed De Stefano V, Rossi E, Paciaroni K, et al. Screening for inherited thrombophilia: indications and therapeutic implications. Haematologica. 2002;87:1095–108.PubMed
85.
Zurück zum Zitat Bertina RM. Genetic approach to thrombophilia. J Endocrinol Investig. 2010;33(2):77–82.CrossRef Bertina RM. Genetic approach to thrombophilia. J Endocrinol Investig. 2010;33(2):77–82.CrossRef
86.
Zurück zum Zitat Rosendaal FR, Helmerhost FM, Vandenbroucke JP. Oral contraceptives, hormone replacement therapy and thrombosis. Thromb Haemost. 2001;86:112–3.PubMed Rosendaal FR, Helmerhost FM, Vandenbroucke JP. Oral contraceptives, hormone replacement therapy and thrombosis. Thromb Haemost. 2001;86:112–3.PubMed
87.
Zurück zum Zitat Korkmaz S, Ileri M, Hisar I, Yetkin E, Kosar F. Increased levels of soluble adhesion molecules, E-selectin and P-selectin, in patients with infective endocarditis and embolic events. Eur Heart J. 2001;22(10):874–8.PubMedCrossRef Korkmaz S, Ileri M, Hisar I, Yetkin E, Kosar F. Increased levels of soluble adhesion molecules, E-selectin and P-selectin, in patients with infective endocarditis and embolic events. Eur Heart J. 2001;22(10):874–8.PubMedCrossRef
88.
Zurück zum Zitat Durante-Mangoni E, Iossa D, Nappi F, et al. Inherited hyper-homocysteinemia as a cause of nonbacterial thrombotic endocarditis. J Heart Valve Dis. 2011;20:232–3.PubMed Durante-Mangoni E, Iossa D, Nappi F, et al. Inherited hyper-homocysteinemia as a cause of nonbacterial thrombotic endocarditis. J Heart Valve Dis. 2011;20:232–3.PubMed
89.
Zurück zum Zitat Eldibany MM, Caprini JA. Hyperhomocysteinemia and thrombosis: an overview. Arch Pathol Lab Med. 2007;131:872–84.PubMed Eldibany MM, Caprini JA. Hyperhomocysteinemia and thrombosis: an overview. Arch Pathol Lab Med. 2007;131:872–84.PubMed
Metadaten
Titel
The Role of Hemostasis in Infective Endocarditis
verfasst von
Emanuele Durante-Mangoni
Rosa Molaro
Domenico Iossa
Publikationsdatum
01.11.2014
Verlag
Springer US
Erschienen in
Current Infectious Disease Reports / Ausgabe 11/2014
Print ISSN: 1523-3847
Elektronische ISSN: 1534-3146
DOI
https://doi.org/10.1007/s11908-014-0435-8

Weitere Artikel der Ausgabe 11/2014

Current Infectious Disease Reports 11/2014 Zur Ausgabe

Skin, Soft Tissue, Bone and Joint Infectious Diseases (N Safdar, Section Editor)

Mycobacterial Skin and Soft Tissue Infection

Tropical, Travel and Emerging Infections (L Chen, Section Editor)

Neurocysticercosis: An Update

Central Nervous System Infections (J Lyons, Section Editor)

Spinal Epidural Abscess

Tropical, Travel and Emerging Infections (L Chen, Section Editor)

Recent Advances in Clinical Parasitology Diagnostics

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag

Battle of Experts: Sport vs. Spritze bei Adipositas und Typ-2-Diabetes

11.05.2024 DDG-Jahrestagung 2024 Kongressbericht

Im Battle of Experts traten zwei Experten auf dem Diabeteskongress gegeneinander an: Die eine vertrat die Auffassung „Sport statt Spritze“ bei Adipositas und Typ-2-Diabetes, der andere forderte „Spritze statt Sport!“ Am Ende waren sie sich aber einig: Die Kombination aus beidem erzielt die besten Ergebnisse.

Vorsicht, erhöhte Blutungsgefahr nach PCI!

10.05.2024 Koronare Herzerkrankung Nachrichten

Nach PCI besteht ein erhöhtes Blutungsrisiko, wenn die Behandelten eine verminderte linksventrikuläre Ejektionsfraktion aufweisen. Das Risiko ist umso höher, je stärker die Pumpfunktion eingeschränkt ist.

Triglyzeridsenker schützt nicht nur Hochrisikopatienten

10.05.2024 Hypercholesterinämie Nachrichten

Patienten mit Arteriosklerose-bedingten kardiovaskulären Erkrankungen, die trotz Statineinnahme zu hohe Triglyzeridspiegel haben, profitieren von einer Behandlung mit Icosapent-Ethyl, und zwar unabhängig vom individuellen Risikoprofil.

Gibt es eine Wende bei den bioresorbierbaren Gefäßstützen?

In den USA ist erstmals eine bioresorbierbare Gefäßstütze – auch Scaffold genannt – zur Rekanalisation infrapoplitealer Arterien bei schwerer PAVK zugelassen worden. Das markiert einen Wendepunkt in der Geschichte dieser speziellen Gefäßstützen.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.