Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis

Introducción: La sepsis representa una entidad que es generada por respuesta sistémica a la infección, inicialmente en 1992 se definió enfocada en el síndrome de respuesta inflamatoria sistémica(7), en el 2016 se modificó y ahora es considerada por The Third International Consensus Definitions for S...

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Autores:
Rueda Galvis, Myriam Vanessa
Tipo de recurso:
Fecha de publicación:
2018
Institución:
Universidad Autónoma de Bucaramanga - UNAB
Repositorio:
Repositorio UNAB
Idioma:
spa
OAI Identifier:
oai:repository.unab.edu.co:20.500.12749/1734
Acceso en línea:
http://hdl.handle.net/20.500.12749/1734
Palabra clave:
Systemic inflammatory response syndrome
Septic cardiomyopathy
Sepsis
Troponin I
Medicine
Internal medicine
Investigations
Complications
Patients
Prevention and control
Third consensus
Mortality
Systolic dysfunction
Diastolic dysfunction
Septic shock
Intensive care unit
Síndrome de respuesta inflamatoria sistémica
Miocardiopatía séptica
Sepsis
Troponina I
Medicina
Medicina interna
Investigaciones
Complicaciones
Pacientes
Prevención y control
Tercer consenso
NT pro BNP
Mortalidad
Disfunción sistólica
Disfunción diastólica
Choque séptico
Unidad de cuidados intensivos
Rights
openAccess
License
http://creativecommons.org/licenses/by-nc-nd/2.5/co/
id UNAB2_1d4dfbef12b865c783ff92859ce96514
oai_identifier_str oai:repository.unab.edu.co:20.500.12749/1734
network_acronym_str UNAB2
network_name_str Repositorio UNAB
repository_id_str
dc.title.spa.fl_str_mv Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
dc.title.translated.eng.fl_str_mv Strength of association between Troponin I, NT-pro BNP and adverse outcomes in sepsis
title Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
spellingShingle Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
Systemic inflammatory response syndrome
Septic cardiomyopathy
Sepsis
Troponin I
Medicine
Internal medicine
Investigations
Complications
Patients
Prevention and control
Third consensus
Mortality
Systolic dysfunction
Diastolic dysfunction
Septic shock
Intensive care unit
Síndrome de respuesta inflamatoria sistémica
Miocardiopatía séptica
Sepsis
Troponina I
Medicina
Medicina interna
Investigaciones
Complicaciones
Pacientes
Prevención y control
Tercer consenso
NT pro BNP
Mortalidad
Disfunción sistólica
Disfunción diastólica
Choque séptico
Unidad de cuidados intensivos
title_short Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
title_full Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
title_fullStr Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
title_full_unstemmed Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
title_sort Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis
dc.creator.fl_str_mv Rueda Galvis, Myriam Vanessa
dc.contributor.advisor.spa.fl_str_mv Machado Romero, Carlos Alfonso
Higuera Cobos, Juan Diego
Ochoa Vera, Miguel Enrique
dc.contributor.author.spa.fl_str_mv Rueda Galvis, Myriam Vanessa
dc.contributor.cvlac.*.fl_str_mv https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0000898465
https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001543126
https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001692834
dc.contributor.orcid.*.fl_str_mv https://orcid.org/0000-0002-4552-3388
https://orcid.org/0000-0003-2622-9412
dc.contributor.scopus.*.fl_str_mv https://www.scopus.com/authid/detail.uri?authorId=36987156500
dc.contributor.researchgate.*.fl_str_mv https://www.researchgate.net/profile/Miguel_Ochoa7
dc.contributor.researchgroup.spa.fl_str_mv Grupo de Investigación en Ciencias y Educación en Salud
Grupo de Investigaciones Clínicas
dc.subject.keywords.eng.fl_str_mv Systemic inflammatory response syndrome
Septic cardiomyopathy
Sepsis
Troponin I
Medicine
Internal medicine
Investigations
Complications
Patients
Prevention and control
Third consensus
Mortality
Systolic dysfunction
Diastolic dysfunction
Septic shock
Intensive care unit
topic Systemic inflammatory response syndrome
Septic cardiomyopathy
Sepsis
Troponin I
Medicine
Internal medicine
Investigations
Complications
Patients
Prevention and control
Third consensus
Mortality
Systolic dysfunction
Diastolic dysfunction
Septic shock
Intensive care unit
Síndrome de respuesta inflamatoria sistémica
Miocardiopatía séptica
Sepsis
Troponina I
Medicina
Medicina interna
Investigaciones
Complicaciones
Pacientes
Prevención y control
Tercer consenso
NT pro BNP
Mortalidad
Disfunción sistólica
Disfunción diastólica
Choque séptico
Unidad de cuidados intensivos
dc.subject.lemb.spa.fl_str_mv Síndrome de respuesta inflamatoria sistémica
Miocardiopatía séptica
Sepsis
Troponina I
Medicina
Medicina interna
Investigaciones
Complicaciones
Pacientes
Prevención y control
dc.subject.proposal.none.fl_str_mv Tercer consenso
NT pro BNP
Mortalidad
Disfunción sistólica
Disfunción diastólica
Choque séptico
Unidad de cuidados intensivos
description Introducción: La sepsis representa una entidad que es generada por respuesta sistémica a la infección, inicialmente en 1992 se definió enfocada en el síndrome de respuesta inflamatoria sistémica(7), en el 2016 se modificó y ahora es considerada por The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) como una respuesta no regulada a la infección que causa disfunción orgánica múltiple y pone en peligro la vida. Los biomarcadores cardiacos (Troponina I, NT pro BNP) se demostraron útiles en la predicción de desenlaces adversos en sepsis, sin embargo con el advenimiento de la nueva definición esta relación no está probada. Métodos: Este es un estudio de evaluación de prueba diagnóstica en participantes del estudio ―Asociación entre la actividad de las Metaloproteinasas de matriz extracelular (MMPs) y la disfunción cardiovascular en pacientes con sepsis. Se calculó la asociación de NT pro BNP, troponina I y mortalidad, choque séptico, disfunción sistólica /diastólica e ingreso a UCI. Resultados: Se analizaron 289 registros. La mediana de edad de los pacientes fue de 63 años con un rango de edad entre 49-77 años. La mediana de NT-pro BNP fue 2099 (RIQ: 533-9051) y de la troponina I 0.1 (RIQ: 0.1-0.2). La mediana del SOFA de 4 (RIQ: 0-13), del APACHE II 13 (RIQ: 8-19) . El origen más frecuente de la sepsis fue tracto urinario (39.1%). El 28.37% (82) de los casos en la cohorte fallecieron. La disfunción sistólica estuvo presente en 39.83 %, la disfunción diastólica 69.11%. El 55.71% fueron manejados en unidad de cuidados intensivo, 47.06% presentaban sepsis. Se encontró una relación positiva estadísticamente significativa (p<0.001) entre niveles séricos de NT pro BNP, troponina I y mortalidad, disfunción sistólica y choque séptico, con AUC con capacidad predictiva pobre. No se halló asociación con NT pro BNP, troponina I y disfunción diastólica o ingreso a UCI. Conclusiones: Aún con criterios más específicos de clasificación de sepsis existe una asociación significativa entre biomarcadores de injuria miocárdica en sepsis y desenlaces adversos. Sus características psicométricas no son buenas, en este estudio son iguales a las de las escalas de riesgo conocidas a la fecha (SOFA-APACHE II)
publishDate 2018
dc.date.issued.none.fl_str_mv 2018
dc.date.accessioned.none.fl_str_mv 2020-06-26T19:59:54Z
dc.date.available.none.fl_str_mv 2020-06-26T19:59:54Z
dc.type.driver.none.fl_str_mv info:eu-repo/semantics/masterThesis
dc.type.local.spa.fl_str_mv Tesis
dc.type.redcol.none.fl_str_mv http://purl.org/redcol/resource_type/TM
dc.identifier.uri.none.fl_str_mv http://hdl.handle.net/20.500.12749/1734
dc.identifier.instname.spa.fl_str_mv instname:Universidad Autónoma de Bucaramanga - UNAB
dc.identifier.reponame.spa.fl_str_mv reponame:Repositorio Institucional UNAB
url http://hdl.handle.net/20.500.12749/1734
identifier_str_mv instname:Universidad Autónoma de Bucaramanga - UNAB
reponame:Repositorio Institucional UNAB
dc.language.iso.spa.fl_str_mv spa
language spa
dc.relation.references.spa.fl_str_mv Rueda Galvis, Myriam Vanessa (2018). Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis. Bucaramanga (Santander, Colombia) : Universidad Autónoma de Bucaramanga UNAB
1. Torio, C.M, Andrews, R.M. (2013). National in patient hospital costs: the most expensive conditions by payer, Statistical Brief #160. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs.. http://www.ncbi.nlm.nih.gov/books NBK169005/.
2. Hotchkiss, R.S., Swanson, P.E., Freeman, B.D., et al. (2011) Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. Critical Care Medicine, 27(7), 1230-1251.
3. Hotchkiss, R.S., Monneret, G., Payen,D. (2013). Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Natural Reviews Immunology, 13(12), 862-874.
4. Singer, M., Clifford S.D., Seymour W., et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 315(8),801-810.
5. Parrillo, J.E., Parker ,M.M., Natanson, C., et al. (1990). Septic shock in humans: advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Annals of Internal Medicine, 113,227-42.
6. Vincent, J.L., de Mendonça, A., Cantraine, F, et al. (1998). Working Group on ―Sepsis-Related Problems‖ of the European Society of Intensive Care Medicine. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Critical Care Medicine, 26(11), 1793-1800.
7. Bone, R.C., Balk, R.A., Cerra, F.B., et al. (1992). American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Critical Care Medicine, 20(6), 864-874.
8. Mervyn, S. (2016). The new sepsis consensus definitions (Sepsis-3): the good, the not so bad, and the actually quite pretty. Intensive Care Medicine. Publicado online 23 Diciembre 2016. DOI 10.1007/s00134-016-4600-4
9. Gaieski, D.F., Edwards J.M., Kallan M.J., et al. (2013). Benchmarking the incidence and mortality of severe sepsis in the United States. Critical Care Medicine, 41(5),1167-1174.
10. Vincent, J.L., Marshall J.C., Namendys-Silva S.A., et al. (2014). Assessment of the worldwide burden of critical illness: the Intensive Care Over Nations (ICON) audit. Lancet Respiratory Medicine, 2(5),380-386.
11. Wang W., Sawicki G., Schulz R. (2002). Peroxynitrite-induced myocardial injury is mediated through matrix metalloproteinase-2. Cardiovascular Research, 53, 165–174
12. Alvarez, S., Vico, T., Vanasco, V. (2016) Cardiac dysfunction, mitocondrial architecture, energy production, and inflammatory pathways: interrelated aspects in endotoxemia and sepsis. The International Journal of Biochemistry & Cell Biology, 81(Pt B), 307-314.
13. De Angelo J. (1999) . Nitric oxide scavengers in the treatment of shock associated with systemic inflammatory response syndrome. Expert Opinion Pharmacotherapy, (1), 19-29.
14. Cimolai, M.C., Alvarez, S., Bode C., et al.(2015). Mitochondrial Mechanisms in Septic Cardiomyopathy. Internal Journal of Molecular Scinces, (16), 17763-17778.
15. Romero-Bermejo, F.J., Ruiz-Bailen, M., Gil-Cebrian, J., et al. (2011). Sepsis-induced cardiomyopathy. Current Cardiology Reviews, (7), 163-183.
16. Ince, C., Mayeux, P.R., Nguyen, T, el al. (2016). The Endothelium in Sepsis. Shock, (45), 259-270
17. Dauphinee, S.M., Karsan, A., 2006. Lipopolysaccharide signaling in endothelial cells. Laboratory Investigation Journal , 86, 9-22.
18. Morikawa, A., Koide, N., Kato, Y., et al. 2000. Augmentation of nitric oxide production by gamma interferon in a mouse vascular endothelial cell line and its modulation by tumor necrosis factor alpha and lipopolysaccharide. Infection and Immunity Journal. 68, 6209-6214.
19. Liaudet, L., Soriano, F.G., Szabó, C. (2000) . Pathophysiological role of nitric oxide in inflammation, in: Nitric Oxide, biology and pathology. Critical Care Medicine, 28(4), 841-872.
20. Thiemermann, C., Vane, J., (1990). Inhibition of nitric oxide synthesis reduces the hypotension induced by bacterial lipopolysaccharides in the rat in vivo. European Journal of Pharmacology, 182, 591-595.
21. Blanco, J., Muriel-Bombin, A., Sagredo, V., Taboada, F., Gandia, F., Tamayo, L., Collado, J., Garcia-Labattut, A., Carriedo, D., Valledor, M., De Frutos, M., Lopez, M.J., Caballero, A., Guerra, J., Alvarez, B., Mayo, A., Villar, J., (2008). Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Critical Care, 12(6), R158.
22. McDonough, K.H., Virag, J.I., (2006). Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury. Frontiers Bioscience, 11, 23-32.
23. Poelaert, J., Declerck, C., Vogelaers, D., et al, (1997). Left ventricular systolic and diastolic function in septic shock. Intensive Care Medicine, 23, 553-560.
24. Smeding, L., Plotz, F.B., Groeneveld, A.B., et al. (2012). Structural changes of the heart during severe sepsis or septic shock. Shock, 37, 449-456.
25. Larche, J., Lancel, S., Hassoun, S.M., et al. (2006). Inhibition of mitochondrial permeability transition prevents sepsis- induced myocardial dysfunction and mortality. Journal of the American College of Cardiology, 48, 377-385.
26. Levy, R.J., Piel, D.A., Acton, P.D., et al. (2005). Evidence of myocardial hibernation in the septic heart. Critical Care Medicine, 33, 2752- 2756.
27. Piantadosi, C.A., Suliman, H.B. (2012). Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes. Biochimica et Biophysica Acta, 1820, 532-541.
28. Vanasco, V., Saez, T., Magnani, N.D., et al. (2014). Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery. Free Radical Biology and Medicine, 77, 1-9.
29. Vieillard-Baron A. (2001). Septic cardiomyopathy. Annals of Intensive Care, 1, 6–7.
30. Hochstadt, A., Meroz, Y., Landesberg, G. (2011). Myocardial dysfunction in severe sepsis and septic shock: more questions than answers?. Journal of Cardiothoracic and Vasc Anesthesia, 25 (3), 526–35.
31. dos Santos, C.C., Gattasm, D.J., Tsoporis, J.N., et al. (2010). Sepsis-induced myocardial depression is associated with transcriptional changes in energy metabolism and contractile related genes: a physiological and gene expression based approach. Critical Care Medicine, 38 (3), 894–902.
32. Stengl, M., Bartak, F., Sykora, R., et al. (2010). Reduced L-type calcium current in ventricular myocytes from pigs with hyperdynamic septic shock. Critical Care of Medicine, 38(2), 580–7.
33. Antonucci, E., Fiaccadori, E., Donadello, K., et al. (2013). Myocardial depression in sepsis: From pathogenesis to clinical manifestations and treatment. Journal of Critical Care, 29(4), 500-11.
34. Repessé, X., Charron, C., Vieillard-Baron, A. (2013). Evaluation of left ventricular systolic function revisited in septic shock. Critical Care, 17(4), 164.
35. Vieillard-Baron, A., Caille, V., Charron, C., et al. (2008). Actual incidence of global left ventricular hypokinesia in adult septic shock. Critical Care Medicine, 36(6), 1701-6
36. Parker, M.M., Shelhamer, J.H., Bacharach, S.L., et al. (1984) Profound but reversible myocardial depression in patients with septic shock. Annals of Internal Medicine, 100:483–90.
37. Guarracino, F., Baldassarri, R., Pinsky, M.R. (2013). Ventriculo-arterial decoupling in acutely altered hemodynamic states. Critical Care, 17(2), 213–20.
38. Landesberg, G., Gilon, D., Meroz, Y., et al. (2012). Diastolic dysfunction and mortality in severe sepsis and septic shock. European Heart Journal, 33(7), 895–903.
39. Roosens, C.D., Ama, R., Leather, H.A., et al. (2006). Hemodynamic effects of different lung- protective ventilation strategies in closed-chest pigs with normal lungs. Critical Care of Medicine, 34(12), 2990–6.
40. Pinsky, M.R. (2005). Cardiovascular issues in respiratory care. Chest, 128, 592–7.
41. Latini, R., Caironi, R., Masson, S. (2016). Cardiac dysfunction and circulating cardiac markers during sepsis. Minerva anestesiologica , 82(6), 697-710
42. Maeder, M,, Fehr, T., Rickli, H., et al. (2006). Sepsis associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest, 129:1349-66
43. Rajaram, S.S., Desai, N.K., Kalra, A., et al.(2013). Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Systematic Review, 28(2),1–59.
44. Sandham, J.D, Hull, R.D., Brant, R.F., et al. (2003). A randomized, controlled trial of the use of pulmonary-artery catheters in high risk surgical patients. The New England Journal of Medicine,348(1), 5-14.
45. Wheeler, A.P., Bernard, G.R, Thompson, B.T., et al. (2006). Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. The New England Journal of Medicine, 354(41), 2213-24.
46. Brett, J., Gerlach, H., Nawroth, P., et al. (1989). Tumor necrosis factor/cachectin increases permeability of endothelial cell monolayers by a mechanism involving regulatory G proteins. The Journal of Experimental Medicine, 169(6), 1977–91
47. Landesberg, G., Jaffe A.S., Gilon D., et al. (2014). Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation. Critical Care Medicine, 42(4), 790-800.
48. Markou, N., Gregorakos, L., Myrianthefs, P. (2011). Increased blood troponin levels in ICU patients. Current Opininon Critical Care, 1(5)7, 454–463.
49. Brivet, F.G., Jacobs, F.M., Colin, P., et al. (2006). Cardiac troponin level is not an independent predictor of mortality in septic patients requiring medical intensive care unit admission. Critical Care, 10(1), 404.
50. Bessiére, F., Khenifer, S., Dubourg, I., et al. (2013). Prognostic value of troponins in sepsis: a meta-analysis. Intensive Care Medicine , 39(7), 1181–1189
51. Spies, C., Haude, V., Fitzner, R., Schroder, K., et al. (1998). Serum cardiac troponin T as a prognostic marker in early sepsis. Chest, 113, 1055–1063
52. Bouhemad, B., Nicolas-Robin, A., Arbelot, C., et al. (2008). Isolated and reversible impairment of ventricular relaxation in patients with septic shock. Critical Care Medicine, 36(3) , 766–774
53. Clerico, A. (2002). Pathophysiological and clinical relevance of circulating levels of cardiac natriuretic hormones: Are they merely markers of cardiac disease? Clinical Chemistry and Laboratory Medicine, 40(8), 752-60
54. Ueda, S., Nishio, K., Akai, Y., et al. (2006). Prognostic value of increased plasma levels of brain natriuretic peptide in patients with septic shock. Shock, 26(2), 134-139
55. Cuthbertson, B.H., Patel, R.R., Croal B.L., et al. (2005), B-type natriuretic peptide and the prediction of outcome in patients admitted to intensive care. Anaesthesia, 60(1), 16-21.
56. Tomaru, K.K., Arai, M., Yokoyama, T., et al. (2002). Transcriptional activation of the BNP gene by lipopolysaccharide is mediated through GATA elements in neonatal rat cardiac myocytes. Journal of Mollecular and Cellular Cardiology, 34(6), 649-659.
57. Turner, K.L., Moore, L.J., Todd, S.R., et al. (2011). Identification of cardiac dysfunction in sepsis with B-type natriuretic peptide. Journal of the American Collegues Surgeons, 213(1), 139–46.
58. Long, B., Koyfman, A. (2017). Ready for Prime Time? Biomarkers in Sepsis. Emergency Medicine Clinics of North America, 35, 109–122.
59. Wang, F., Wu, Y., Tang, L., et al. (2012). Brain natriuretic peptide for prediction of mortality in patients with sepsis: a systematic review and meta-analysis . Critical Care, 16:R74.
60. Post, F., Weilemann, L.S., Messow, C.M., et al. (2008). B-type natriuretic peptide as a marker for sepsis induced myocardial depression in intensive care patients. Critical Care Medicine, 36(11),3030-3037.
61. Mokart, D., Sannini, A., Brun, J.P., et al. (2007). N- terminal pro-brain natriuretic peptide as an early prognostic factor in cancer patients developing septic shock. Critical Care , 11(2), R37.
62. Seung, R., Kim, W.Y., Won, H.J., et al. (2015). Prognostic Value of B-type Natriuretic Peptide With the Sequential Organ Failure Assessment Score in Septic Shock . American Journal of medical sciencies, 349 (4), 287–291.
63. Müller-Werdan, U., Werdan, K. (1999). Septic cardiomyopathy. Current Opinion in Critical Care, 5,415–421.
64. Parker, M.M., Shelhamer, J.H., Natanson, C., el al. (1989). Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: heart rate as an early predictor of prognosis. Critical Care Medicine, 15(10),923–929.
65. Hestenes, S.M., Halvorsen P.S., Skulstad, H., et al.(2014). Advantages of Strain Echocardiography in Assessment of Myocardial Function in Severe Sepsis: An Experimental Study. Critical Care Medicine, 42(6), 432-440.
66. Werdan, K., Oelke, A., Hettwer, S., et al. (2011). Septic cardiomyopathy: Hemodynamic quantification, occurrence, and prognostic implications. Clinical Research in Cardiology, 100(8), 661–668.
67. Brown, S., Pittman, J., Hirshberg, E.L., et al. (2012) Diastolic dysfunction and mortality in early severe sepsis and septic shock: a prospective, observational echocardiography study. Critical Ultrasound Journal, 4(1), 8.
68. Bouhemad, B., Nicolas-Robin, A., Benois, A., et al. (2003). Echocardiographic Doppler assessment of pulmonary capillary wedge pressure in surgical patients with postoperative circulatory shock and acute lung injury. Anesthesiology, 98(5), 1091–1100.
69. Vicent, J.L, Moreno R., Takala., et al. (1996). The SOFA (Sepsis realted organ failure assessment) score to describe organ dysfunction/ failure. Intensive Care Medicine, 22(), 707-710.
70. Ferreira, F.L., Bota, D.P., Bross, A., et al. (2001). Serial evaluation of the SOFA score to predict outcome in critically ill patients. JAMA, 286(14):1754-8
71. 72. Knaus, W.A., Draper, E.A., Wagner , D.P., et al. (1985). APACHE II: everity of disease clasification system. Critical Care Medicine, 13(10), 818-820.
72. Capuzzo, M., Valpondi, V., Sgarbi, A. (2000). Validation of severity scoring systems SAPS II and APACHE II in a single-center population.Intensive Care Medicine, 26(12), 1779.
73. Zimmerman J.E., Kramer, A.A., McNair, D.S., et al. (2006) Acute Physiology and Chronic Health Evaluation (APACHE) IV: hospital mortality assessment for today's critically ill patients. Critical Care of Medicine, 34(5):1297-310.
74. Swets J. (1988). Measuring the Accuracy of Diagnostic Systems. American Association for the Advancement of Science, 240 (4857), 1285- 1293.
75. Mokart D, Brun JP, Faucher M., et al (2007) : N- terminal pro-brain natriuretic peptide as an early prognostic factor in cancer patients developing septic shock. Critical Care of Medicine, (11):37.
76. Roch A., Alladet-Servent, J., Michelet P., et al. (2005): NH2 terminal pro- brain natriuretic peptide plasma level as an early marker of prognosis and cardiac dysfunction in septic shock patients Critical Care of Medicine, 33(5): 1001-1007.
77. Chen Y., Li C. (2009) : Prognostic significance of brain natriuretic peptide obtained in the ED in patients with SIRS or sepsis. American Journal of Emergency Medicine, 27: 701-706.
78. Klouche, K., Pommet, S., Amigues, L., et al (2014) Plasma Brain Natriuretic Peptide and Troponin Levels in Severe Sepsis and Septic Shock : Relationships With Systolic Myocardial Dysfunction and Intensive Care Unit Mortality. Journal or Intensive Care Medicine, 29(4):229-37
79. Charpentier J, Luyt CE, Fulla Y, et al. (2004) Brain natriuretic peptide: a marker of myocardial dysfunction and prognosis during severe sepsis. Critical Care of Medicine. 32(3):660-665.
80. Maeder M, Ammann P, Kiowski W, Rickli H. (2005) B-type natriuretic peptide in patients with sepsis and preserved left ventricular ejection fraction. European Journal of Heart Failure. 2005;7(7):1164-1167.
81. Landesber, G., Jaffe, A., Gilon, Dan., et al. (2014) Troponin Elevation in Severe Sepsis and Septic Shock: The Role of Left Ventricular Diastolic Dysfunction and Right Ventricular Dilatation. Critical Care of Medicine. 42:790–800.
82. Redfield MM, Jacobsen SJ, Burnett JC Jr, et al.(2003) Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JaMa. 289:194-202.
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dc.publisher.grantor.spa.fl_str_mv Universidad Autónoma de Bucaramanga UNAB
dc.publisher.faculty.spa.fl_str_mv Facultad Ciencias de la Salud
dc.publisher.program.spa.fl_str_mv Especialización en Medicina Interna
institution Universidad Autónoma de Bucaramanga - UNAB
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spelling Machado Romero, Carlos Alfonso9d3238ed-2da9-474d-a7c3-f672667a87cf-1Higuera Cobos, Juan Diego186d9eee-08a0-49b0-aa1d-20f6d2234f70-1Ochoa Vera, Miguel Enriquebf83ca83-93c9-401e-91d3-b424889e868f-1Rueda Galvis, Myriam Vanessaf568b178-79af-4ba3-a303-03d25bad2c29-1https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0000898465https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001543126https://scienti.minciencias.gov.co/cvlac/visualizador/generarCurriculoCv.do?cod_rh=0001692834https://orcid.org/0000-0002-4552-3388https://orcid.org/0000-0003-2622-9412https://www.scopus.com/authid/detail.uri?authorId=36987156500https://www.researchgate.net/profile/Miguel_Ochoa7Grupo de Investigación en Ciencias y Educación en SaludGrupo de Investigaciones Clínicas2020-06-26T19:59:54Z2020-06-26T19:59:54Z2018http://hdl.handle.net/20.500.12749/1734instname:Universidad Autónoma de Bucaramanga - UNABreponame:Repositorio Institucional UNABIntroducción: La sepsis representa una entidad que es generada por respuesta sistémica a la infección, inicialmente en 1992 se definió enfocada en el síndrome de respuesta inflamatoria sistémica(7), en el 2016 se modificó y ahora es considerada por The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) como una respuesta no regulada a la infección que causa disfunción orgánica múltiple y pone en peligro la vida. Los biomarcadores cardiacos (Troponina I, NT pro BNP) se demostraron útiles en la predicción de desenlaces adversos en sepsis, sin embargo con el advenimiento de la nueva definición esta relación no está probada. Métodos: Este es un estudio de evaluación de prueba diagnóstica en participantes del estudio ―Asociación entre la actividad de las Metaloproteinasas de matriz extracelular (MMPs) y la disfunción cardiovascular en pacientes con sepsis. Se calculó la asociación de NT pro BNP, troponina I y mortalidad, choque séptico, disfunción sistólica /diastólica e ingreso a UCI. Resultados: Se analizaron 289 registros. La mediana de edad de los pacientes fue de 63 años con un rango de edad entre 49-77 años. La mediana de NT-pro BNP fue 2099 (RIQ: 533-9051) y de la troponina I 0.1 (RIQ: 0.1-0.2). La mediana del SOFA de 4 (RIQ: 0-13), del APACHE II 13 (RIQ: 8-19) . El origen más frecuente de la sepsis fue tracto urinario (39.1%). El 28.37% (82) de los casos en la cohorte fallecieron. La disfunción sistólica estuvo presente en 39.83 %, la disfunción diastólica 69.11%. El 55.71% fueron manejados en unidad de cuidados intensivo, 47.06% presentaban sepsis. Se encontró una relación positiva estadísticamente significativa (p<0.001) entre niveles séricos de NT pro BNP, troponina I y mortalidad, disfunción sistólica y choque séptico, con AUC con capacidad predictiva pobre. No se halló asociación con NT pro BNP, troponina I y disfunción diastólica o ingreso a UCI. Conclusiones: Aún con criterios más específicos de clasificación de sepsis existe una asociación significativa entre biomarcadores de injuria miocárdica en sepsis y desenlaces adversos. Sus características psicométricas no son buenas, en este estudio son iguales a las de las escalas de riesgo conocidas a la fecha (SOFA-APACHE II)RESUMEN Y PALABRAS CLAVE ............................................................................................... 8 SUMMARY AND KEYWORDS .................................................................................................. 9 INTRODUCCIÓN ................................................................................................................... 10 1. OBJETIVOS ................................................................................................................... 13 Objetivos Específicos .......................................................................................................................... 13 2. PLANTEAMIENTO DEL PROBLEMA .................................................................................... 14 3.MARCO TEÓRICO Y ESTADO DEL ARTE .............................................................................. 16 3.1 Fisiopatología de la sepsis: ........................................................................................................... 16 3.2 Disfunción cardiaca en sepsis, fisiopatología : ............................................................................ 17 3.3 Alteraciones hemodinámicas en miocardiopatía séptica: ........................................................... 21 3.4 Definición de cardiomiopatía séptica: .......................................................................................... 22 3.5 Ventilación mecánica y cardiomiopatía séptica : ......................................................................... 24 3.6 Métodos diagnósticos de cardiomiopatía séptica ....................................................................... 25 3.7 Biomarcadores de origen cardiogénico........................................................................................ 27 3.8 Manifestaciones ecocardiográficas .............................................................................................. 34 3.9 Puntajes de predicción de riesgo: ............................................................................................... 36 4. METODOLOGÍA ................................................................................................................ 39 4.1 Tipo de estudio ............................................................................................................................. 39 4.2 Población ...................................................................................................................................... 39 4.3 Muestra ........................................................................................................................................ 39 4.4 Recolección de la información ..................................................................................................... 40 4.5 Procesamiento y control de calidad ............................................................................................. 42 4.6 Procesamiento y Análisis estadístico ........................................................................................... 42 5. CONSIDERACIONES ÉTICAS .............................................................................................. 43 6. RESULTADOS ................................................................................................................... 45 6.1 Características de base ................................................................................................................. 45 6.2 Desenlaces primarios ................................................................................................................... 45 6.2.1 Exactitud diagnostica de la NT- pro BNP ................................................................................... 46 6.2.2 Exactitud diagnostica de la Troponina I .................................................................................... 48 6.2.3. Desenlace SOFA modificado ..................................................................................................... 49 6.2.4. Desenlace APACHE II modificado ............................................................................................. 50 7. DISCUSIÓN ...................................................................................................................... 51 8.LIMITACIONES Y FORTALEZAS ........................................................................................... 55 9. CONCLUSIONES................................................................................................................ 57 10. BIBLIOGRAFIA ................................................................................................................ 58 TABLAS ................................................................................................................................ 64 FIGURAS .............................................................................................................................. 66 ANEXOS............................................................................................................................... 74 CRONOGRAMA .................................................................................................................... 88EspecializaciónBackground: Sepsis represents an entity that is generated by a systemic response to infection. In1992 was defined based on the systemic inflammatory response syndrome (7), in 2016 it was modified and is now considered by The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) as an unregulated response to infection, that causes multiple organ dysfunction and endangers life. The cardiac biomarkers (Troponin I, NT pro BNP) was useful in the prediction of adverse outcomes in sepsis, however with the new definition this relationship is not proven. Methods: This study is an evaluation study of the diagnostic test in participants of the study "Association between the activity of extracellular matrix metalloproteinases (MMPs) and cardiovascular dysfunction in patients with sepsis. The association of NT pro BNP, troponin I and mortality, septic shock, systolic / diastolic dysfunction and admission to the ICU was calculated. Results: We analyzed 289 records. The median age of the patients was 63 years with an age range between 49-77 years. The median NT-pro BNP was 2099 (RIQ: 533-9051) and troponin I 0.1 (RIQ: 0.1-0.2). The SOFA median of 4 (RIQ: 0-13), of the APACHE II 13 (RIQ: 8-19). The most frequent origin of sepsis was the urinary tract (39.1%). 28.37% (82) of the cases in the cohort died. Systolic dysfunction was present in 39.83%, diastolic dysfunction 69.11%. 55.71% were managed in intensive care unit, 47.06% had sepsis. A statistically significant positive relationship (p <0.001) was found between serum levels of NT pro BNP, troponin I and mortality, systolic dysfunction and septic shock, with AUC with poor predictive capacity. No association was found with NT pro BNP, troponin I and diastolic dysfunction or admission to the ICU. Conclusions: Even with more specific criteria for the classification of sepsis, there is a significant association between biomarkers of myocardial injury in sepsis and adverse outcomes. Its psychometric characteristics are not the best, but in this study are similar to the risk scales known to date (SOFA-APACHE II)Modalidad Presencialapplication/pdfspahttp://creativecommons.org/licenses/by-nc-nd/2.5/co/Abierto (Texto Completo)info:eu-repo/semantics/openAccesshttp://purl.org/coar/access_right/c_abf2Atribución-NoComercial-SinDerivadas 2.5 ColombiaFuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsisStrength of association between Troponin I, NT-pro BNP and adverse outcomes in sepsisEspecialista en Medicina InternaBucaramanga (Santander, Colombia)UNAB Campus BucaramangaUniversidad Autónoma de Bucaramanga UNABFacultad Ciencias de la SaludEspecialización en Medicina Internainfo:eu-repo/semantics/masterThesisTesishttp://purl.org/redcol/resource_type/TMSystemic inflammatory response syndromeSeptic cardiomyopathySepsisTroponin IMedicineInternal medicineInvestigationsComplicationsPatientsPrevention and controlThird consensusMortalitySystolic dysfunctionDiastolic dysfunctionSeptic shockIntensive care unitSíndrome de respuesta inflamatoria sistémicaMiocardiopatía sépticaSepsisTroponina IMedicinaMedicina internaInvestigacionesComplicacionesPacientesPrevención y controlTercer consensoNT pro BNPMortalidadDisfunción sistólicaDisfunción diastólicaChoque sépticoUnidad de cuidados intensivosRueda Galvis, Myriam Vanessa (2018). Fuerza de asociación entre Troponina I, NT-pro BNP y desenlaces adversos en sepsis. Bucaramanga (Santander, Colombia) : Universidad Autónoma de Bucaramanga UNAB1. Torio, C.M, Andrews, R.M. (2013). National in patient hospital costs: the most expensive conditions by payer, Statistical Brief #160. Healthcare Cost and Utilization Project (HCUP) Statistical Briefs.. http://www.ncbi.nlm.nih.gov/books NBK169005/.2. Hotchkiss, R.S., Swanson, P.E., Freeman, B.D., et al. (2011) Apoptotic cell death in patients with sepsis, shock, and multiple organ dysfunction. Critical Care Medicine, 27(7), 1230-1251.3. Hotchkiss, R.S., Monneret, G., Payen,D. (2013). Sepsis-induced immunosuppression: from cellular dysfunctions to immunotherapy. Natural Reviews Immunology, 13(12), 862-874.4. Singer, M., Clifford S.D., Seymour W., et al. (2016). The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3) JAMA, 315(8),801-810.5. Parrillo, J.E., Parker ,M.M., Natanson, C., et al. (1990). Septic shock in humans: advances in the understanding of pathogenesis, cardiovascular dysfunction, and therapy. Annals of Internal Medicine, 113,227-42.6. Vincent, J.L., de Mendonça, A., Cantraine, F, et al. (1998). Working Group on ―Sepsis-Related Problems‖ of the European Society of Intensive Care Medicine. Use of the SOFA score to assess the incidence of organ dysfunction/failure in intensive care units: results of a multicenter, prospective study. Critical Care Medicine, 26(11), 1793-1800.7. Bone, R.C., Balk, R.A., Cerra, F.B., et al. (1992). American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Critical Care Medicine, 20(6), 864-874.8. Mervyn, S. (2016). The new sepsis consensus definitions (Sepsis-3): the good, the not so bad, and the actually quite pretty. Intensive Care Medicine. Publicado online 23 Diciembre 2016. DOI 10.1007/s00134-016-4600-49. Gaieski, D.F., Edwards J.M., Kallan M.J., et al. (2013). Benchmarking the incidence and mortality of severe sepsis in the United States. Critical Care Medicine, 41(5),1167-1174.10. Vincent, J.L., Marshall J.C., Namendys-Silva S.A., et al. (2014). Assessment of the worldwide burden of critical illness: the Intensive Care Over Nations (ICON) audit. Lancet Respiratory Medicine, 2(5),380-386.11. Wang W., Sawicki G., Schulz R. (2002). Peroxynitrite-induced myocardial injury is mediated through matrix metalloproteinase-2. Cardiovascular Research, 53, 165–17412. Alvarez, S., Vico, T., Vanasco, V. (2016) Cardiac dysfunction, mitocondrial architecture, energy production, and inflammatory pathways: interrelated aspects in endotoxemia and sepsis. The International Journal of Biochemistry & Cell Biology, 81(Pt B), 307-314.13. De Angelo J. (1999) . Nitric oxide scavengers in the treatment of shock associated with systemic inflammatory response syndrome. Expert Opinion Pharmacotherapy, (1), 19-29.14. Cimolai, M.C., Alvarez, S., Bode C., et al.(2015). Mitochondrial Mechanisms in Septic Cardiomyopathy. Internal Journal of Molecular Scinces, (16), 17763-17778.15. Romero-Bermejo, F.J., Ruiz-Bailen, M., Gil-Cebrian, J., et al. (2011). Sepsis-induced cardiomyopathy. Current Cardiology Reviews, (7), 163-183.16. Ince, C., Mayeux, P.R., Nguyen, T, el al. (2016). The Endothelium in Sepsis. Shock, (45), 259-27017. Dauphinee, S.M., Karsan, A., 2006. Lipopolysaccharide signaling in endothelial cells. Laboratory Investigation Journal , 86, 9-22.18. Morikawa, A., Koide, N., Kato, Y., et al. 2000. Augmentation of nitric oxide production by gamma interferon in a mouse vascular endothelial cell line and its modulation by tumor necrosis factor alpha and lipopolysaccharide. Infection and Immunity Journal. 68, 6209-6214.19. Liaudet, L., Soriano, F.G., Szabó, C. (2000) . Pathophysiological role of nitric oxide in inflammation, in: Nitric Oxide, biology and pathology. Critical Care Medicine, 28(4), 841-872.20. Thiemermann, C., Vane, J., (1990). Inhibition of nitric oxide synthesis reduces the hypotension induced by bacterial lipopolysaccharides in the rat in vivo. European Journal of Pharmacology, 182, 591-595.21. Blanco, J., Muriel-Bombin, A., Sagredo, V., Taboada, F., Gandia, F., Tamayo, L., Collado, J., Garcia-Labattut, A., Carriedo, D., Valledor, M., De Frutos, M., Lopez, M.J., Caballero, A., Guerra, J., Alvarez, B., Mayo, A., Villar, J., (2008). Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Critical Care, 12(6), R158.22. McDonough, K.H., Virag, J.I., (2006). Sepsis-induced myocardial dysfunction and myocardial protection from ischemia/reperfusion injury. Frontiers Bioscience, 11, 23-32.23. Poelaert, J., Declerck, C., Vogelaers, D., et al, (1997). Left ventricular systolic and diastolic function in septic shock. Intensive Care Medicine, 23, 553-560.24. Smeding, L., Plotz, F.B., Groeneveld, A.B., et al. (2012). Structural changes of the heart during severe sepsis or septic shock. Shock, 37, 449-456.25. Larche, J., Lancel, S., Hassoun, S.M., et al. (2006). Inhibition of mitochondrial permeability transition prevents sepsis- induced myocardial dysfunction and mortality. Journal of the American College of Cardiology, 48, 377-385.26. Levy, R.J., Piel, D.A., Acton, P.D., et al. (2005). Evidence of myocardial hibernation in the septic heart. Critical Care Medicine, 33, 2752- 2756.27. Piantadosi, C.A., Suliman, H.B. (2012). Transcriptional control of mitochondrial biogenesis and its interface with inflammatory processes. Biochimica et Biophysica Acta, 1820, 532-541.28. Vanasco, V., Saez, T., Magnani, N.D., et al. (2014). Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery. Free Radical Biology and Medicine, 77, 1-9.29. Vieillard-Baron A. (2001). Septic cardiomyopathy. Annals of Intensive Care, 1, 6–7.30. Hochstadt, A., Meroz, Y., Landesberg, G. (2011). Myocardial dysfunction in severe sepsis and septic shock: more questions than answers?. Journal of Cardiothoracic and Vasc Anesthesia, 25 (3), 526–35.31. dos Santos, C.C., Gattasm, D.J., Tsoporis, J.N., et al. (2010). Sepsis-induced myocardial depression is associated with transcriptional changes in energy metabolism and contractile related genes: a physiological and gene expression based approach. Critical Care Medicine, 38 (3), 894–902.32. Stengl, M., Bartak, F., Sykora, R., et al. (2010). Reduced L-type calcium current in ventricular myocytes from pigs with hyperdynamic septic shock. Critical Care of Medicine, 38(2), 580–7.33. Antonucci, E., Fiaccadori, E., Donadello, K., et al. (2013). Myocardial depression in sepsis: From pathogenesis to clinical manifestations and treatment. Journal of Critical Care, 29(4), 500-11.34. Repessé, X., Charron, C., Vieillard-Baron, A. (2013). Evaluation of left ventricular systolic function revisited in septic shock. Critical Care, 17(4), 164.35. Vieillard-Baron, A., Caille, V., Charron, C., et al. (2008). Actual incidence of global left ventricular hypokinesia in adult septic shock. Critical Care Medicine, 36(6), 1701-636. Parker, M.M., Shelhamer, J.H., Bacharach, S.L., et al. (1984) Profound but reversible myocardial depression in patients with septic shock. Annals of Internal Medicine, 100:483–90.37. Guarracino, F., Baldassarri, R., Pinsky, M.R. (2013). Ventriculo-arterial decoupling in acutely altered hemodynamic states. Critical Care, 17(2), 213–20.38. Landesberg, G., Gilon, D., Meroz, Y., et al. (2012). Diastolic dysfunction and mortality in severe sepsis and septic shock. European Heart Journal, 33(7), 895–903.39. Roosens, C.D., Ama, R., Leather, H.A., et al. (2006). Hemodynamic effects of different lung- protective ventilation strategies in closed-chest pigs with normal lungs. Critical Care of Medicine, 34(12), 2990–6.40. Pinsky, M.R. (2005). Cardiovascular issues in respiratory care. Chest, 128, 592–7.41. Latini, R., Caironi, R., Masson, S. (2016). Cardiac dysfunction and circulating cardiac markers during sepsis. Minerva anestesiologica , 82(6), 697-71042. Maeder, M,, Fehr, T., Rickli, H., et al. (2006). Sepsis associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and natriuretic peptides. Chest, 129:1349-6643. Rajaram, S.S., Desai, N.K., Kalra, A., et al.(2013). Pulmonary artery catheters for adult patients in intensive care. Cochrane Database Systematic Review, 28(2),1–59.44. Sandham, J.D, Hull, R.D., Brant, R.F., et al. (2003). A randomized, controlled trial of the use of pulmonary-artery catheters in high risk surgical patients. The New England Journal of Medicine,348(1), 5-14.45. Wheeler, A.P., Bernard, G.R, Thompson, B.T., et al. (2006). Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. The New England Journal of Medicine, 354(41), 2213-24.46. Brett, J., Gerlach, H., Nawroth, P., et al. (1989). Tumor necrosis factor/cachectin increases permeability of endothelial cell monolayers by a mechanism involving regulatory G proteins. The Journal of Experimental Medicine, 169(6), 1977–9147. Landesberg, G., Jaffe A.S., Gilon D., et al. (2014). Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic dysfunction and right ventricular dilatation. Critical Care Medicine, 42(4), 790-800.48. Markou, N., Gregorakos, L., Myrianthefs, P. (2011). Increased blood troponin levels in ICU patients. Current Opininon Critical Care, 1(5)7, 454–463.49. Brivet, F.G., Jacobs, F.M., Colin, P., et al. (2006). Cardiac troponin level is not an independent predictor of mortality in septic patients requiring medical intensive care unit admission. Critical Care, 10(1), 404.50. Bessiére, F., Khenifer, S., Dubourg, I., et al. (2013). Prognostic value of troponins in sepsis: a meta-analysis. Intensive Care Medicine , 39(7), 1181–118951. Spies, C., Haude, V., Fitzner, R., Schroder, K., et al. (1998). Serum cardiac troponin T as a prognostic marker in early sepsis. Chest, 113, 1055–106352. Bouhemad, B., Nicolas-Robin, A., Arbelot, C., et al. (2008). Isolated and reversible impairment of ventricular relaxation in patients with septic shock. Critical Care Medicine, 36(3) , 766–77453. Clerico, A. (2002). Pathophysiological and clinical relevance of circulating levels of cardiac natriuretic hormones: Are they merely markers of cardiac disease? Clinical Chemistry and Laboratory Medicine, 40(8), 752-6054. Ueda, S., Nishio, K., Akai, Y., et al. (2006). Prognostic value of increased plasma levels of brain natriuretic peptide in patients with septic shock. Shock, 26(2), 134-13955. Cuthbertson, B.H., Patel, R.R., Croal B.L., et al. (2005), B-type natriuretic peptide and the prediction of outcome in patients admitted to intensive care. Anaesthesia, 60(1), 16-21.56. Tomaru, K.K., Arai, M., Yokoyama, T., et al. (2002). Transcriptional activation of the BNP gene by lipopolysaccharide is mediated through GATA elements in neonatal rat cardiac myocytes. Journal of Mollecular and Cellular Cardiology, 34(6), 649-659.57. Turner, K.L., Moore, L.J., Todd, S.R., et al. (2011). Identification of cardiac dysfunction in sepsis with B-type natriuretic peptide. Journal of the American Collegues Surgeons, 213(1), 139–46.58. Long, B., Koyfman, A. (2017). Ready for Prime Time? Biomarkers in Sepsis. Emergency Medicine Clinics of North America, 35, 109–122.59. Wang, F., Wu, Y., Tang, L., et al. (2012). Brain natriuretic peptide for prediction of mortality in patients with sepsis: a systematic review and meta-analysis . Critical Care, 16:R74.60. Post, F., Weilemann, L.S., Messow, C.M., et al. (2008). B-type natriuretic peptide as a marker for sepsis induced myocardial depression in intensive care patients. Critical Care Medicine, 36(11),3030-3037.61. Mokart, D., Sannini, A., Brun, J.P., et al. (2007). N- terminal pro-brain natriuretic peptide as an early prognostic factor in cancer patients developing septic shock. Critical Care , 11(2), R37.62. Seung, R., Kim, W.Y., Won, H.J., et al. (2015). Prognostic Value of B-type Natriuretic Peptide With the Sequential Organ Failure Assessment Score in Septic Shock . American Journal of medical sciencies, 349 (4), 287–291.63. Müller-Werdan, U., Werdan, K. (1999). Septic cardiomyopathy. Current Opinion in Critical Care, 5,415–421.64. Parker, M.M., Shelhamer, J.H., Natanson, C., el al. (1989). Serial cardiovascular variables in survivors and nonsurvivors of human septic shock: heart rate as an early predictor of prognosis. Critical Care Medicine, 15(10),923–929.65. Hestenes, S.M., Halvorsen P.S., Skulstad, H., et al.(2014). Advantages of Strain Echocardiography in Assessment of Myocardial Function in Severe Sepsis: An Experimental Study. Critical Care Medicine, 42(6), 432-440.66. Werdan, K., Oelke, A., Hettwer, S., et al. (2011). Septic cardiomyopathy: Hemodynamic quantification, occurrence, and prognostic implications. Clinical Research in Cardiology, 100(8), 661–668.67. Brown, S., Pittman, J., Hirshberg, E.L., et al. (2012) Diastolic dysfunction and mortality in early severe sepsis and septic shock: a prospective, observational echocardiography study. Critical Ultrasound Journal, 4(1), 8.68. Bouhemad, B., Nicolas-Robin, A., Benois, A., et al. (2003). Echocardiographic Doppler assessment of pulmonary capillary wedge pressure in surgical patients with postoperative circulatory shock and acute lung injury. Anesthesiology, 98(5), 1091–1100.69. Vicent, J.L, Moreno R., Takala., et al. (1996). The SOFA (Sepsis realted organ failure assessment) score to describe organ dysfunction/ failure. Intensive Care Medicine, 22(), 707-710.70. Ferreira, F.L., Bota, D.P., Bross, A., et al. (2001). Serial evaluation of the SOFA score to predict outcome in critically ill patients. JAMA, 286(14):1754-871. 72. Knaus, W.A., Draper, E.A., Wagner , D.P., et al. (1985). APACHE II: everity of disease clasification system. Critical Care Medicine, 13(10), 818-820.72. Capuzzo, M., Valpondi, V., Sgarbi, A. (2000). Validation of severity scoring systems SAPS II and APACHE II in a single-center population.Intensive Care Medicine, 26(12), 1779.73. Zimmerman J.E., Kramer, A.A., McNair, D.S., et al. (2006) Acute Physiology and Chronic Health Evaluation (APACHE) IV: hospital mortality assessment for today's critically ill patients. Critical Care of Medicine, 34(5):1297-310.74. Swets J. (1988). Measuring the Accuracy of Diagnostic Systems. American Association for the Advancement of Science, 240 (4857), 1285- 1293.75. Mokart D, Brun JP, Faucher M., et al (2007) : N- terminal pro-brain natriuretic peptide as an early prognostic factor in cancer patients developing septic shock. Critical Care of Medicine, (11):37.76. Roch A., Alladet-Servent, J., Michelet P., et al. (2005): NH2 terminal pro- brain natriuretic peptide plasma level as an early marker of prognosis and cardiac dysfunction in septic shock patients Critical Care of Medicine, 33(5): 1001-1007.77. Chen Y., Li C. (2009) : Prognostic significance of brain natriuretic peptide obtained in the ED in patients with SIRS or sepsis. American Journal of Emergency Medicine, 27: 701-706.78. Klouche, K., Pommet, S., Amigues, L., et al (2014) Plasma Brain Natriuretic Peptide and Troponin Levels in Severe Sepsis and Septic Shock : Relationships With Systolic Myocardial Dysfunction and Intensive Care Unit Mortality. Journal or Intensive Care Medicine, 29(4):229-3779. Charpentier J, Luyt CE, Fulla Y, et al. (2004) Brain natriuretic peptide: a marker of myocardial dysfunction and prognosis during severe sepsis. Critical Care of Medicine. 32(3):660-665.80. Maeder M, Ammann P, Kiowski W, Rickli H. (2005) B-type natriuretic peptide in patients with sepsis and preserved left ventricular ejection fraction. European Journal of Heart Failure. 2005;7(7):1164-1167.81. Landesber, G., Jaffe, A., Gilon, Dan., et al. (2014) Troponin Elevation in Severe Sepsis and Septic Shock: The Role of Left Ventricular Diastolic Dysfunction and Right Ventricular Dilatation. Critical Care of Medicine. 42:790–800.82. Redfield MM, Jacobsen SJ, Burnett JC Jr, et al.(2003) Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. 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