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Critical Care Research and Practice
Volume 2012 (2012), Article ID 896430, 9 pages
Myocardial Dysfunction in Sepsis: A Large, Unsolved Puzzle
1Hospital Israelita Albert Einstein, Avenida Albert Einstein 627/701, 05661-901 Morumbi, SP, Brazil
2Department of Intensive Care Unit, Hospital Israelita Albert Einstein, Sao Paulo, Brazil
Received 16 October 2011; Revised 14 December 2011; Accepted 4 January 2012
Academic Editor: D. Annane
Copyright © 2012 Constantino Jose Fernandes Jr. and Murillo Santucci Cesar de Assuncao. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- From the Centers for Disease Control, “Increase in National Hospital Discharge Survey rates for septicemia—United States, 1979–1987,” Journal of the American Medical Association, vol. 263, no. 7, pp. 937–938, 1990.
- D. Annane, P. Aegerter, M. C. Jars-Guincestre, and B. Guidet, “Current epidemiology of septic shock: the CUB-Réa network,” American Journal of Respiratory and Critical Care Medicine, vol. 168, no. 2, pp. 165–172, 2003.
- E. Silva, M. A. Pedro, A. C. Sogayar et al., “Brazilian Sepsis Epidemiological Study (BASES study),” Critical Care, vol. 8, no. 4, pp. R251–R260, 2004.
- E. Rivers, B. Nguyen, S. Havstad et al., “Early goal-directed therapy in the treatment of severe sepsis and septic shock,” New England Journal of Medicine, vol. 345, no. 19, pp. 1368–1377, 2001.
- J. E. Parrillo, “The cardiovascular pathophysiology of sepsis,” Annual Review of Medicine, vol. 40, pp. 469–485, 1989.
- A. Vieillard-Baron, V. Caille, C. Charron, G. Belliard, B. Page, and F. Jardin, “Actual incidence of global left ventricular hypokinesia in adult septic shock,” Critical Care Medicine, vol. 36, no. 6, pp. 1701–1706, 2008.
- J. F. Dhainaut AC and I. Laurent, “Myocardial dysfunction in sepsis,” Sepsis, vol. 4, no. 2, pp. 89–97, 2000.
- C. J. Wiggers, “Myocardial depression in shock. A survey of cardiodynamic studies,” American Heart Journal, vol. 33, no. 5, pp. 633–650, 1947.
- L. D. Maclean, W. W. Spink, M. B. Visscher, and M. H. Weil, “Studies on the circulatory changes in the dog produced by endotoxin from gram-negative microorganisms,” The Journal of Clinical Investigation, vol. 35, no. 11, pp. 1191–1198, 1956.
- C. J. Fernandes Júnior, N. Akamine, and E. Knobel, “Myocardial depression in sepsis,” Shock, vol. 30, supplement 1, pp. 14–17, 2008.
- V. H. Moon, “The pathology of secondary shock,” The American Journal of Pathology, vol. 24, no. 2, pp. 235–273, 1948.
- C. J. Fernandes Júnior, M. Iervolino, R. A. Neves, E. L. Sampaio, E. Knobel, and D. R. Sustovich, “The myocardium in sepsis: anatomo-pathologic aspects,” Arquivos Brasileiros de Cardiologia, vol. 50, no. 3, pp. 175–178, 1988.
- C. J. Fernandes Júnior, M. Iervolino, R. A. Neves, E. L. M. Sampaio, and E. Knobel, “Interstitial myocarditis in sepsis,” American Journal of Cardiology, vol. 74, no. 9, p. 958, 1994.
- C. Natanson, P. W. Eichenholz, R. L. Danner et al., “Endotoxin and tumor necrosis factor challenges in dogs simulate the cardiovascular profile of human septic shock,” Journal of Experimental Medicine, vol. 169, no. 3, pp. 823–832, 1989.
- A. F. Suffredini, R. E. Fromm, M. M. Parker et al., “The cardiovascular response of normal humans to the administration of endotoxin,” New England Journal of Medicine, vol. 321, no. 5, pp. 280–287, 1989.
- J. A. Russell, J. Boyd, T. Nakada, S. Thair, and K. R. Walley, “Molecular mechanisms of sepsis,” Contributions to Microbiology, vol. 17, pp. 48–85, 2011.
- S. Akira, S. Uematsu, and O. Takeuchi, “Pathogen recognition and innate immunity,” Cell, vol. 124, no. 4, pp. 783–801, 2006.
- M. Flesch, H. Kilter, B. Cremers et al., “Effects of endotoxin on human myocardial contractility involvement of nitric oxide and peroxynitrite,” Journal of the American College of Cardiology, vol. 33, no. 4, pp. 1062–1070, 1999.
- B. S. Cain, D. R. Meldrum, C. A. Dinarello et al., “Tumor necrosis factor-α and interleukin-1β synergistically depress human myocardial function,” Critical Care Medicine, vol. 27, no. 7, pp. 1309–1318, 1999.
- J. A. Thomas, S. B. Haudek, T. Koroglu et al., “IRAK1 deletion disrupts cardiac Toll/IL−1 signaling and protects against contractile dysfunction,” American Journal of Physiology, vol. 285, no. 2, pp. H597–H606, 2003.
- O. Avlas, R. Fallach, A. Shainberg, E. Porat, and E. Hochhauser, “Toll-like receptor 4 stimulation initiates an inflammatory response that decreases cardiomyocyte contractility,” Antioxidants and Redox Signaling, vol. 15, no. 7, pp. 1895–1909, 2011.
- R. E. Cunnion, G. L. Schaer, and M. M. Parker, “The coronary circulation in human septic shock,” Circulation, vol. 73, no. 4, pp. 637–644, 1986.
- A. M. Lefer and J. Martin, “Origin of myocardial depressant factor in shock,” The American Journal of Physiology, vol. 218, no. 5, pp. 1423–1427, 1970.
- R. McConn, J. K. Greineder, F. Wasserman, and G. H. Clowes Jr., “Is there a humoral factor that depresses ventricular function in sepsis?” Circulatory Shock, vol. 1, supplement, pp. 9–22, 1979.
- A. Kumar, V. Thota, L. Dee, J. Olson, E. Uretz, and J. E. Parrillo, “Tumor necrosis factor α and interleukin 1β are responsible for in vitro myocardial cell depression induced by human septic shock serum,” Journal of Experimental Medicine, vol. 183, no. 3, pp. 949–958, 1996.
- L. C. Casey, R. A. Balk, and R. C. Bone, “Plasma cytokine and endotoxin levels correlate with survival in patients with the sepsis syndrome,” Annals of Internal Medicine, vol. 119, no. 8, pp. 771–778, 1993.
- A. Billiau and F. Vandekerckhove, “Cytokines and their interactions with other inflammatory mediators in the pathogenesis of sepsis and septic shock,” European Journal of Clinical Investigation, vol. 21, no. 6, pp. 559–573, 1991.
- J. L. Vincent, J. Bakker, G. Marecaux, L. Schandene, R. J. Kahn, and E. Dupont, “Administration of anti-TNF antibody improves left ventricular function in septic shock patients; Results of a pilot study,” Chest, vol. 101, no. 3, pp. 810–815, 1992.
- U. Müller-Werdan, H. Schumann, H. Loppnow et al., “Endotoxin and tumor necrosis factor α exert a similar proinflammatory effect in neonatal rat cardiomyocytes, but have different cardiodepressant profiles,” Journal of Molecular and Cellular Cardiology, vol. 30, no. 5, pp. 1027–1036, 1998.
- E. Abraham, R. Wunderink, H. Silverman et al., “Efficacy and safety of monoclonal antibody to human tumor necrosis factor α in patients with sepsis syndrome: a randomized, controlled, double-blind, multicenter clinical trial,” Journal of the American Medical Association, vol. 273, no. 12, pp. 934–941, 1995.
- M. Bujak and N. G. Frangogiannis, “The role of IL−1 in the pathogenesis of heart disease,” Archivum Immunologiae et Therapiae Experimentalis, vol. 57, no. 3, pp. 165–176, 2009.
- U. Muller-Werdan, M. Buerke, H. Ebelt et al., “Septic cardiomyopathy—a not yet discovered cardiomyopathy?” Experimental and Clinical Cardiology, vol. 11, no. 3, pp. 226–236, 2006.
- M. S. Finkel, C. V. Oddis, T. D. Jacob, S. C. Watkins, B. G. Hattler, and R. L. Simmons, “Negative inotropic effects of cytokines on the heart mediated by nitric oxide,” Science, vol. 257, no. 5068, pp. 387–389, 1992.
- A. D. Niederbichler, L. M. Hoesel, M. V. Westfall et al., “An essential role for complement C5a in the pathogenesis of septic cardiac dysfunction,” Journal of Experimental Medicine, vol. 203, no. 1, pp. 53–61, 2006.
- R. Schulz, T. Rassaf, P. B. Massion, M. Kelm, and J. L. Balligand, “Recent advances in the understanding of the role of nitric oxide in cardiovascular homeostasis,” Pharmacology and Therapeutics, vol. 108, no. 3, pp. 225–256, 2005.
- M. T. Ziolo and D. M. Bers, “The real estate of NOS signaling location, location, location,” Circulation Research, vol. 92, no. 12, pp. 1279–1281, 2003.
- F. Ichinose, E. S. Buys, T. G. Neilan et al., “Cardiomyocyte-specific overexpression of nitric oxide synthase 3 prevents myocardial dysfunction in murine models of septic shock,” Circulation Research, vol. 100, no. 1, pp. 130–139, 2007.
- M. Bougaki, R. J. Searles, K. Kida, J. Yu, E. S. Buys, and F. Ichinose, “NOS3 protects against systemic inflammation and myocardial dysfunction in murine polymicrobial sepsis,” Shock, vol. 34, no. 3, pp. 281–290, 2010.
- D. Dawson, C. A. Lygate, M. H. Zhang, K. Hulbert, S. Neubauer, and B. Casadei, “nNOS gene deletion exacerbates pathological left ventricular remodeling and functional deterioration after myocardial infarction,” Circulation, vol. 112, no. 24, pp. 3729–3737, 2005.
- T. Rassaf, L. W. Poll, P. Brouzos et al., “Positive effects of nitric oxide on left ventricular function in humans,” European Heart Journal, vol. 27, no. 14, pp. 1699–1705, 2006.
- R. Ullrich, M. Scherrer-Crosbie, K. D. Bloch et al., “Congenital deficiency of nitric oxide synthase 2 protects against endotoxin-induced myocardial dysfunction in mice,” Circulation, vol. 102, no. 12, pp. 1440–1446, 2000.
- J. L. Balligand, D. Ungureanu, R. A. Kelly et al., “Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium,” Journal of Clinical Investigation, vol. 91, no. 5, pp. 2314–2319, 1993.
- P. Pacher, J. S. Beckman, and L. Liaudet, “Nitric oxide and peroxynitrite in health and disease,” Physiological Reviews, vol. 87, no. 1, pp. 315–424, 2007.
- A. C. Sharma, S. J. Motew, S. Farias et al., “Sepsis alters myocardial and plasma concentrations of endothelin and nitric oxide in rats,” Journal of Molecular and Cellular Cardiology, vol. 29, no. 5, pp. 1469–1477, 1997.
- M. Chopra and A. C. Sharma, “Distinct cardiodynamic and molecular characteristics during early and late stages of sepsis-induced myocardial dysfunction,” Life Sciences, vol. 81, no. 4, pp. 306–316, 2007.
- H. F. Galley, “Oxidative stress and mitochondrial dysfunction in sepsis,” British Journal of Anaesthesia, vol. 107, no. 1, pp. 57–64, 2011.
- C. B. Lorigados, F. G. Soriano, and C. Szabo, “Pathomechanisms of myocardial dysfunction in sepsis,” Endocrine, Metabolic and Immune Disorders, vol. 10, no. 3, pp. 274–284, 2010.
- T. Peng, X. Lu, and Q. Feng, “NADH oxidase signaling induces cyclooxygenase-2 expression during lipopolysaccharide stimulation in cardiomyocytes,” FASEB Journal, vol. 19, no. 2, pp. 293–295, 2005.
- H. Schmidt, U. Müller-Werdan, T. Hoffmann et al., “Autonomic dysfunction predicts mortality in patients with multiple organ dysfunction syndrome of different age groups,” Critical Care Medicine, vol. 33, no. 9, pp. 1994–2002, 2005.
- P. Y. Hahn, P. Wang, S. M. Tait, Z. F. Ba, S. S. Reich, and I. H. Chaudry, “Sustained elevation in circulating catecholamine levels during polymicrobial sepsis,” Shock, vol. 4, no. 4, pp. 269–273, 1995.
- L. L. Wu, S. L. Yang, R. C. Yang et al., “G protein and adenylate cyclase complex-mediated signal transduction in the rat heart during sepsis,” Shock, vol. 19, no. 6, pp. 533–537, 2003.
- K. Zorn-Pauly, B. Pelzmann, P. Lang et al., “Endotoxin impairs the human pacemaker current IF,” Shock, vol. 28, no. 6, pp. 655–661, 2007.
- S. Liu and K. D. Schreur, “G protein-mediated suppression of L-type Ca2+ current by interleukin- 1β in cultured rat ventricular myocytes,” American Journal of Physiology, vol. 268, no. 2, pp. C339–C349, 1995.
- J. Zhong, T. C. Hwang, H. R. Adams, and L. J. Rubin, “Reduced L-type calcium current in ventricular myocytes from endotoxemic guinea pigs,” American Journal of Physiology, vol. 273, no. 5, pp. H2312–H2324, 1997.
- L. L. Wu, Y. Ji, L. W. Dong, and M. S. Liu, “Calcium uptake by sarcoplasmic reticulum is impaired during the hypodynamic phase of sepsis in the rat heart,” Shock, vol. 15, no. 1, pp. 49–55, 2001.
- B. Tavernier, D. Garrigue, C. Boulle, B. Vallet, and P. Adnet, “Myofilament calcium sensitivity is decreased in skinned cardiac fibres of endotoxin-treated rabbits,” Cardiovascular Research, vol. 38, no. 2, pp. 472–479, 1998.
- C. J. Fernandes Júnior, N. Akamine, and E. Knobel, “Cardiac troponin: a new serum marker of myocardial injury in sepsis,” Intensive Care Medicine, vol. 25, no. 10, pp. 1165–1168, 1999.
- H. M. Piper, P. Schwartz, and R. Spahr, “Early enzyme release from myocardial cells is not due to irreversible cell damage,” Journal of Molecular and Cellular Cardiology, vol. 16, no. 4, pp. 385–388, 1984.
- K. M. Ver Elst, H. D. Spapen, D. N. Nguyen, C. Garbar, L. P. Huyghens, and F. K. Gorus, “Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock,” Clinical Chemistry, vol. 46, no. 5, pp. 650–657, 2000.
- A. Turner, M. Tsamitros, and R. Bellomo, “Myocardial cell injury in septic shock,” Critical Care Medicine, vol. 27, no. 9, pp. 1775–1780, 1999.
- N. J. Mehta, I. A. Khan, V. Gupta, K. Jani, R. M. Gowda, and P. R. Smith, “Cardiac troponin I predicts myocardial dysfunction and adverse outcome in septic shock,” International Journal of Cardiology, vol. 95, no. 1, pp. 13–17, 2004.
- E. P. Rivers, J. McCord, R. Otero, G. Jacobsen, and M. Loomba, “Clinical utility of B-type natriuretic peptide in early severe sepsis and septic shock,” Journal of Intensive Care Medicine, vol. 22, no. 6, pp. 363–373, 2007.
- E. Kandil, J. Burack, A. Sawas et al., “B-type natriuretic peptide: a biomarker for the diagnosis and risk stratification of patients with septic shock,” Archives of Surgery, vol. 143, no. 3, pp. 242–246, 2008.
- K. L. Turner, L. J. Moore, S. R. Todd et al., “Identification of cardiac dysfunction in sepsis with B-type natriuretic peptide,” Journal of the American College of Surgeons, vol. 213, no. 1, pp. 139–146, 2011.
- S. M. Perman, A. M. Chang, J. E. Hollander et al., “Relationship between B-type natriuretic peptide and adverse outcome in patients with clinical evidence of sepsis presenting to the emergency department,” Academic Emergency Medicine, vol. 18, no. 2, pp. 219–222, 2011.
- B. Bouhemad, A. Nicolas-Robin, C. Arbelot, M. Arthaud, F. Féger, and J. J. Rouby, “Acute left ventricular dilatation and shock-induced myocardial dysfunction,” Critical Care Medicine, vol. 37, no. 2, pp. 441–447, 2009.
- A. Morelli, S. De Castro, J. L. Teboul et al., “Effects of levosimendan on systemic and regional hemodynamics in septic myocardial depression,” Intensive Care Medicine, vol. 31, no. 5, pp. 638–644, 2005.
- D. Barraud, V. Faivre, T. Damy et al., “Levosimendan restores both systolic and diastolic cardiac performance in lipopolysaccharide-treated rabbits: comparison with dobutamine and milrinone,” Critical Care Medicine, vol. 35, no. 5, pp. 1376–1382, 2007.
- E. Rezende, M. Assuncao, G. Leão, and M. Silva, “Is it possible to use levosimedan to treat cardiovascular dysfunction in septic patients?” Critical Care, vol. 7, supplement 3, p. P37, 2003.