IJCS | Volume 31, Nº6, November / December 2018

649 1. Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al. The Third International Consensus definitions for sepsis and septic shock (Sepsis-3). JAMA. 2016;315(8):801-10. 2. Court O, Kumar A, Parrillo J, Kumar A. Clinical review: myocardial depression in sepsis and septic shock. Crit Care. 2000;6(6):500-8. 3. Bouhemad B, Nicolas-Robin A, Arbelot C, ArthaudM, Feger F, Rouby JJ. Isolated and reversible impairment of ventricular relaxation in patients with septic shock. Crit Care Med. 2008;36(3):766-74. 4. Burns JR, Menapace FJ. Acute reversible cardiomyopathy complicating toxic shock syndrome. Arch Intern Med. 1982;142(5):1032-4. 5. Zethelius B, Berglund L, Sundström J, Ingelsson E, Basu S, Larsson A, et al. Use of multiple biomarkers to improve the prediction of death from cardiovascular causes. N Engl J Med. 2008;358(20):2107-16. 6. Kakihana Y, Ito T, NakaharaM, Yamaguchi K, Yasuda T. Sepsis-induced myocardial dysfunction: pathophysiology andmanagement. J Intensive Care. 2016 Mar 23;4:22. 7. Kumar A, Thota V, Dee L, Olson J, Uretz E, Parrillo JE. Tumor necrosis factor alpha and interleukin 1 beta are responsible for in vitromyocardial cell depression induced by human septic shock serum. J Exp Med. 1996;183(3):949-58. 8. dos Santos CC, Gattas DJ, Tsoporis JN, Smeding L, Kabir G, Massom H, et al. Sepsis-induced myocardial depression is associated with transcriptional changes in energy metabolism and contractile related genes: a physiological and gene expression based approach. Crit Care Med. 2010;38(3):894-902. 9. Cimolai MC, Alvarez S, Bode C, Bugger H. Mitochondrial mechanisms in septic cardiomyopathy. Int J Mol Sci. 2015;16(8):17763-78. 10. Sharma AC, Motew SJ, Farias S, Alden KJ, Bosmann HB, LawWR, et al. Sepsis alters myocardial and plasma concentrations of endothelin and nitric oxide in rats. J Mol Cell Cardiol. 1997;29(5):1469-77. 11. Stengl M, Bargak F, Sykora R, Chvojka J, Benes J, Krouzecky J, et al. Reduced L-type calcium current in ventricular myocytes from pigs with hyperdynamic septic shock. Crit Care Med. 2010;38(2):580-7. 12. Kimmoun A, Levy B. Treatment of myocardial dysfunction in sepsis: the toll-like receptor antagonist approach. Shock. 2011;36(6):633-4. 13. Gao M, Ha T, Zhang X, Liu L, Wang X, Kelley J, et al. Toll-like receptor 3 plays a central role in cardiac dysfunction during polymicrobial sepsis. Crit Care Med. 2012;40(8):2390-9. 14. SilvermanHJ, Penaranda R, Orens JB, Lee NH. Impaired beta-adrenergic receptor stimulation of cyclic adenosine monophosphate in human References Jorge et al. Myocardial dysfunction and mortality in sepsis Int J Cardiovasc Sci. 2018;31(6)643-651 Review Article as independent markers of mortality in this clinical scenario. 77,78 Brueckmann et al., 79 for example, followed 57 patients diagnosed with severe sepsis and observed that patients with NT-proBNP levels > 1400 pmol/L showed a 3.9 times greater risk (relative risk [RR] 3.9, 95%CI 1.6 – 9.7) of dying from sepsis than patients with lower NT-proBNP values (p < 0.001). 79 Khoury et al. 80 studied 259 patients with sepsis and without cardiac failure and concluded using multivariate analysis that BNP is a strong predictor of in-hospital mortality at 90 days and 60 months, in addition to a better prognostic predictor than the Sepsis-related Organ Failure Assessment (SOFA) score for mortality at 90 days, and a better prognostic predictor of mortality at 60 months in low-risk groups. 80 Final considerations Evidence points to an association betweenmyocardial dysfunction and sepsis as a relatively frequent event. The relationship between systolic dysfunction and mortality is still not defined, nor is the mechanism by which the diastolic dysfunction and the right ventricular dysfunction affect so adversely the evolution of patients with sepsis. There are no studies evaluating the effects of a differentiated strategy of treatment on the outcome of these patients. These gaps offer the opportunity for research and development of knowledge that can contribute to the treatment of such patients and, in the final analysis, improve their prognosis. Author contributions Conception and design of the research: Campista MS. Writing of the manuscript: Campista MS, Guedes MA. Critical revision of themanuscript for intellectual content: Jorge AJL, Campista MS, Martins WA. Supervision / as the major investigador: Jorge AJL. Potential Conflict of Interest No potential conflict of interest relevant to this article was reported. Sources of Funding There were no external funding sources for this study. Study Association This article is part of the thesis of master submitted by Márcio da Silva Campista, from Universidade Federal Fluminense. Ethics approval and consent to participate This article does not contain any studies with human participants or animals performed by any of the authors.