Case report: severe reversible cardiomyopathy associated with systemic inflammatory response syndrome in the setting of diabetic hyperosmolar hyperglycemic non-ketotic syndrome

BMC Cardiovascular Disorders

Joaquin Lado¹  Hatice Duygu Baser¹  Raymond Wade¹  Justin Berk¹ 

[1] Department of Internal Medicine, Texas Tech University Health Sciences Center, School of Medicine, 3601 4th St Stop 9410, Lubbock 79416, TX, USA

关键词: Hyperosmolar hyperglycemic non-ketotic syndrome;    Non-thyroidal illness syndrome;    Systemic inflammatory response syndrome;    Diabetes;    Cardiomyopathy;   

Others  :  1229136
DOI  :  10.1186/s12872-015-0112-3

 received in 2015-06-24, accepted in 2015-09-24,  发布年份 2015

【 摘 要 】

Background

This case study features a woman who presented with clinical and laboratory findings consistent with hyperosmolar hyperglycemic non-ketotic syndrome (HHNS), systemic inflammatory response syndrome (SIRS), and non-thyroidal illness syndrome (NTIS) who was noted to have a transient decrease in myocardial function. To our knowledge, this is the first case discussing the overlapping pathophysiological mechanisms could increase susceptibility to SIRS-induced cardiomyopathy. It is imperative that this clinical question be investigated further as such a relationship may have significant clinical implications for prevention and future treatments, particularly in patients similar to the one presented in this clinical case.

Case presentation

A 53-year old Caucasian female presented to the Emergency Department for cough, nausea, vomiting and “feeling sick for 3 weeks.” Labs were indicative of diabetic ketoacidosis. Initial electrocardiograms were suggestive of possible myocardial infarction and follow-up echocardiogram showed severely depressed left ventricular systolic function which resolved upon treatment of ketoacidosis.

Conclusion

We suggest that her cardiomyopathy could have three synergistic sources: SIRS, HHNS and NTIS. Overlapping mechanisms suggest uncontrolled diabetes mellitus and NTIS could increase susceptibility to SIRS-induced cardiomyopathy as seen in this case. HHNS and SIRS cause cardiac tissue injury through mechanisms including impairment of fatty acid oxidation and formation of reactive oxygen species, as well as modifying the function of membrane calcium channels. As a result, it is conceivable that diabetes may amplify the deleterious effects of inflammatory stressors on cardiac myocytes. This novel case report offers a path for future research into prevention and treatment of SIRS-induced cardiomyopathy in, but not exclusive to, the setting of diabetes.

【 授权许可】

   
2015 Berk et al.

【 图 表 】

Fig. 1.

Fig. 2.

Fig. 3.

Fig. 4.

【 参考文献 】

• [1]Gogos CA, Giali S, Paliogianni F, Dimitracopoulos G, Bassaris HP, Vagenakis AG: Interleukin-6 and C-reactive protein as early markers of sepsis in patients with diabetic ketoacidosis or hyperosmosis. Diabetologia 2001, 44:1011-1014.
• [2]Poelaert J, Declerck C, Vogelaers D, Colardyn F, Visser CA: Left ventricular systolic and diastolic function in septic shock. Intensive Care Med 1997, 23:553-560.
• [3]Landesberg G, Gilon D, Meroz Y, Georgieva M, Levin PD, Goodman S, et al.: Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J 2012, 33:895-903.
• [4]Ren J, Wu S: A burning issue: do sepsis and systemic inflammatory response syndrome (SIRS) directly contribute to cardiac dysfunction? Front Biosci J Virtual Libr 2006, 11:15-22.
• [5]Finkel MS, Oddis CV, Jacob TD, Watkins SC, Hattler BG, Simmons RL: Negative inotropic effects of cytokines on the heart mediated by nitric oxide. Science 1992, 257:387-389.
• [6]Schulz R, Nava E, Moncada S: Induction and potential biological relevance of a Ca2 + −independent nitric oxide synthase in the myocardium. Br J Pharmacol 1992, 105:575-580.
• [7]Ziolo MT, Kohr MJ, Wang H: Nitric oxide signaling and the regulation of myocardial function. J Mol Cell Cardiol 2008, 45:625-632.
• [8]Rudiger A, Singer M: Mechanisms of sepsis-induced cardiac dysfunction. Crit Care Med 2007, 35:1599-1608.
• [9]Werdan K, Schmidt H, Ebelt H, Zorn-Pauly K, Koidl B, Hoke RS, et al.: Impaired regulation of cardiac function in sepsis, SIRS, and MODS. Can J Physiol Pharmacol 2009, 87:266-274.
• [10]Pagani FD, Baker LS, Hsi C, Knox M, Fink MP, Visner MS: Left ventricular systolic and diastolic dysfunction after infusion of tumor necrosis factor-alpha in conscious dogs. J Clin Invest 1992, 90:389-398.
• [11]Yokoyama T, Vaca L, Rossen RD, Durante W, Hazarika P, Mann DL: Cellular basis for the negative inotropic effects of tumor necrosis factor-alpha in the adult mammalian heart. J Clin Invest 1993, 92:2303-2312.
• [12]Hobai IA, Buys ES, Morse JC, Edgecomb J, Weiss EH, Armoundas AA, et al.: SERCA Cys674 sulphonylation and inhibition of L-type Ca2+ influx contribute to cardiac dysfunction in endotoxemic mice, independent of cGMP synthesis. Am J Physiol Heart Circ Physiol 2013, 305:H1189-1200.
• [13]Kao Y-H, Chen Y-C, Cheng C-C, Lee T-I, Chen Y-J, Chen S-A: Tumor necrosis factor-alpha decreases sarcoplasmic reticulum Ca2 + −ATPase expressions via the promoter methylation in cardiomyocytes. Crit Care Med 2010, 38:217-222.
• [14]Goldhaber JI, Kim KH, Natterson PD, Lawrence T, Yang P, Weiss JN: Effects of TNF-alpha on [Ca2+] i and contractility in isolated adult rabbit ventricular myocytes. Am J Physiol 1996, 271(4 Pt 2):H1449-1455.
• [15]Gulick T, Chung MK, Pieper SJ, Lange LG, Schreiner GF: Interleukin 1 and tumor necrosis factor inhibit cardiac myocyte beta-adrenergic responsiveness. Proc Natl Acad Sci U S A 1989, 86:6753-6757.
• [16]Balligand JL, Ungureanu D, Kelly RA, Kobzik L, Pimental D, Michel T, et al.: Abnormal contractile function due to induction of nitric oxide synthesis in rat cardiac myocytes follows exposure to activated macrophage-conditioned medium. J Clin Invest 1993, 91:2314-2319.
• [17]Raymond RM: When does the heart fail during shock? Circ Shock 1990, 30:27-41.
• [18]Solomon MA, Correa R, Alexander HR, Koev LA, Cobb JP, Kim DK, et al.: Myocardial energy metabolism and morphology in a canine model of sepsis. Am J Physiol 1994, 266(2 Pt 2):H757-768.
• [19]Brealey D, Brand M, Hargreaves I, Heales S, Land J, Smolenski R, et al.: Association between mitochondrial dysfunction and severity and outcome of septic shock. Lancet 2002, 360:219-223.
• [20]Langley RJ, Tsalik EL, Velkinburgh JC V, Glickman SW, Rice BJ, Wang C, et al.: An Integrated Clinico-Metabolomic Model Improves Prediction of Death in Sepsis. Sci Transl Med 2013, 5:195ra95.
• [21]Crossland H, Constantin-Teodosiu D, Gardiner SM, Constantin D, Greenhaff PL: A potential role for Akt/FOXO signalling in both protein loss and the impairment of muscle carbohydrate oxidation during sepsis in rodent skeletal muscle. J Physiol 2008, 586(Pt 22):5589-5600.
• [22]Gellerich FN, Trumbeckaite S, Hertel K, Zierz S, Müller-Werdan U, Werdan K, et al.: Impaired energy metabolism in hearts of septic baboons: diminished activities of Complex I and Complex II of the mitochondrial respiratory chain. Shock Augusta Ga 1999, 11:336-341.
• [23]Drosatos K, Drosatos-Tampakaki Z, Khan R, Homma S, Schulze PC, Zannis VI, et al.: Inhibition of c-Jun-N-terminal kinase increases cardiac peroxisome proliferator-activated receptor alpha expression and fatty acid oxidation and prevents lipopolysaccharide-induced heart dysfunction. J Biol Chem 2011, 286:36331-36339.
• [24]Feingold K, Kim MS, Shigenaga J, Moser A, Grunfeld C: Altered expression of nuclear hormone receptors and coactivators in mouse heart during the acute-phase response. Am J Physiol Endocrinol Metab 2004, 286:E201-207.
• [25]Singer M: The role of mitochondrial dysfunction in sepsis-induced multi-organ failure. Virulence 2014, 5:66-72.
• [26]Carré JE, Singer M: Cellular energetic metabolism in sepsis: the need for a systems approach. Biochim Biophys Acta 2008, 1777:763-771.
• [27]Levy RJ, Deutschman CS: Evaluating myocardial depression in sepsis. Shock Augusta Ga 2004, 22:1-10.
• [28]Merx MW, Weber C: Sepsis and the Heart. Circulation 2007, 116:793-802.
• [29]Zanotti-Cavazzoni SL, Hollenberg SM: Cardiac dysfunction in severe sepsis and septic shock. Curr Opin Crit Care 2009, 15:392-397.
• [30]Fernandes CJ Jr, de Assuncao MSC: Myocardial dysfunction in sepsis: a large. Unsolved Puzzle Crit Care Res Pract 2012, 2012:1-9.
• [31]Stentz FB, Umpierrez GE, Cuervo R, Kitabchi AE: Proinflammatory cytokines, markers of cardiovascular risks, oxidative stress, and lipid peroxidation in patients with hyperglycemic crises. Diabetes 2004, 53:2079-2086.
• [32]Bugger H, Abel ED: Molecular mechanisms of diabetic cardiomyopathy. Diabetologia 2014, 57:660-671.
• [33]Wartofsky L, Burman KD: Alterations in thyroid function in patients with systemic illness: the “euthyroid sick syndrome.”. Endocr Rev 1982, 3:164-217.
• [34]Kaptein EM, Beale E, Chan LS: Thyroid hormone therapy for obesity and nonthyroidal illnesses: a systematic review. J Clin Endocrinol Metab 2009, 94:3663-3675.
• [35]Castro I, Quisenberry L, Calvo R-M, Obregon M-J, Lado-Abeal J: Septic shock non-thyroidal illness syndrome causes hypothyroidism and conditions for reduced sensitivity to thyroid hormone. J Mol Endocrinol 2013, 50:255-266.
• [36]Iervasi G, Pingitore A, Landi P, Raciti M, Ripoli A, Scarlattini M, et al.: Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation 2003, 107:708-713.
• [37]Ladenson PW, Sherman SI, Baughman KL, Ray PE, Feldman AM: Reversible alterations in myocardial gene expression in a young man with dilated cardiomyopathy and hypothyroidism. Proc Natl Acad Sci U S A 1992, 89:5251-5255.
• [38]Hamilton MA, Stevenson LW, Fonarow GC, Steimle A, Goldhaber JI, Child JS, et al.: Safety and hemodynamic effects of intravenous triiodothyronine in advanced congestive heart failure. Am J Cardiol 1998, 81:443-447.