The value of heat shock protein (HSP) 60 on in-hospital and short-term prognosis in patients with acute ST segment elevation myocardial infarction

Yıl 2020, Cilt: 4 Sayı: 2, 130 - 134, 01.02.2020

Mustafa Çelik , Recep Karataş Ahmet Yılmaz , Fikret Keleş Nazif Aygül , Hüsamettin Vatansev , Erdoğan Sökmen , Ahmet Erseçgin

https://doi.org/10.28982/josam.601334

Öz

Aim: HSP60 has previously been shown to be an independent risk factor for congestive heart failure. Recently, increased HSP60 values have been shown to be associated with increased mortality in patients hospitalized with acute heart failure. The purpose of our study was to determine whether HSP 60 is an independent predictor of in-hospital or short-term mortality in patients with acute ST segment elevation myocardial infarction (STEMI) and to assess whether it may be used as an early predictor of in-hospital heart failure or cardiogenic shock development in the same population.
Methods: A total of 221 patients over 18 years of age presenting within 12 hours after the onset of symptoms with STEMI between 2011 and 2013 were enrolled to our study. Our study was designed as a prospective cohort. Several clinical conditions, such as clinical heart failure, development of cardiogenic shock and death during hospitalization were recorded together with the data pertaining to the length of hospital stay, MI localization, revascularization strategy and risk factors associated with coronary heart disease. Patients were called 1 month after discharge to find out if anyone had died.
Results: HSP 60 values were significantly higher in patients who died during hospitalization (P=0.004) or within 1 month after discharge (P=0.020). These results were independent from other factors associated with mortality following STEMI. Significant association was found between HSP60 value and in-hospital development of cardiogenic shock (P=0.03) or heart failure (P=0.03).
Conclusion: HSP60 was found to be independently associated with increased mortality in patients admitted for STEMI and therefore may be used as a promising predictor of mortality.

Anahtar Kelimeler

Myocardial infarction, HSP60, Prognosis, Inflammation, Atherosclerosis

Akut ST elevasyonlu miyokard infaktüsünde ısı şok proteini 60’ın hastane içi ve kısa dönem prognostik değeri

Öz

Amaç: HSP60'ın daha önce konjestif kalp yetmezliği için bağımsız bir risk faktörü olduğu gösterilmiştir. Son zamanlarda artan HSP60 değerinin mortalite ile ilişkili olduğu gösterilmiştir. Çalışmanın amacı HSP 60'ın akut ST segment yükselmeli miyokard enfarktüslü (STEMI) hastalarda bağımsız bir hastane içi veya kısa süreli mortalite belirleyicisi olup olmadığını belirlemek ve aynı popülasyonda kardiyojenik şok gelişimi ve hastanede kalp yetmezliğinin erken bir belirleyicisi olarak kullanılıp kullanılmayacağını değerlendirmektir.
Yöntemler: Çalışmamıza 2011-2013 yılları arasında STEMI semptomlarının başlamasından sonraki 12 saat içinde başvuran 18 yaş üstü 221 hasta alındı. Çalışmamız prospektif kohort olarak dizayn edildi. Klinik kalp yetmezliği, kardiyojenik şok gelişimi ve hastanede yatış sırasındaki ölüm gibi çeşitli klinik durumlar, hastanede kalış süresi, MI lokalizasyonu, revaskülarizasyon stratejisi ve koroner kalp hastalığı ile ilişkili risk faktörleri ile ilgili verilerle birlikte kaydedildi. Hastaların taburcu olduktan 1 ay sonra mortalite açısından telefonla aranarak bilgi alındı.
Bulgular: Hastanede yatış sırasında ölen hastalarda (P=0,004) veya taburcu olduktan sonraki 1 ay içinde HSP 60 değerleri anlamlı olarak daha yüksekti (P=0,020). Bu sonuçlar STEMI sonrası mortalite ile ilişkili diğer faktörlerden bağımsızdı. HSP 60 değeri ile hastanede kardiyojenik şok (P=0,03) veya kalp yetmezliği (P=0,03) arasında anlamlı bir ilişki izlendi.
Sonuç: HSP60'ın STEMI ile başvuran hastalarda artmış mortalite ile bağımsız olarak ilişkili olduğu ve bu nedenle umut verici bir mortalite belirleyicisi olarak kullanılabileceği düşünülebilir.

Anahtar Kelimeler

Miyokard enfarktüsü, HSP60, Prognoz, İnflamasyon, Ateroskleroz

Kaynakça

• 1. Fuster V, Badimon L, Badimon JJ, Chesebro JJ. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med. 1992;326(4):242-50.
• 2. Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature. 1993;362(6423):801-9.
• 3. Lai BT, Chin NW, Stanek AE, Keh W, Lanks KW. Quantitation and intracellular localization of the 85K heat shock protein by using monoclonal and polyclonal antibodies. Mol Cell Biol. 1984;4(12):2802-10.
• 4. Padmini E, Vijaya GB, Usha RM. Pollution induced nitrative stress and heat shock protein 70 overexpression in fish liver mitochondria. Sci Total Environ. 2009;407(4):1307-17.
• 5. Liu B, Dai J, Zheng H, Stoilova D, Sun S, Li Z. Cell surface expression of an endoplasmic reticulum resident heat shock protein gp96 triggers MyD88-dependent systemic autoimmune diseases. Proc Natl Acad Sci USA. 2003;100(26):15824-9.
• 6. Chan SH, Wang LL, Chang KF, Ou CC, Chan JY. Altered temporal profile of heat shock factor 1 phosphorylation and heat shock protein 70 expression induced by heat shock in nucleus tractus solitarii of spontaneously hypertensive rats. Circulation. 2003;107(2):339-45.
• 7. Varbiro S, Biro A, Cervenak J, Cervenak L, Singh M, Banhidy F, et al. Human anti-60 kD heat shock protein autoantibodies are characterized by basic features of natural autoantibodies. Acta Physiol Hung. 2010;97(1):1-10.
• 8. Xu Q, Schett G, Perschinka H, Mayr M, Egger G, Oberhollenzer F, et al. Serum soluble heat shock protein 60 is elevated in subjects with atherosclerosis in a general population. Circulation. 2000;102(1):14-20.
• 9. Pockley AG, Wu R, Lemne C, Kiessling R, de Faire U, Frostegard J. Circulating heat shock protein 60 is associated with early cardiovascular disease. Hypertension. 2000;36(2):303-7.
• 10. Steg PG, James SK, Atar D, Badano LP, Blömstrom LC, Borger MA, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33(20):2569-19.
• 11. Xu Q. Role of heat shock proteins in atherosclerosis. Arterioscler Thromb Vasc Biol. 2002;22(10):1547-59.
• 12. Zhang X, He MA, Cheng L, Zhou L, Zeng H, Wang J, et al. Joint effects of antibody to heat shock protein 60, hypertension, and diabetes on risk of coronary heart disease in Chinese. Clin Chem. 2008;54(6):1046-52.
• 13. Moseley PL. Heat shock proteins and heat adaptation of the whole organism. J Appl Physiol. 1997;83(5):1413-7.
• 14. Welch WJ, Suhan JP. Cellular and biochemical events in mammalian cells during and after recovery from physiological stress. J Cell Biol. 1986;103(5):2035-52.
• 15. Helmbrecht K, Zeise E, Rensing L. Chaperones in cell cycle regulation and mitogenic signal transduction. Cell Prolif. 2000;33(6):341-65.
• 16. Kaufmann SH. Heat-shock proteins: a link between rheumatoid arthritis and infection? Curr Opin Rheumatol. 1990;2(3):430-5.
• 17. Cohen IR, Young DB. Autoimmunity, microbial immunity and the immunological homunculus. Immunol Today. 1991;12(4):105-10.
• 18. Wick G, Knoflach M, Xu Q. Autoimmune and inflammatory mechanisms in atherosclerosis. Annu Rev Immunol. 2004;22:361-403.
• 19. Xiao Q, Mandal K, Schett G, Mayr M, Wick G, Oberhollenzer F, et al. Association of serum-soluble heat shock protein 60 with carotid atherosclerosis: clinical significance determined in a follow-up study. Stroke. 2005;36(12):2571-6.
• 20. Kol A, Bourcier T, Lichtman AH, Libby P. Chlamydial and human heat shock protein 60s activate human vascular endothelium, smooth muscle cells, and macrophages. J Clin Invest. 1999;103(4):571-7.
• 21. Maguire M, Poole S, Coates AR, Tormay P, Wheeler JC, Henderson B. Comparative cell signalling activity of ultrapure recombinant chaperonin 60 proteins from prokaryotes and eukaryotes. Immunology. 2005;115(2):231-8.
• 22. Kol A, Sukhova GK, Lichtman AH, Libby P. Chlamydial heat shock protein 60 localizes in human atheroma and regulates macrophage tumor necrosis factor-alpha and matrix metalloproteinase expression. Circulation. 1998;98(4):300-7.
• 23. Fong IW, Chiu B, Viira E, Tucker W, Wood H, Peeling RW. Chlamydial heat-shock protein-60 antibody and correlation with Chlamydia pneumoniae in atherosclerotic plaques. J Infect Dis. 2002;186(10):1469-73.
• 24. Biasucci LM, Liuzzo G, Ciervo A, Petrucca A, Piro M, Angiolillo DJ. Antibody response to chlamydial heat shock protein 60 is strongly associated with acute coronary syndromes. Circulation. 2003;107(24):3015-7.
• 25. Burian K, Kis Z, Virok D, Endresz V, Prohaszka Z, Duba J, et al. Independent and joint effects of antibodies to human heat-shock protein 60 and Chlamydia pneumoniae infection in the development of coronary atherosclerosis. Circulation. 2001;103(11):1503-8.
• 26. Multhoff G, Issels R. The role of heat shock proteins in the stimulation of an immune response. Biol Chem. 1998;379(3):295–300.
• 27. Toga W, Tanonaka K, Takeo S. Changes in Hsp60 level of the failing heart following acute myocardial infarction and the effect of long-term treatment with trandolapril. Biol Pharm Bull. 2007;30(1):105-10.
• 28. Schett G, Metzler B, Kleindienst R, Amberger A, Recheis H, Xu Q, et al. Myocardial injury leads to a release of heat shock protein (hsp) 60 and a suppression of the anti-hsp65 immune response. Cardiovasc Res. 1999;42(3):685-95.
• 29. Hochleitner BW, Hochleitner EO, Obrist P, Eberl T, Amberger A, Xu Q, et al. Fluid shear stress induces heat shock protein 60 expression in endothelial cells in vitro and in vivo. Arterioscler Thromb Vasc Biol. 2000;20(3):617-23.
• 30. Bonanad C, Nunez J, Sanchis J, Bodi V, Chaustre F, Chillet M, et al. Serum heat shock protein 60 in acute heart failure: a new biomarker? Congest Heart Fail. 2013;19(1):6-10.