Is IGF-1 level actually lowered in the early stage following an acute myocardial infarction and is IGF-1 associated with the left ventricle dysfunction or cardiac events?

Year 2020, Volume: 3 Issue: 1, 1 - 6, 15.01.2020

Yücel Yılmaz , Fatih Tanrıverdi , Mustafa Duran , Mustafa Altay Namık Kemal Eryol

https://doi.org/10.32322/jhsm.504184

Abstract

Background: Insulin-like growth factor
(IGF) is the primary mediator of growth hormone. IGF-1 may have an important
role in protecting the myocardial functions following an acute myocardial
infarction (AMI). Literature reveals only a limited number of studies
investigating the relationship between the serum IGF-1/IGF binding protein-3 (IGFBP-3)
levels and the left ventricular functions post AMI.  We aimed to determine
IGF-1 and IGFBP-3 levels and evaluate their effect on cardiac functions post
AMI.

Material and Method: Sixty five patients who were included
in the study and the control group had 26 patients. Blood samples of the
patients were obtained on the second day of their admission. The patients
underwent echocardiographic examination on the 7^th day of their
hospitalization.

Results: The serum IGF-1 and IGFBP-3 levels of the patient group were
higher than those of the control group; however only IGF-1 levels were
statistically significant (243,2±87,9 ng/mL versus 177,2±81,8 ng/mL p=0,001).
The increase in the wall thickness and LV chamber size did not correlate with
the decrease in LVEF and IGF-1/IGFBP-3 levels. The patients who had minor
cardiac events had lower IGF-1 levels but this was not statistically
significant (210.5±88.5 versus 253.1±86.1 p>0.05).

Conclusion: IGF-1 and IGFBP-3 levels elevated
following an the early AMI, but these markers were not correlated with the
echocardiographical measurements in early post MI period.

Keywords

Insulin-like growth factor, Insulin-like growth factor binding proteins, acute myocardial infarction

Serum IGF-1 düzeyleri akut miyokard infarktüsü sonrası gerçekten azalır mı ve sol ventrikül disfonksiyonu ile ilişkili midir?

Abstract

Giriş; İnsülin benzeri büyüme faktörü (İGF), büyüme hormonunun primer mediatördür. İGF-1 akut miyokard infarktüsü (AMİ) sonrası miyokard fonksiyonlarının korunmasında önemli olabilir. Literatürde AMI sonrası İGF-1/İGF binding protein-3 (IGFBP-3) ​​düzeyleri ile sol ventrikül fonksiyonları arasındaki ilişkiyi araştıran sınırlı sayıda çalışma vardır. Bizim amacımız, AMİ sonrası serum İGF-1 ve İGFBP-3 düzeylerini belirlemek ve kardiyak fonksiyonlar üzerindeki etkisini değerlendirmektir.

Çalışma planı; Çalışamaya koroner yoğun bakım ünitesine yatırılan ve kabul edilme kriterlerine sahip olan 65 hasta alındı. Kontrol grubu daha önce koroner arter hastalığı olmayan ve dışlanma kriterlerine sahip olmayan 26 kişiden oluşturuldu. Hastaların kan örnekleri aç olarak yatışının ikinci gününde alındı. Serum İGF-1 ve İGFBP-3 düzeyleri ölçüldü. Hastaların ekokardiyografik değerlendirmesi ortalama yatışının 7. gününde yapıldı.

Bulgular; Hasta grubunun serum İGF-1 ve İGFBP-3 düzeyleri kontrol grubuna göre daha yüksek tespit edildi. Ancak sadece IGF-1 düzeyleri (243,2 ± 87,9 ng / ml ve 177,2 ± 81,8 ng / ml p = 0.001) istatistiksel olarak anlamlı idi. Sol ventrikül (SV) duvar kalınlığı ve boşluk boyutlarındaki artış veya SV ejeksiyon fraksiyonlarındaki azalma ile İGF-1/İGFBP-3 düzeyleri arasında ilişki saptanmadı. Hasta grubunda minör kardiyak olaylar ile düşük İGF-1 düzeyleri arasında istatiksel olarak anlamlı olmayan bir ilişki tespit edildi. (253,1 ± 86,1 ve 210,5 ± 88,5 p> 0.05).

Sonuç; Daha önceki benzer çalışma sonuçlarından farklı olarak AMİ sonrası serum İGF-1 düzeylerinde yükselme tespit ettik. Ancak İGF-1 düzeyleri ile hastane içi kardiyak olaylar ve ekokardiyografik parametreler arasında ilişki bulamadık. AMİ ile İGF / İGFBP düzeyleri arasındaki bağlantılar karmaşık gibi görünmektedir ve bu ilişkiyi açıklamak için daha ileri çalışmalar gereklidir.

Keywords

: İnsülin benzeri büyüme faktörü, insülin benzeri büyüme faktörü bağlayıcı proteinler, akut miyokard infarktüsü

References

• 1. Delafontaine P. Insulin-like growth factor I and its binding proteins in the cardiovascular system. Cardiovasc Res. 1995;30:825–834.
• 2. Wang J, Niu W, Nikiforov Y, et al. Targeted overpression of IGF-1 evokes distinct patterns of organ remodeling in smooth muscle cell tissue beds of transgenic mice. J Clin Invest. 1997;100:1425–1439.
• 3. LeRoith D, Werner H, Beitner-Johnson D, et al. Molecular and cellular aspects of the insulin like growth factor I receptor. Endocr Rev. 1995;16:143–159.
• 4. Sowers JR. Insulin and insulin-like growth factor 1 (IGF-1) effects on Ca2+ and nitric oxide in diabetes. In: Levin ER, Nadler JL (eds) Endocrinology of Cardiovascular Function. Boston: Kluwer Academic Publishers 1998a, pp. 139–158.
• 5. Wang L, Ma W, Markovich R, et al. Regulation of cardiomyocyte apoptotic signaling by insulin-like growth factor I. Circ Res. 1998;83: 516–522.
• 6. Li B, Setoguchi M, Wang X, et al. Insulin-like growth factor-1 attenuates the detrimental impact of nonocclusive coronary artery constriction on the heart. Circ Res. 1999;84:1007–1019.
• 7. Colao A. The GH–IGF-I axis and the cardiovascular system: clinical implications. Clinical Endocrinology 2008; 69: 347–358.
• 8. Tunstall-Pedoe H, Kuulasmaa K, Amouyel P, et al. Myocardial infarction and coronary deaths in the World Health Organization MONICA Project: registration procedures, event rates, and case-fatality rates in 38 populations from 21 countries in four continents. Circulation 1994;90:583–612.
• 9. Devereux RB, de Simone G, Koren MJ, et al. Left ventricular mass as a predictor of development of hypertension. Am J Hypertens. 1991;4:603S–607S.
• 10. Kaplan RC, Strickler HD, Rohan TE, et al. Insulin-Like Growth Factors and Coronary Heart Disease. Cardiol Rev. 2005;13:35-39.
• 11. Ruidavets JB, Luc G, Machez E, et al. Effects of insulin-like growth factor 1 in preventing acute coronary syndromes:The PRIME study. Atherosclerosis 2011;218:464-469.
• 12. Sekuri C, Arslan O, Utük O, et al. Serum level of insulin-like growth factor-1 and insulin-like growth factor binding protein-3 in acute coronary syndromes and relationship with prognosis. Anadolu Kardiyol Derg. 2004;4:209-212
• 13. Friberg L, Werner S, Eggertsen G, et al. Growth hormone and insulin-like growth factor-1 in acute myocardial infarction. Eur Heart J. 2000;21:1547-1554.
• 14. Yamaguchi H, Komamura K, Choraku M, et al. Impact of Serum Insulin-like Growth factor-1 on Early Prognosis in Acute Myocardial Infarction. Inter Med. 2008;47:819-825.
• 15. Hajsadeghi S, Mohseni H, Moradi M, et al. Evaluating the Association Between Insulin–Like Growth Factor-1 Values and Short-Term Survival Rates Following Acute Myocardial Infarction. Clin Med Insights Cardiol. 2011;5:7–11.
• 16. Lee WL, Chen JW, Ting CT, et al. Changes of the insulin-like growth factor I system during acute myocardial infarction: implications on left ventricular remodeling. J Clin Endocrinol Metab. 1999;84:1575-1581.
• 17. Friehs I, Stamm C, Cao-Danh H, et al. Insulin-like growth factor-1 improves postischemic recovery in hypertrophied hearts. Ann Thorac Surg. 2001;72:1650 –1656.
• 18. Li Q, Li B, Wang X, et al. Overexpression of insulin-like growth factor-1 in mice protects from myocyte death after infarction, attenuating ventricular dilation, wall stress, and cardiac hypertrophy. J Clin Invest. 1997;100:1991–1999.
• 19. Lee WL, Chen JW, Ting CT, et al. Insulin-like growth factor I improves cardiovascular function and suppresses apoptosis of cardiomyocytes in dilated cardiomyopathy. Endocrinology 1999;140:4831– 4840.
• 20. Bennett MR, Evan GI, Schwartz SM. Apoptosis of human vascular smooth muscle cells derived from normal vessels and coronary atherosclerotic plaques. J Clin Invest. 1995;95:2266 –2274.
• 21. Mallat Z, Tedgui A. Current perspective on the role of apoptosis in atherothrombotic disease. Circ Res. 2001;88:998–1003.
• 22. Bornfeldt KE, Raines EW, Nakano T, et al. Insulin-like growth factor-I and platelet-derived growth factor-BB induce directed migration of human arterial smooth muscle cells via signaling pathways that are distinct from those of proliferation. J Clin Invest. 1994;93:1266–1274.
• 23. Muniyappa R, Walsh MF, Rangi JS, et al. Insulin like growth factor 1 increases vascular smooth muscle nitric oxide production. Life Sci. 1997;61:925–931.
• 24. Tsukahara H, Gordienko DV, Tonshoff B, et al. Direct demonstration of insulin-like growth factor-I-induced nitric oxide production by endothelial cells. Kidney Int. 1994;45:598–604.
• 25. Davani EY, Brumme Z, Singhera GK, et al. Insulin-like growth factor-1 protects ischemic murine myocardium from ischemia/reperfusion associated injury. Crit Care. 2003;7:176-183.
• 26. Akagi Y, Liu W, Zebrowski B, et al. Regulation of vascular endothelial growth factor expression in human colon cancer by insulin-like growth factor-I. Cancer Res. 1998;58:4008–4014.
• 27. Friehs I, Stamm C, Cao-Danh H, et al. Insulin-like growth factor-1 improves postischemic recovery in hypertrophied hearts. Ann Thorac Surg. 2001;72:1650 –1656.
• 28. Kotlyar AA, Vered Z, Goldberg I, et al. Insulin-like growth factor I and II preserve myocardial structure in postinfarct swine. Heart 2001;86:693-700.
• 29. Conti E, Andreotti F, Sciahbasi A, et al. Markedly reduced insulin-like growth factor-1 in the acute phase of myocardial infarction. J Am Coll Cardiol. 2001;38:26 –32.
• 30. Davies MJ. The composition of coronary artery plaques (letter). N Engl J Med. 1997;336:1312–1314.
• 31. Berenson GS, Srinivasan SR, Bao W, et al. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults: The Bogalusa Heart Study. N Engl J Med. 1998; 338:1650–1656.