Inquiring about the link between urotensin-II and coronary collateral development in coronary artery patients with and without diabetes

Year 2023, , 371 - 375, 27.10.2023

Yasin Karakuş Nusret Açıkgöz

https://doi.org/10.38053/acmj.1330608

Abstract

Aims: Coronary collateral circulation consists of vascular channels activated to maintain perfusion in major epicardial coronary arteries in severe stenosis or occlusion. Yet, coronary collateral development (CCD) in diabetic patients was previously proven to be poor. Urotesin-II (U-II) is famous for being the most potent vasoconstrictor agent, and plasma levels are known to elevate in diabetic patients and play an important role in diabetic complications. In this study, we inquired about the link between U-II levels and the development of coronary collaterals between diabetic and non-diabetic patients with coronary artery disease (CAD).
Methods: We recruited 31 diabetic and 30 non-diabetic patients with 95% or more coronary artery stenosis or occlusion and considered Rentrop’s classification for grading collaterals. In this sense, while Rentrop grades 0-1 are regarded as poor CCD, Rentrop grades 2-3 correspond to well-developed collaterals. Moreover, we compared the patients’ serum levels of U-II by the degree of CCD.
Results: The findings revealed that demographic characteristics did not significantly differ between the groups (p >0.05). Although CCD seemed worse in diabetic patients than those without diabetes (DM), the finding was not statistically significant. However, the diabetic patients had significantly higher U-II levels than non-diabetic patients (388.1±314.2 vs. 229.8±216.9, p=0.026). Despite not being significant, U-II levels were higher in patients with poor CCD than those with well-developed collaterals in the non-diabetic group (370.6±298; 178.6±158.3, p=0.2). In the diabetic group, on the other hand, U-II levels were significantly higher in patients with poor CCD and significantly lower in patients with good CCD (582.7±316.4 and 180.4±121.6, respectively; p <0.0001 for both).
Conclusion: Overall, our findings demonstrated a significant association between U-II levels and the development of coronary collateral circulation in patients with DM. We also determined that U-II levels were low in diabetic patients with good CCD, while those with poor CCD had higher levels of U-II.

Keywords

Diabetes, coronary collateral circulation, urotensin II

References

• Ralapanawa U, Sivakanesan R. Epidemiology and the magnitude of coronary artery disease and acute coronary syndrome: a narrative review. J Epidemiol Glob Health. 2021;11(2):169-177.
• Aytan Y, Koşar F. Kollateral dolaşım. MN Kardiyoloji. 2000;7(1): 64-70
• Lorenzi M, Nordberg JA, Toledo S. High glucose prolongs cell-cycle traversal of cultured human endothelial cells. Diabetes. 1987;36(11):1261-1267.
• Islam MM, Ali A, Khan NA, et al. Comparative study of coronary collaterals et al. in diabetic and nondiabetic patients by angiography. Mymensingh Med J. 2006;15(2):170-175.
• Langham RG, Kelly Darren J, Gow Renae M, et al. Increased expression of urotensin II and urotensin II receptor in human diabetic nephropathy. Am J Kidney Dis. 2004;44(5): 826-831.
• Ong KL, Lam KS, Cheung BM. Urotensin II: its function in health and its function in disease. Cardiovasc Drugs Ther. 2005;19(1):65-75.
• Cohen M, Rentrop KP. Limitation of myocardial ischemia by collateral circulation during sudden controlled coronary artery occlusion in human subjects: a prospective study. Circulation. 1986;74(3):469-476.
• Williams DO, Amsterdam EA, Miller RR, Mason Dean T. Functional significance of coronary collateral vessels in patients with acute myocardial infarction: relation to pump performance, cardiogenic shock and survival. Am J Cardiol. 1976;37(3):345-351.
• Wingard DL, Barrett-Connors E Heart disease and diabetes. In: Diabetes in America, 2nd ed. (Ed. Harris M), p. 429-456. Bethesda: National Institutes of Health, 1995.
• Lorenzi M, Nordberg JA, Toledo S. High glucose prolongs cell-cycle traversal of cultured human endothelial cells. Diabetes. 1987;36(11):1261-1267.
• Abacı A, Oğuzhan A, Kahraman S, et al. Effect of diabetes mellitus on formation of coronary collateral vessels. Circulation. 1999;99(17):2239-2242.
• E Tatli, A Altun, M Büyüklü, Barotçu Ahmet. Coronary collateral vessel development after acute myocardial infarction. Exp Clin Cardiol. 2007;12(2):97-99.
• Moreno PR, Alvaro MM, Palacios IF, et al. Coronary composition and macrophage infiltration in atherectomy specimens from patients with diabetes mellitus. Circulation. 2000;102(18):2180-2184.
• Suguro T, Watanabe T, Kodate S, et al. Increased plasma urotensin-II levels are associated with diabetic retinopathy and carotid atherosclerosis in type 2 diabetes. Clin Sci. 2008;115(11):327-334.
• Totsune, K, Takahashi K, Arihara Z, Sone M, Ito S, Murakami O. Increased plasma urotensin II levels in patients with diabetes mellitus. Clin Sci (Lond). 2003;104(1):1-5.
• Yu Q, Wei P, Xu L, et al. Urotensin II enhances advanced aortic atherosclerosis formation and delays plaque regression in hyperlipidemic rabbits. Int J Mol Sci. 2023;24(4):3819.
• Bousette N, Patel L, Douglas SA, Ohlstein EH, Giaid A. Increased expression of urotensin II and its cognate receptor GPR14 in atherosclerotic lesions of the human aorta. Atherosclerosis. 2004;176(1):117-123.
• Suguro T, Watanabe T, Ban Y, et al. Increased human urotensin II levels are correlated with carotid atherosclerosis in essential hypertension. Am J Hypertens. 2007;20(2):211-217.
• Khan SQ, Bhandari SS, Quinn P, Davies JE, Ng LL. Urotensin II is raised in acute myocardial infarction and low levels predict risk of adverse clinical outcome in humans. Int J Cardiol. 2007;117(3):323-328.
• Cook-Mills JM, Marchese ME, Valencia HA.Vascular cell adhesion molecule-1 expression and signaling during disease: regulation by reactive oxygen species and antioxidants. Antioxid Redox Signal. 2011;15(6):1607-1638.