The Relationship Between HbA1c and Contrast-Induced Nephropathy in Patients with Non-ST Elevation Myocardial Infarction and Non- Established Diabetes Mellitus

Year 2021, Volume: 3 Issue: 4, 172 - 176, 29.10.2021

Onur Baydar

https://doi.org/10.46310/tjim.882755

Cited By: 1

Abstract

Background: Diabetes Mellitus (DM) is an important cardiovascular risk factor and 50% of newly diagnosed diabetic patients have coronary artery disease. HbA1c levels in these patients have an effect on prognosis. Development of contrast agent-induced nephropathy (CIN) is common in patients who have undergone percutaneous coronary intervention (PCI) without ST elevation myocardial infarction (NSTEMI) and is associated with increased mortality and morbidity. In our study, the relationship between HbA1c and the development of CIN was investigated in NSTEMI patients who did not have a previous diagnosis of DM and receive treatment.
Methods: In our study, 359 (189, 52.6% male) patients who were not diagnosed with DM and did not receive treatment were retrospectively analyzed for NSTEMI diagnosis. HbA1c and creatinine values before the procedure and post-procedure creatinine values were evaluated. CIN; It was defined as an increase of 25% or 0.5 mg / dl compared to the basal value in serum creatinine measured 48-72 hours after the procedure.
Results: CIN was detected in 56 (15.6%) of all patients. Among the group with and without CIN; There was no difference between gender, amount of contrast material, pre-procedure eGFR, troponin and ejection fraction values. Only in the group with CIN, the patients were older and the number of hypertensive patients was significantly higher (Table 1). As a result of coronary angiography, medical follow-up was made for 46 (12.7%) patients, coronary stent in 271 (74.7%) and coronary bypass in 40 (11%) patients. In addition, in-hospital mortality was detected in 17 (4.7%) patients. HbA1c and fasting glucose levels were found significantly higher in the group developing CIN (6.1 ± 1.0 vs 5.5 ± 0.6, p <0.001, 133.8 mg/dl ± 65.9 vs 110.9 mg/dl ± 48.7, p: 0.002, respectively). But only the HbA1c value was determined to be an independent predictor in the logistic regression analysis of CIN (OR: 2.3, p <0.001, CI: 1.6-3.2).

Conclusion: CIN was more common in NSTEMI patients with high HbA1c who were not diagnosed with DM and were not treated.In addition, HbA1c value was an independent predictor of CIN development.

Keywords

HbA1c, nephropathy, myocardial infarction

References

• 1. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet 2003;361:13-20. doi: 10.1016/S0140-6736(03)12113-7.
• 2. Marenzi G, Lauri G, Assanelli E, et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll Cardiol 2004;44:1780-5. doi: 10.1016/j.jacc.2004.07.043.
• 3. Ishihara M, Inoue I, Kawagoe T, et al. Impact of acute hyperglycemia on left ventricular function after reperfusion therapy in patients with a first anterior wall acute myocardial infarction. Am Heart J 2003;146: 674-8. doi: 10.1016/S0002-8703(03)00167-4.
• 4. Nakamura T, Ako J, Kadowaki T, et al. Impact of acute hyperglycemia during primary stent implantation in patients with STelevation myocardial infarction. J Cardiol 2009;53:2727. doi: 10.1016/j.jjcc.2008.11.011.
• 5. Barbieri L, Verdoia M, Schaffer A, Cassetti E, Di Giovine G, Marino P, Suryapranata H, De Luca G. Pre-diabetes and the risk of contrast induced nephropathy in patients undergoing coronary angiography or percutaneous intervention. Diabetes Res Clin Pract. 2014;106:458–64. doi: 10.1016/j.diabres.2014.09.041.
• 6. Hamm CW, Bassand JP, Agewall S, et al; ESC Committee for Practice Guidelines. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Task Force for the Management of Acute Coronary Syndromes (ACS) in Patients Presenting Without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2011;32(23):2999-3054. doi: 10.1714/1038.11322.
• 7. Expert Panel on Detection Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the third report of the National Cholesterol Education Program (NCEP) expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (adult treatment panel III). JAMA. 2001; 285(19):2486-97. doi: 10.1001/jama.285.19.2486.
• 8. Levey AS, Beto JA, Coronado BE, et al. National Kidney Foundation Task Force on Cardiovascular Disease. Controlling the epidemic of cardiovascular disease in chronic renal disease. What do we know? What do we need to learn? Where do we go from here? Am J Kidney Dis 1998 Nov;32(5 Suppl 3):S1-199.
• 9. Thomsen HS. European Society of Urogenital Radiology (ESUR) guidelines on the safe use of iodinated contrast media. Eur J Radiol. 2006;60(3):307-13. doi: 10.1016/j.ejrad.2006.06.020.
• 10. Tepel M, Aspelin P, Lameire N. Contrast-induced nephropathy: a clinical and evidence-based approach. Circulation. 2006;113(14): 1799-1806. doi: 10.1161/CIRCULATIONAHA.105.595090.
• 11. Selvin E, Marinopoulos S, Berkenblit G, Rami T, Brancati FL, Powe NR, Golden SH. Meta-analysis: Glycosylated hemoglobin and cardiovascular disease in diabetes mellitus. Ann Internal Med. 2004;141:421–31. doi: 10.7326/0003-4819-141-6-200409210-00007.
• 12. Balkau B, Shipley M, Jarrett RJ, Pyorala K, Pyörälä K, Pyörälä M, Forhan A, Eschwège E. High blood glucose concentration is a risk factor for mortality in middle-aged nondiabetic men. 20-year follow-up in the Whitehall Study, the Paris Prospective Study, and the Helsinki Policemen Study. Diabetes Care. 1998;21:360–367. doi: 10.2337/diacare.21.3.360.
• 13. Xu Y, Wang L, He J, Bi Y, Li M, Wang T, Wang L, Jiang Y, Dai M, Lu J, et al. Prevalence and control of diabetes in Chinese adults. JAMA. 2013;310:948–959. doi: 10.1001/jama.2013.168118.
• 14. McCullough PA, Wolyn R, Rocher LL, Levin RN, Oneill WW. Acute renal failure after coronary intervention: Incidence, risk factors, and relationship to mortality. Am J Med. 1997;103:368–375. doi: 10.1016/s0002-9343(97)00150-2.
• 15. Goldstein DE, Little RR, Lorenz RA, Malone JI, Nathan DM, Peterson CM. American Diabetes Association: Tests of glycemia in diabetes. Diabetes Care. 2004;27(Suppl 1):S91–S93.
• 16. Yang Z, Laubach VE, French BA, et al. Acute hyperglycemia enhances oxidative stress and exacerbates myocardial infarction by activating nicotinamide adenine dinucleotide phosphate oxidase during reperfusion. J Thorac Cardiovasc Surg 2009;137: 723-9. doi: 10.1016/j.jtcvs.2008.08.056.
• 17. Undas A, Wiek I, Stepien E, et al. Hyperglycemia is associated with enhanced thrombin formation, platelet activation, and fibrin clot resistance to lysis in patients with acute coronary syndrome. Diabetes Care 2008;31:1590-5. doi: 10.2337/dc08-0282.
• 18. Worthley MI, Holmes AS, Willoughby SR, et al. The deleterious effects of hyperglycemia on platelet function in diabetic patients with acute coronary syndromes. Mediation by superoxide production, resolution with intensive insulin administration. J Am Coll Cardiol 2007;49: 304-10. doi: 10.1016/j.jacc.2006.08.053.