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The Relationship Between Serum Urotensin II Level and Contrast-Induced Nephropathy and One-year Clinical Follow-up Findings in Patients with Coronary Slow Phenomenon Undergoing Percutaneous Coronary Intervention

Year 2019, , 442 - 454, 16.09.2019
https://doi.org/10.31832/smj.596933

Abstract

Background:
Coronary slow-reflow phenomenon (CSFP) and
Contrast-Induced
Nephropathy (CIN) are
associated with an increased risk of major
cardiovascular adverse events.

This study aimed to evaluate the relationship between serum
Urotensin
II molecule (U-II
)
levels and CIN in patients with CSFP undergoing percutaneous coronary
intervention (PCI).

Methods: We
enrolled  227  patients (161 male and 66 female; mean age:
61,44 ± 12,44 years) with angiographically diagnosed CSFP. The patients were
divided into two groups according to CIN development (Non-CIN (n=206) and CIN
group (n=21)).

Results: CIN
was observed in 9,25%(n=21) of the CSFP patients. Serum U-II level was
significantly higher in CIN group than in non-CIN group (6,79±2,2 vs. 3±1,29,
p<0.001). One year clinical follow-up findings including all-cause mortality
(7(33,3%) vs. 24(11,7%), p=0,013), cardiovascular death(7(33,3%) vs. 18(8,7%),
p=0,003) and
Major Adverse
cardiovascular events
(MACE) (10(47,6%) vs. 46(22,4%), p: 0,011) were
significantly higher in CIN group. We also performed forward conditional
logistic regression analysis and found that U-II (Odds ratio (OR)= 3,983; 95%
confidence interval (CI): 2,25 to 7,052; p < 0.001) and Mehran score (OR=1,228,
95% CI: 1,083-1,393, p=0,001) were independently predicted CIN development in patients
with CSFP.







Conclusions:
Baseline serum U-II concentrations and higher Mehran scores are independently
associated with CIN in CSFP patients. One year clinical follow-up findings
including all-cause mortality, cardiovascular death and MACE were significantly
higher in CIN group, but stroke and myocardial infarction rates were similar in
both groups.

Supporting Institution

Bezmialem Vakıf Üniversitesi

Project Number

5.2016/17

Thanks

The author thanks Betul Cetintulum Huyut, PhD. Cand., for her statistical analysis contributions in preparing this manuscript.

References

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  • 3. Chaudhry MA, Smith M, Hanna EB, Lazzara R. Diverse spectrum of presentation of coronary slow flow phenomenon: a concise review of the literature. Cardiol Res Pract. 2012;2012:383181.
  • 4. Yarlioglues M, Yalcinkaya D, Celik IE, Duran M. CHA2DS2VASc Score and Coronary No-Reflow Phenomenon. Angiology. 2019 May 23:3319719851698. doi: 10.1177/0003319719851698.
  • 5. Kelly RF, Sompalli V, Sattar P, Khankari K. Increased TIMI frame counts in cocaine users: a case for increased microvascular resistance in the absence of epicardial coronary disease or spasm. Clin Cardiol 2003;26:319–22.
  • 6. Quisi A, Alıcı G. The relationship between serum rheumatoid factor level and no-reflow phenomenon in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. J Clin Lab Anal. 2018 Nov;32(9):e22598. doi: 10.1002/jcla.22598.
  • 7. Jaffe R, Dick A, Strauss BH. Prevention and treatment of microvascular obstruction-related myocardial injury and coronary no-reflow following percutaneous coronary intervention: a systematic approach. JACC Cardiovasc Interv. 2010;3:695‐704.
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  • 17. Coca SG, Peixoto AJ, Garg AX, Krumholz HM, Parikh CR. The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. Am J Kidney Dis. 2007;50:712-720.
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  • 21. Ong KL, Lam KS, Cheung BM. Urotensin II: its function in health and its role in disease. Cardiovasc Drugs Ther 2005; 19: 65-75.
  • 22. Am Fam Physician. JNC 8 Guidelines for the Management of Hypertension in Adults, 2014 Oct 1;90(7):503-504.
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  • 25. Acquatella H, Asch FM, Barbosa MM, Barros M, Bern C, Cavalcante JL, et al. Recommendations for Multimodality Cardiac Imaging in Patients with Chagas Disease: A Report from the American Society of Echocardiography in Collaboration With the InterAmerican Association of Echocardiography (ECOSIAC) and the Cardiovascular Imaging Department of the Brazilian Society of Cardiology (DIC-SBC). J Am Soc Echocardiogr. 2018 Jan;31(1):3-25. doi: 10.1016/j.echo.2017.10.019.
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  • 27. Cin VG, Pekdemir H, Camsar A, Cicek D, Akkuş MN, Parmaksız T, et al. Diffuse intimal thickening of coronary arteries in slow coronary flow. Jpn Heart J 2003;44, 907–919.
  • 28. Yıldız A, Gur M, Yılmaz R, Demirbag R, Polat M, Selek S, et al. Association of paraoxonase activity and coronary blood flow. Atherosclerosis 2008; 197, 257–263.
  • 29. Enli Y, Turk M, Akbay R, Evrengul H, Tanrıverdi H, Kuru O,et al. Oxidative stress parameters in patients with slow coronary flow. Adv Ther 2008; 25, 37–44.
  • 30. Kopetz V, Kennedy J, Heresztyn T, Stafford I, Willoughby SR, Beltrame JF. Endothelial function, oxidative stress and inflammatory studies in chronic coronary slow flow phenomenon patients. Cardiology 2012; 121, 197–203.
  • 31. Zengin H, Erbay AR, Okuyucu A, Alaçam H, Yüksel S, Meriç M, et al. The relationship between coronary slow flow phenomenon and urotensin-II: A prospective and controlled study. Anatol J Cardiol. 2015 Jun;15(6):475-9. doi: 10.5152/akd.2014.5481.
  • 32. Balment RJ, Song W, Ashton N. Urotensin II: ancient hormone with new functions in vertebrate body fluid regulation. Ann NY Acad Sci 2005;1040:66–73.33. Iglewski M, Grant SR. Urotensin II-induced signaling involved in proliferation of vascular smooth muscle cells. Vasc Health Risk Manag 2010; 6, 723–734.
  • 34. Song N, Ding W, Chu S, Zhao J, Dong X, Di B, et al. Urotensin II stimulates vascular endothelial growth factor secretion from adventitial fibroblasts in synergy with angiotensin II. Circ J 2012; 76, 1267–1273.
  • 35. Goldenberg I, Matetzky S. Nephropathy induced by contrast media: pathogenesis, risk factors and preventive strategies. Can Med Assoc J 2005;172: 1461–71.
  • 36. Marenzi G, De Metrio M, Rubino M, Lauri G, Cavallero A, Assanelli E, et al. Acute hyperglycemia and contrast-induced nephropathy in primary percutaneous coronary intervention. Am Heart J. 2010 Dec;160(6):1170-7. doi: 10.1016/j.ahj.2010.09.022.
  • 37. Cowburn PJ, Patel H, Pipes RR, Parker JD. Contrast nephropathy post cardiac resynchronization therapy: an under-recognized complication with important morbidity. Eur J Heart Fail. 2005 Aug;7(5):899-903.
  • 38. Shacham Y, Steinvil A, Arbel Y. Acute kidney injury among ST elevation myocardial infarction patients treated by primary percutaneous coronary intervention: a multifactorial entity. J Nephrol. 2016;29(2):169-74.
  • 39. Maioli M, Toso A, Leoncini M, Gallopin M, Musilli N, Bellandi F. Persistent renal damage after contrast-induced acute kidney injury incidence, evolution, risk factors, and prognosis. Circulation. 2012;125(25):3099-107.
  • 40. Kumar S, Nair RK, Aggarwal N, Abbot AK, Muthukrishnan J, Kumar KV. Risk factors for contrast-induced nephropathy after coronary angiography. Saudi J Kidney Dis Transpl. 2017;28(2): 318-24.
  • 41. Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention. J Am Coll Cardiol. 2004;44(7):1393-99.
  • 42. Sun XP, Li J, Zhu WW, Li DB, Chen H, Li HW et al. Platelet to Lymphocyte Ratio Predicts Contrast-Induced Nephropathy in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Angiology. 2018 Jan;69(1):71-78.
  • 43. Kocas C, Yildiz A, Abaci O, Karaca OS, Firdin N, Dalgic Y, et al. Platelet-to-Lymphocyte Ratio Predicts Contrast-Induced Nephropathy in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome. Angiology. 2015 Nov;66(10):964-8.
  • 44. Ulus T, Isgandarov K, Yilmaz AS, Uysal S, Vasi I, Dural M, et al. Monocyte to High-Density Lipoprotein Ratio Predicts Contrast-Induced Nephropathy in Patients With Acute Coronary Syndrome. Angiology. 2018 Nov;69(10):909-916.
  • 45. Kaya A, Kaya Y, Topcu S, Günaydin ZY, Kurt M, Tanboğa IH, et al. Neutrophil-to-lymphocyte ratio predicts contrast-induced nephropathy in patients undergoing primary percutaneous coronary intervention. Angiology. 2014 Jan;65(1):51-6.
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Perkütan Koroner Girişim Yapılan Koroner Yavaş Akım Olgularında, Serum Urotensin II Düzeyi ve Kontrast Kaynaklı Nefropati Gelişimi ile Bir Yıllık Klinik Takip Bulguları Arasındaki İlişki

Year 2019, , 442 - 454, 16.09.2019
https://doi.org/10.31832/smj.596933

Abstract

Amaç: Koroner yavaş akıntı
fenomeni (CSFP) ve kontrast kaynaklı nefropati (CIN), artmış kardiyovasküler
advers olay riski ile ilişkilidir. Bu çalışmada, CSFP'li perkütan koroner
girişim (PCI) yapılan hastalarda serum Urotensin II molekülü (U-II) düzeyleri
ile CIN arasındaki ilişkiyi değerlendirmeyi amaçladık.



Yöntem: Anjiyografik
olarak CSFP tanısı alan 227 hasta (161 erkek ve 66 kadın; ort. yaş: 61,44 ±
12,44) çalışmaya alındı. Hastalar CIN gelişmesine (CIN Dışı (n = 206) ve CIN
grubuna (n = 21)) göre iki gruba ayrıldı.



Bulgular: CSFP
hastalarının% 9,25'inde (n = 21) CIN gözlendi. Serum U-II düzeyi CIN grubunda
CIN olmayan gruba göre anlamlı derecede yüksek saptandı (6,79 ± 2,2 vs. 3 ±
1,29, p <0,001). Tüm nedenlere bağlı mortalite (7 (% 33,3) ve 24 (% 11,7), p
= 0,013), kardiyovasküler ölüm (7 (% 33,3) ve 18 (8, % 7), p = 0,003) ve Majör
olumsuz kardiyovasküler olaylar (MACE) (10 (% 47,6) vs. 46 (% 22,4), p: 0,011)
CIN grubunda anlamlı derecede yüksekti. Ayrıca ileri koşullu lojistik regresyon
analizi yapıldı ve CSFP'li hastalarda U-II (Oran oranı (OR) = 3,983;% 95 güven
aralığı (CI): 2,25 ila 7,052; p <0,001) ve Mehran skorunun (OR = 1,228, %95
CI: 1,083-1,393, p = 0,001) bağımsız olarak CIN gelişimininin
öngördürücülerinin olduğu saptandı.



Sonuç: Yüksek
serum U-II konsantrasyonları ve yüksek Mehran skorları CSFP hastalarında
bağımsız olarak CIN gelişimi ile ilişkili bulunmuştur. Bir yıllık klinik
takipte, tüm nedenlere bağlı ölüm, kardiyovasküler ölüm ve MACE bulguları CIN
grubunda anlamlı derecede yüksek saptandı, ancak inme ve miyokard infarktüsü
oranları her iki grupta da benzer bulundu.

Project Number

5.2016/17

References

  • 1. Hawkins BM, Stavrakis S, Rousan TA, Abu-Fadel M, Schechter E. Coronary slow flow--prevalence and clinical correlations. Circ J. 2012;76(4):936-42.
  • 2. Rezkalla SH, Stankowski RV, Hanna J, Kloner RA. Management of No-Reflow Phenomenon in the Catheterization Laboratory. JACC Cardiovasc Interv. 2017 Feb 13;10(3):215-223. doi: 10.1016/j.jcin.2016.11.059.
  • 3. Chaudhry MA, Smith M, Hanna EB, Lazzara R. Diverse spectrum of presentation of coronary slow flow phenomenon: a concise review of the literature. Cardiol Res Pract. 2012;2012:383181.
  • 4. Yarlioglues M, Yalcinkaya D, Celik IE, Duran M. CHA2DS2VASc Score and Coronary No-Reflow Phenomenon. Angiology. 2019 May 23:3319719851698. doi: 10.1177/0003319719851698.
  • 5. Kelly RF, Sompalli V, Sattar P, Khankari K. Increased TIMI frame counts in cocaine users: a case for increased microvascular resistance in the absence of epicardial coronary disease or spasm. Clin Cardiol 2003;26:319–22.
  • 6. Quisi A, Alıcı G. The relationship between serum rheumatoid factor level and no-reflow phenomenon in patients with acute ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. J Clin Lab Anal. 2018 Nov;32(9):e22598. doi: 10.1002/jcla.22598.
  • 7. Jaffe R, Dick A, Strauss BH. Prevention and treatment of microvascular obstruction-related myocardial injury and coronary no-reflow following percutaneous coronary intervention: a systematic approach. JACC Cardiovasc Interv. 2010;3:695‐704.
  • 8. Brosh D, Assali AR, Mager A, Porter A, Hasdai D, Teplitsky I, et al. Effect of no-reflow during primary percutaneous coronary intervention for acute myocardial infarction on six-month mortality. Am J Cardiol. 2007;99:442‐445.
  • 9. Silvain J, Collet JP, Montalescot G. Contrast-induced nephropathy: the sin of primary percutaneous coronary intervention? Eur Heart J. 2014;35(23):1504-1506.
  • 10. Caruso M, Balasus F, Incalcaterra E, Ruggieri A, Evola S, Fattouch K, et al. Contrast-induced nephropathy after percutaneous coronary intervention in simple lesions: risk factors and incidence are affected by the definition utilized. Intern Med. 2011;50(9):983-989.
  • 11. Sadat U. Radiographic contrast-media-induced acute kidney injury: pathophysiology and prophylactic strategies. ISRN Radiol. 2013;2013:496438.
  • 12. Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002;105:2259– 64.
  • 13. McCullough PA, Wolyn R, Rocher LL, Levin RN, O’Neill WW. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med 1997;103:368–75.
  • 14. Brillet G, Aubry P, Schmidt A, Catella L, Julien L, Benard S. Hospital costs of contrast-induced nephropathy. Value Health. 2015;18(7):A510.
  • 15. Sigterman TA, Krasznai AG, Snoeijs MG, Heijboer R, Schurink GW, Bouwman LH. Contrast induced nephropathy and long-term renal decline after percutaneous transluminal angioplasty for symptomatic peripheral arterial disease. Eur J Vasc Endovasc Surg. 2016;51(3):386-393.
  • 16. Mitchell AM, Kline JA, Jones AE, Tumlin JA. Major adverse events one year after acute kidney injury after contrast-enhanced computed tomography. Ann Emerg Med. 2015;66:267-274.e4. doi: 10.1016/j.annemergmed.2015.04.028.
  • 17. Coca SG, Peixoto AJ, Garg AX, Krumholz HM, Parikh CR. The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. Am J Kidney Dis. 2007;50:712-720.
  • 18. Neyra JA, Shah S, Mooney R, Jacobsen G, Yee J, Novak JE. Contrast-induced acute kidney injury following coronary angiography: a cohort study of hospitalized patients with or without chronic kidney disease. Nephrol Dial Transplant. 2013;28:1463–1471.
  • 19. Kharbanda RK, Deanfield JE. Functions of the healthy endothelium. Coron Artery Dis 2001; 12: 485-91.
  • 20. Maguire JJ, Kuc RE, Davenport AP. Orphan-receptor ligand human urotensin II: receptor localization in human tissues and comparison of vasoconstrictor responses with endothelin-1. Br J Pharmacol 2000; 131: 441-6.
  • 21. Ong KL, Lam KS, Cheung BM. Urotensin II: its function in health and its role in disease. Cardiovasc Drugs Ther 2005; 19: 65-75.
  • 22. Am Fam Physician. JNC 8 Guidelines for the Management of Hypertension in Adults, 2014 Oct 1;90(7):503-504.
  • 23. Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the expert committee on the diagnosis and classification of diabetes mellitus. Diabetes Care. 2003;26(Suppl 1): S5‐20.
  • 24. National Cholesterol Education Program Expert Panel on Detection evaluation, and treatment of high blood cholesterol in adults. 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) final report. Circulation. 2002;106:3143‐3421.
  • 25. Acquatella H, Asch FM, Barbosa MM, Barros M, Bern C, Cavalcante JL, et al. Recommendations for Multimodality Cardiac Imaging in Patients with Chagas Disease: A Report from the American Society of Echocardiography in Collaboration With the InterAmerican Association of Echocardiography (ECOSIAC) and the Cardiovascular Imaging Department of the Brazilian Society of Cardiology (DIC-SBC). J Am Soc Echocardiogr. 2018 Jan;31(1):3-25. doi: 10.1016/j.echo.2017.10.019.
  • 26. Tambe AA, Demany MA, Zimmerman HA, Mascarenhas E. Angina pectoris and slow flow velocity of dye in coronary arteries – A new angiographic finding. Am Heart J 84, 66–71 (1972).
  • 27. Cin VG, Pekdemir H, Camsar A, Cicek D, Akkuş MN, Parmaksız T, et al. Diffuse intimal thickening of coronary arteries in slow coronary flow. Jpn Heart J 2003;44, 907–919.
  • 28. Yıldız A, Gur M, Yılmaz R, Demirbag R, Polat M, Selek S, et al. Association of paraoxonase activity and coronary blood flow. Atherosclerosis 2008; 197, 257–263.
  • 29. Enli Y, Turk M, Akbay R, Evrengul H, Tanrıverdi H, Kuru O,et al. Oxidative stress parameters in patients with slow coronary flow. Adv Ther 2008; 25, 37–44.
  • 30. Kopetz V, Kennedy J, Heresztyn T, Stafford I, Willoughby SR, Beltrame JF. Endothelial function, oxidative stress and inflammatory studies in chronic coronary slow flow phenomenon patients. Cardiology 2012; 121, 197–203.
  • 31. Zengin H, Erbay AR, Okuyucu A, Alaçam H, Yüksel S, Meriç M, et al. The relationship between coronary slow flow phenomenon and urotensin-II: A prospective and controlled study. Anatol J Cardiol. 2015 Jun;15(6):475-9. doi: 10.5152/akd.2014.5481.
  • 32. Balment RJ, Song W, Ashton N. Urotensin II: ancient hormone with new functions in vertebrate body fluid regulation. Ann NY Acad Sci 2005;1040:66–73.33. Iglewski M, Grant SR. Urotensin II-induced signaling involved in proliferation of vascular smooth muscle cells. Vasc Health Risk Manag 2010; 6, 723–734.
  • 34. Song N, Ding W, Chu S, Zhao J, Dong X, Di B, et al. Urotensin II stimulates vascular endothelial growth factor secretion from adventitial fibroblasts in synergy with angiotensin II. Circ J 2012; 76, 1267–1273.
  • 35. Goldenberg I, Matetzky S. Nephropathy induced by contrast media: pathogenesis, risk factors and preventive strategies. Can Med Assoc J 2005;172: 1461–71.
  • 36. Marenzi G, De Metrio M, Rubino M, Lauri G, Cavallero A, Assanelli E, et al. Acute hyperglycemia and contrast-induced nephropathy in primary percutaneous coronary intervention. Am Heart J. 2010 Dec;160(6):1170-7. doi: 10.1016/j.ahj.2010.09.022.
  • 37. Cowburn PJ, Patel H, Pipes RR, Parker JD. Contrast nephropathy post cardiac resynchronization therapy: an under-recognized complication with important morbidity. Eur J Heart Fail. 2005 Aug;7(5):899-903.
  • 38. Shacham Y, Steinvil A, Arbel Y. Acute kidney injury among ST elevation myocardial infarction patients treated by primary percutaneous coronary intervention: a multifactorial entity. J Nephrol. 2016;29(2):169-74.
  • 39. Maioli M, Toso A, Leoncini M, Gallopin M, Musilli N, Bellandi F. Persistent renal damage after contrast-induced acute kidney injury incidence, evolution, risk factors, and prognosis. Circulation. 2012;125(25):3099-107.
  • 40. Kumar S, Nair RK, Aggarwal N, Abbot AK, Muthukrishnan J, Kumar KV. Risk factors for contrast-induced nephropathy after coronary angiography. Saudi J Kidney Dis Transpl. 2017;28(2): 318-24.
  • 41. Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention. J Am Coll Cardiol. 2004;44(7):1393-99.
  • 42. Sun XP, Li J, Zhu WW, Li DB, Chen H, Li HW et al. Platelet to Lymphocyte Ratio Predicts Contrast-Induced Nephropathy in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention. Angiology. 2018 Jan;69(1):71-78.
  • 43. Kocas C, Yildiz A, Abaci O, Karaca OS, Firdin N, Dalgic Y, et al. Platelet-to-Lymphocyte Ratio Predicts Contrast-Induced Nephropathy in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome. Angiology. 2015 Nov;66(10):964-8.
  • 44. Ulus T, Isgandarov K, Yilmaz AS, Uysal S, Vasi I, Dural M, et al. Monocyte to High-Density Lipoprotein Ratio Predicts Contrast-Induced Nephropathy in Patients With Acute Coronary Syndrome. Angiology. 2018 Nov;69(10):909-916.
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Details

Primary Language English
Subjects Health Care Administration
Journal Section Articles
Authors

Mustafa Huyut 0000-0001-8740-1429

Project Number 5.2016/17
Publication Date September 16, 2019
Submission Date July 25, 2019
Published in Issue Year 2019

Cite

AMA Huyut M. The Relationship Between Serum Urotensin II Level and Contrast-Induced Nephropathy and One-year Clinical Follow-up Findings in Patients with Coronary Slow Phenomenon Undergoing Percutaneous Coronary Intervention. Sakarya Tıp Dergisi. September 2019;9(3):442-454. doi:10.31832/smj.596933

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