The relationship Between Multivessel Disease and Monocyte/HDL-C Ratio In Patients Presenting with Acute Coronary Syndrome

Abstract

Background: Acute coronary syndromes are among the most common causes of death worldwide. Inflammation has an important place in the etiology and pathogenesis of ACS (acute coronary syndrome). To date, many diffe-rent parameters have been used to assess inflammation. Monocyte HDL ratio (MHR) is a new marker of inflamma-tion that has come into use in recent years. The aim of our study is to determine the clinical significance of MHR in patients presenting with ACS.
Materials and Methods: In this retrospective study, 195 patients who applied to our clinic with the diagnosis of acute coronary syndrome and underwent coronary angiography were included. Routine hematological and biochemical parameters of all patients were analyzed retrospectively. MHR was obtained by dividing the number of monocytes by HDL cholesterol. The patients were divided into 3 groups according to their MHR tertiles. All 3 groups were compared for angiographic features and MHR.
Results: There was no significant difference between the 3 groups in terms of baseline demographic characteris-tics. However, it was determined that the frequency of 3-vessel disease increased gradually as MHR increased. (12%, 33%, 52%, respectively, p<0.001). In the correlation analysis, age (r= 0.326 , p<0.001) and MHR (r=0.347 , p<0.001) were positively correlated with the number of vessels with critical stenosis. In the multivariate logistic regression analysis, age (hazard ratio: 1.052; 95% confidence interval: 1.020 - 1.085; p = 0.001), MHR (hazard ratio: 1.075, 95% confidence interval: 1.192 - 5.087; p <0.001) and diabetes mellitus (hazard ratio: 2.462 ; 95% confidence interval: 1.192 – 5.087; p = 0.015 ) were identified as independent predictors of multivessel disease. Taking the MHR cut-off value ≥ 19.1 predicted multivessel disease in patients with acute coronary syndrome, with a sensitivity of 71.9% and a specificity of 61.8%.
Conclusions: MHR is a new marker of inflammation. In our study, we found that MHR independently predicted multivessel disease in patients presenting with ACS.


Keywords: Monocyte/HDL ratio; Acute coronary syndrome; Inflammation; Multivessel disease

Akut Koroner Sendrom ile Gelen Hastalarda Çok Damar Hastalığı ile Monosit/HDL-C Oranı Arasındaki İlişki

Abstract

Amaç: Akut koroner sendromlar tüm dünyada ölümün en sık nedenleri arasındadır. İnflamasyon akut koroner sendrom (AKS) etyoloji ve patogenezinde önemli bir yere sahiptir. Bugüne kadar inflamasyonu değerlendirmek için bir çok farklı parametre kullanılmıştır. Monosit /HDL-C oranı (MHO) son yıllarda kullanıma giren yeni bir inflamasyon belirtecidir. Çalışmamızın amacı, AKS ile başvuran hastalarda MHO’nun klinik önemini saptamaktır. Materyal ve metod: Bu retrospektif çalışmaya, akut koroner sendrom tanısıyla kliniğimize başvurmuş ve koroner anjiyografi yapılmış 195 hasta dahil edildi. Tüm hastaların rutin hematolojik ve biyokimyasal parametreleri geriye dönük olarak incelendi. Monosit sayısının HDL kolesterole bölünmesi ile MHO elde edildi. Hastalar MHO tertillerine göre 3 gruba ayrıldı. Her 3 grup, anjiyografik özellikler ve MHO açısından karşılaştırıldı. Bulgular: Her 3 grup arasında bazal demografik karakteristikler açısından anlamlı bir farklılık saptanmadı. Ancak, MHO arttıkça 3 damar hastalığı sıklığının da giderek arttığı tespit edildi. (sırasıyla % 12, %33 , %52, P<0.001). Korelasyon analizinde yaş (r= 0.326 , p<0.001) ve MHO’nın (r=0.347 , p<0.001) kritik darlık bulunan damar sayısı ile pozitif şekilde korele olduğu tespit edildi. Yapılan çok değişkenli lojistik regresyon analizinde yaş (risk oranı: 1.052; %95 güven aralığı: 1.020 - 1.085; P =0.001), MHO (risk oranı:1.075, %95 güven aralığı: 1.192 – 5.087; P <0.001) ve Diyabetes mellitus (risk oranı:2.462 ; %95 güven aralığı : 1.192 – 5.087; P =0.015 ) 3 damar hastalığının bağımsız prediktörleri olarak tespit edildi. MHO sınır değerinin ≥ 19.1 alınması, % 71.9 duyarlılık ve % 61.8 özgüllük ile akut koroner sendromlu hastalarda çok damar hastalığını öngördü. Sonuç: MHO yeni bir inflamasyon belirtecidir. Çalışmamızda MHO’nun AKS ile başvuran hastalarda çok damar hastalığını bağımsız bir şekilde öngördüğünü tespit ettik. Anahtar kelimeler: Monosit/HDL oranı ; Akut koroner sendrom; İnflamasyon ; Çok damar hastalığı

Keywords

• monosit/HDL-C oranı
• Akut koroner sendrom
• İnflamasyon
• Çok damar hastalığı

References

1. 1. Makki N, Brennan TM, Girotra S. Acute coronary syndrome. J Intensive Care Med. 2015 ;30(4):186-200
2. 2. Grech ED, Ramsdale DR. Acute coronary syndrome: unstable angina and non-ST segment elevation myocardial infarction. BMJ. 2003 ;326(7401):1259-61.
3. 3. Wachira JK, Stys TP. Cardiovascular disease and bridging the diagnostic gap. S D Med. 2013 ;66(9):366-9.
4. 4. Mehta SR, Bossard M. Acute Coronary Syndromes and Multivessel Disease: Completing the Evidence. JACC Cardiovasc Interv. 2020 ;13(13):1568-1570.
5. 5. Sager HB, Nahrendorf M. Inflammation: a trigger for acute coronary syndrome. Q J Nucl Med Mol Imaging. 2016 ;60:185-93.
6. 6. Fiechter M, Ghadri JR, Jaguszewski M, Siddique A, Vogt S, Haller RB, et al. Impact of inflammation on adverse cardiovascular events in patients with acute coronary syndromes. J Cardiovasc Med (Hagerstown). 2013 ;14(11):807-14.
7. 7. Ancuta P, Wang J, Gabuzda D. CD16+ monocytes produce IL-6, CCL2,and matrix metalloproteinase-9 upon interaction with CX3CL1-expressing endothelial cells. J Leukoc Biol 2006;80:1156–6
8. 8. Nozawa N, Hibi K, Endo M, Sugano T, Ebina T, Kosuge M, et al. Association between circulating monocytes and coronary plaque progression in patients with acute myocardial infarction. Circ J. 2010 ;74(7):1384-91.

9. 9. Afiune Neto A, Mansur Ade P, Avakian SD, Gomes EP, Ramires JA. Monocitose é um marcador de risco independente para a doença arterial coronariana [Monocytosis is an independent risk marker for coronary artery disease]. Arq Bras Cardiol. 2006 ;86(3):240-4.
10. 10. Kuvin JT, Rämet ME, Patel AR, Pandian NG, Mendelsohn ME, Karas RH. A novel mechanism for the beneficial vascular effects of high-density lipoprotein cholesterol: enhanced vasorelaxation and increased endothelial nitric oxide synthase expression. Am Heart J. 2002 ;144(1):165-72.
11. 11. Kundi H, Gok M, Kiziltunc E, Cetin M, Cicekcioglu H, Cetin ZG, et al. Relation Between Monocyte to High-Density Lipoprotein Cholesterol Ratio With Presence and Severity of Isolated Coronary Artery Ectasia. Am J Cardiol. 2015 1;116(11):1685-9.
12. 12. Oylumlu M, Oylumlu M, Arik B, Demir M, Ozbek M, Arslan B, et al. Monocyte to high-density lipoprotein cholesterol and lymphocyte to monocyte ratios are predictors of in-hospital and long-term mortality in patients with acute coronary syndrome. Int J Clin Pract. 2021 ;75(5):e13973.
13. 13. Wu TT, Zheng YY, Chen Y, Yu ZX, Ma YT, Xie X. Monocyte to high-density lipoprotein cholesterol ratio as long-term prognostic marker in patients with coronary artery disease undergoing percutaneous coronary intervention. Lipids Health Dis. 2019 22;18(1):180.
14. 14. Cetin EH, Cetin MS, Canpolat U, Aydin S, Topaloglu S, Aras D, et al. Monocyte/HDL-cholesterol ratio predicts the definite stent thrombosis after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Biomark Med. 2015;9(10):967-77.
15. 15. Uno K, Nicholls SJ. Biomarkers of inflammation and oxidative stress in atherosclerosis. Biomark Med. 2010 ;4(3):361-73.
16. 16. Libby P, Ridker PM, Hansson GK. Progress and challenges in translating the biology of atherosclerosis. Nature. 2011 ;473(7347):317-25.
17. 17. Tabas I, García-Cardeña G, Owens GK. Recent insights into the cellular biology of atherosclerosis. J Cell Biol. 2015 ;209(1):13-22.
18. 18. Johnsen SH, Fosse E, Joakimsen O, Mathiesen EB, Stensland-Bugge E, Njølstad I, et al. Monocyte count is a predictor of novel plaque formation: a 7-year follow-up study of 2610 persons without carotid plaque at baseline the Tromsø Study. Stroke. 2005 ;36(4):715-9.
19. 19. Kuvin JT, Rämet ME, Patel AR, Pandian NG, Mendelsohn ME, Karas RH. A novel mechanism for the beneficial vascular effects of high-density lipoprotein cholesterol: enhanced vasorelaxation and increased endothelial nitric oxide synthase expression. Am Heart J. 2002 ;144(1):165-72.
20. 20. Cooper HA, Exner DV, Waclawiw MA, Domanski MJ. White blood cell count and mortality in patients with ischemic and nonischemic left ventricular systolic dysfunction (an analysis of the Studies Of Left Ventricular Dysfunction [SOLVD]). Am J Cardiol. 1999 ;84(3):252-7.
21. 21. Horne BD, Anderson JL, John JM, Weaver A, Bair TL, Jensen KR, Renlund DG, Muhlestein JB; Intermountain Heart Collaborative Study Group. Which white blood cell subtypes predict increased cardiovascular risk? J Am Coll Cardiol. 2005 ;45(10):1638-43.
22. 22. Açıkgöz SK, Açıkgöz E, Şensoy B, Topal S, Aydoğdu S. Monocyte to high-density lipoprotein cholesterol ratio is predictive of in-hospital and five-year mortality in ST-segment elevation myocardial infarction. Cardiol J. 2016;23(5):505-512.
23. 23. Cetin EH, Cetin MS, Canpolat U, Aydin S, Topaloglu S, Aras D, Aydogdu S. Monocyte/HDL-cholesterol ratio predicts the definite stent thrombosis after primary percutaneous coronary intervention for ST-segment elevation myocardial infarction. Biomark Med. 2015;9(10):967-77.
24. 24. Akboga MK, Balci KG, Maden O, Ertem AG, Kirbas O, Yayla C, et al. Usefulness of monocyte to HDL-cholesterol ratio to predict high SYNTAX score in patients with stable coronary artery disease. Biomark Med. 2016;10(4):375-83.
25. 25. Tok D, Turak O, Yayla Ç, Ozcan F, Tok D, Çağlı K. Monocyte to HDL ratio in prediction of BMS restenosis in subjects with stable and unstable angina pectoris. Biomark Med. 2016 ;10(8):853-60.
26. 26. Yilmaz S, Akboga MK, Sen F, Balcı KG, Aras D, Temizhan A, et al. Usefulness of the monocyte-to-high-density lipoprotein cholesterol ratio to predict bare metal stent restenosis. Biomark Med. 2016 ;10(9):959-66.
27. 27. Ucar FM. A potential marker of bare metal stent restenosis: monocyte count - to- HDL cholesterol ratio. BMC Cardiovasc Disord. 2016 ;16(1):186.
28. 28. Balta S, Celik T, Ozturk C, Kaya MG, Aparci M, Yildirim AO, et al. The relation between monocyte to HDL ratio and no-reflow phenomenon in the patients with acute ST-segment elevation myocardial infarction. Am J Emerg Med. 2016 ;34(8):1542-7.
29. 29. Zhang Y, Li S, Guo YL, Wu NQ, Zhu CG, Gao Y, et al. Is monocyte to HDL ratio superior to monocyte count in predicting the cardiovascular outcomes: evidence from a large cohort of Chinese patients undergoing coronary angiography. Ann Med. 2016 ;48(5):305-12.
30. 30. Balta S, Celik T, Ozturk C, Kaya MG, Aparci M, Yildirim AO, et al. The relation between monocyte to HDL ratio and no-reflow phenomenon in the patients with acute ST-segment elevation myocardial infarction. Am J Emerg Med. 2016 ;34(8):1542-7.
31. 31. Farooq V, van Klaveren D, Steyerberg EW, Meliga E, Vergouwe Y, Chieffo A, et al. Anatomical and clinical characteristics to guide decision making between coronary artery bypass surgery and percutaneous coronary intervention for individual patients: development and validation of SYNTAX score II. Lancet. 2013 ;381(9867):639-50.
32. 32. Brunetti ND. 'Hot stuff': inflammatory lymphocyte populations in acute coronary syndrome. Cell Mol Immunol. 2015 ;12:513-4.
33. 33. Hansson GK. Inflammation, atherosclerosis, and coronary artery disease. N Engl J Med. 2005;352:1685-1695.
34. 34. Burgess S, Juergens CP, Yang W, Shugman IM, Idris H, Nguyen T, et al. Cardiac mortality, diabetes mellitus, and multivessel disease in ST elevation myocardial infarction. Int J Cardiol. 2021 ;323:13-18.
35. 35. Combadière C, Potteaux S, Rodero M, Simon T, Pezard A, Esposito B, et al. Combined inhibition of CCL2, CX-3CR1,and CCR5 abrogates Ly6C(hi) and Ly6C(lo) monocytosis and almost abolishes atherosclerosis in hypercholesterolemic mice. Circulation. 2008; 117:1649–57.
36. 36. Ghattas A, Griffiths HR, Devitt A, Lip GY, Shantsila E. Monocytes in coronaryartery disease and atherosclerosis: where are we now? J Am Coll Cardiol.2013;62(17):1541–51.
37. 37. Westerterp M, Gourion-Arsiquaud S, Murphy AJ, Shih A, Cremers S, LevineRL, et al. Regulation of hematopoietic stem and pro genitor cell mobilization by cholesterol efflux pathways. Cell Stem Cell.2012;11(2):195–206.
38. 38. Ansell BJ, Navab M, Hama S, Kamranpour N, Fonarow G, Hough G, et al. Inflammatory/antiinflammatory properties of high-density lipoprotein distinguish patients from control subjects better than high-density lipoprotein cholesterol levels and are favorably affected by simvastatin treatment. Circulation. 2003 2;108(22):2751-6.
39. 39. Yvan-Charvet L, Pagler T, Gautier EL, Avagyan S, Siry RL, Han S, et al. Tall AR.ATP-binding cassette transporters and HDL suppress hematopoietic stem cell proliferation. Science. 2010;328(5986):1689–93.
40. 40. Kuvin JT, Rämet ME, Patel AR, Pandian NG, Mendelsohn ME, Karas RH. Anovel mechanism for the beneficial vascular effects of high-densitylipoprotein cholesterol: enhanced vasorelaxation and increased endothelialnitric oxide synthase expression. Am Heart J. 2002;144(1):165–72.