The Risk Factors of Coronary Heart Disease and its Relationship with Endothelial Nitric Oxide Synthase

Authors

  • Eka Fithra Elfi Department of Cardiology and Vascular Medicine, Faculty of Medicine, Universitas Andalas, Padang, Indonesia
  • Eva Decroli Department of Internal Medicine, Faculty of Medicine, Universitas Andalas, Dr. M. Djamil General Hospital, Padang
  • Ellyza Nasrul Department of Clinical Pathology, Faculty of Medicine, Universitas Andalas, Padang, Indonesia
  • Yanwirasti Yanwirasti Department of Anatomy, Faculty of Medicine, Universitas Andalas, Padang, Indonesia
  • Eryati Darwin Department of Histology and Immunology, Faculty of Medicine, Andalas University, Padang, Indonesia

DOI:

https://doi.org/10.3889/oamjms.2021.6062

Keywords:

Coronary heart disease, Endothelial nitric oxide synthase, Risk factors

Abstract

BACKGROUND: Coronary heart disease (CHD) is the leading cause of death and start with injury to the endothelium of a coronary artery. The common feature of endothelial dysfunction is a decrease of nitric oxide (NO) bioavailability that regulated by endothelial NO synthase (eNOS) activity.

AIM: The aim of our study was to study the relationship between risk factors of CHD patients with the level of eNOS.

METHODS: Thirty-seven outpatients in cardiology department of the regional public hospital diagnosed as CHD were included in our study. Thirty healthy individuals were included as the control group. Risk factors of CHD were identified according to anamnesis and laboratory finding. eNOS was measured by ELISA methods.

RESULTS: Endothelial NOS levels were significantly higher in the CHD when compared to the controls (p < 0.05). The most dominant risk factor for CHD is overweight, and followed by dyslipidemia, smoking, hypertension, history of CHD, and diabetes mellitus. eNOS in CHD patients who had one risk factor was 37.598 ± 0.1541 ng/ml, two risk factors 42.154 ± 22.329 ng/ml, three risk factors 25.329 ± 6.083 ng/ml, four risk factors 22.483 ± 4.022 ng/ml, and five risk factors 15.994 ± 4.774 ng/ml. There were significant differences in the average eNOS levels based on the number of risk factors (p < 0.05), and a tendency that more risk factors in CHD patients, the lower the average level of eNOS.

CONCLUSION: In our study, eNOS levels showed highly significant relation with CHD and related to the number of risk factors those the CHD patients had.

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References

World Health Organization. Global health risks: mortality and burden of disease attributable to selected major risks. Geneva, Switzerland: World Health Organization; 2009.

World Health Organization. Cardiovascular diseases (CVDs). Geneva, Switzerland: World Health Organization; 2017.

Ferreira-González I. The epidemiology of coronary heart disease. Rev Esp Cardiol. 2014; 67:139–144. https://doi.org/10.1016/j.rec.2013.10.002 DOI: https://doi.org/10.1016/j.rec.2013.10.002

Siswanto. Basic Health Research 2018. Directorate of Non- Communicable Disease Prevention and Control, Research and Development Council. Ministry of Health of the Republic of Indonesia. 2019.

Ganz P, Hsue PY. Endothelial dysfunction in coronary heart disease is more than a systemic process. Eur Heart J. 2013; 34(27):2025–7. DOI: https://doi.org/10.1093/eurheartj/eht199

Gutiérrez E, Flammer AJ, Lerman LO, Elı́zaga J, Lerman A, Fernández-Avilés F. Endothelial dysfunction over the course of coronary artery disease. Eur Heart J. 2013; 34(41):3175–81. DOI: https://doi.org/10.1093/eurheartj/eht351

Widmer RJ, Lerman A. Endothelial dysfunction and cardiovascular disease. Glob Cardiol Sci Pract. 2014; 2014(3):291–308. DOI: https://doi.org/10.5339/gcsp.2014.43

Sayols-Baixeras S, Lluís-Ganella C, Lucas G, Elosua R. Pathogenesis of coronary artery disease: focus on genetic risk factors and identification of genetic variants. Appl Clin Genet. 2014; 7:15–32. DOI: https://doi.org/10.2147/TACG.S35301

Ambrose JA, Singh M. Pathophysiology of coronary artery disease leading to acute coronary syndromes. F1000Prime Rep. 2015; 7:08. DOI: https://doi.org/10.12703/P7-08

Bergheanu SC, Bodde MC, Jukema JW. Pathophysiology and treatment of atherosclerosis: Current view and future perspective on lipoprotein modification treatment. Neth Heart J. 2017; 25(4): 231–42. DOI: https://doi.org/10.1007/s12471-017-0959-2

Hajar R. Risk factors for coronary artery disease: historical perspectives. Heart Views. 2017; 18(3):109–14. DOI: https://doi.org/10.4103/HEARTVIEWS.HEARTVIEWS_106_17

Förstermann U, Sessa WC. Nitric oxide synthases: regulation and function. Eur Heart J. 2012; 33(7):829–37. DOI: https://doi.org/10.1093/eurheartj/ehr304

Heiss C, Rodriguez-Mateos A, Kelm M. Central role of eNOS in the maintenance of endothelial homeostasis. Antioxid Redox Signal. 2015; 22(14):1230–42. DOI: https://doi.org/10.1089/ars.2014.6158

Park KH, Park WJ. Endothelial dysfunction: clinical implications in cardiovascular disease and therapeutic approaches. J Korean Med Sci. 2015; 30(9):1213–25. DOI: https://doi.org/10.3346/jkms.2015.30.9.1213

Hadi AR, Cornelia S, Carr CS, Al Suwaidi J. Endothelial dysfunction: cardiovascular risk factors, therapy, and outcome. Vasc Health Risk Manag. 2005; 1(3):183–98.

Kwaifa IK, Bahari H, Yong YK, Md Noor S. Endothelial dysfunction in obesity-induced inflammation: molecular mechanisms and clinical implications. Biomolecules. 2020;10(2):291. DOI: https://doi.org/10.3390/biom10020291

Ali, H. Standard operating procedures for ELISA of Biomedical Laboratory of Medical Faculty Universitas Andalas, Padang Indonesia, 2019

Zhang Y. Cardiovascular Diseases in American Women. Nutr Metab Cardiovasc Dis. 2010; 20(6):386–393. DOI: https://doi.org/10.1016/j.numecd.2010.02.001

Förstermann U, Münzel T. Endothelial nitric oxide synthase in vascular disease. From Marvel to Menace. Circulation. 2006; 113:1708–14. DOI: https://doi.org/10.1161/CIRCULATIONAHA.105.602532

Maas AHEM, Appelman YEA. Gender differences in coronary heart disease. Neth Heart J. 2010; 18(12):598–602. DOI: https://doi.org/10.1007/s12471-010-0841-y

Smith AR, Visioli F, Frei B, and Hagen TM. Age-related changes in endothelial nitric oxide synthase phosphorylation and nitric oxide dependent vasodilation: evidence for a novel mechanism involving sphingomyelinase and ceramide-activated phosphatase. Aging Cell, 2006; 5:391–400. DOI: https://doi.org/10.1111/j.1474-9726.2006.00232.x

Fuster JJ, Ouchi N, Gokce N,1 and Walsh K. Obesity-induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease. Circ Res., 2016; 118(11):1786–1807. DOI: https://doi.org/10.1161/CIRCRESAHA.115.306885

Wagner L, Laczy B, Tamaskó M, Mazák M, Markó L, Molnár LA, et al. Cigarette smoke-induced alterations in endothelial nitric oxide synthase phosphorylation: role of protein kinase C. Endothelium. 2007; 14(4-5):245–55. DOI: https://doi.org/10.1080/10623320701606707

World Tobacco Free Day. Center for Data and Information, Ministry of Health of the Republic of Indonesia. Info Datin 2014.

Konukoglu D, Uzun H. Endothelial dysfunction and hypertension. Adv Exp Med Biol. 2016:1–31. DOI: https://doi.org/10.1007/5584_2016_90

Vinkhuyzen AA, Wray NR, Yang J, Goddard ME, Visscher PM. Estimation and partition of heritability in human populations using whole-genome analysis methods. Annu Rev Genet. 2013; 47:75–95. DOI: https://doi.org/10.1146/annurev-genet-111212-133258

Said MA, van de Vegte YJ, Zafar MM, van der Ende MY, Raja GK, Verweij N, van der PHarst. Contributions of interactions between lifestyle and genetics on coronary artery disease risk. Curr Cardiol Rep. 2019; 21(89):1–8. DOI: https://doi.org/10.1007/s11886-019-1177-x

Förstermann U, Xia N, Li H. Roles of vascular oxidative stress and nitric oxide in the pathogenesis of atherosclerosis. Circ Res. 2017; 120:713–35. DOI: https://doi.org/10.1161/CIRCRESAHA.116.309326

Pizzino G, Irrera N, Cucinotta M, Pallio G, Mannino F, Arcoraci V, et al. Oxidative stress: harms and benefits for human health. Oxid Med Cell Longev. 2017; 2017; 1–13. DOI: https://doi.org/10.1155/2017/8416763

Kawashima S and Yokoyama M. Dysfunction of endothelial nitric oxide synthase and atherosclerosis. Arterioscler Thromb Vasc Biol. 2004; 24(6):998–1005. DOI: https://doi.org/10.1161/01.ATV.0000125114.88079.96

Hong FF, Liang XY, Liu W, Sha LV, He SJ, Kuang HB, et al. lRoles of eNOS in atherosclerosis treatment. Inflamm Res. 2019; 68:429–441. https://doi.org/10.1007/s00011-019-01229-9 DOI: https://doi.org/10.1007/s00011-019-01229-9

Daiber A, Xia N, Steven S, Oelze M, Hanf A, Kröller-Schön S,1 Münzel, Li H. New therapeutic implications of endothelial nitric oxide synthase (eNOS) function/dysfunction in cardiovascular disease. Int J Mol Sci. 2019; 20(1):187. DOI: https://doi.org/10.3390/ijms20010187

Besedina A. NO-Synthase Activity in Patients with Coronary Heart Disease Associated with Hypertension of Different Age Groups. J Med Biochem., 2016; 35(1):43–49. DOI: https://doi.org/10.1515/jomb-2015-0008

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Published

2021-06-18

How to Cite

1.
Elfi EF, Decroli E, Nasrul E, Yanwirasti Y, Darwin E. The Risk Factors of Coronary Heart Disease and its Relationship with Endothelial Nitric Oxide Synthase. Open Access Maced J Med Sci [Internet]. 2021 Jun. 18 [cited 2024 Jul. 3];9(B):451-6. Available from: https://oamjms.eu/index.php/mjms/article/view/6062