CORRELATION OF LIPOPROTEIN(a) AND CORONARY ARTERY DISEASES

Authors

  • Gazmend Zylbeari Faculty of Medical Sciences, University of Tetovo. Tetovo. North Macedonia.
  • Zamira Bexheti South East European University. Tetovo. North Macedonia.
  • Elita Zylbeari-Masha Clinical Hospital, Tetovo, North Macedonia.
  • Art Zylbeari Clinical Hospital, Tetovo, North Macedonia.
  • Lutfi Zylbeari Faculty of Medical Sciences, University of Tetovo. Tetovo. North Macedonia. http://orcid.org/0009-0001-3668-1413

DOI:

https://doi.org/10.58885/ijllis.v12i3.44.gz

Abstract

INTRODUCTION: Cardiovascular diseases (CVD) continue to be one of the leading causes of mortality worldwide. While factors such as diabetes, sedentariness, psychostress, genetic predisposition, hypertension, smoking, and hyperlipidemia are well-known in the etiology of atherosclerosis (Ath) of coronary arteries. Recent studies have also identified high concentrations of lipoproteins (a) [Lp(a)] as a risk factor. In fact, high concentrations of Lp(a) above 30mg/dl (reference value-30mg/dl) have been found to be a risk factor for Ath, leading experts to develop medications aimed at reducing Lp(a) concentrations and preventing atherosclerotic manifestations. The European Atherosclerosis Society has also released clinical guidelines for testing and treating high concentrations of Lp(a) as part of the global assessment of cardiovascular risk.

THE GOAL OF THE STUDY: The goal of this study is to investigate the concentration of Lp(a) in patients with coronary disease and its connection to the presentation of atherosclerosis of the coronary arteries in patients with CVD compared to a control group of healthy individuals. Through this study, we hope to gain a better understanding of the role of Lp(a) in CVD and its potential as a target for prevention and treatment. By identifying and addressing risk factors like high Lp(a) concentrations, we can work towards reducing the global burden of CVD and improving health outcomes for individuals around the world.

THE AIM OF THE STUDY: The aim of this study is to determine the concentration of lipoprotein(a) in patients with coronary disease, its connectivity and role in the presentation of atherosclerosis of the coronary arteries in patients with CVD compared to the control group of healthy individuals.

MATERIAL AND METHODS: As working material, the blood taken from the vein of patients with coronary disease was used - N0=80, (with an identical average age of 55.70±6.00 years old, of which 35 were female while 45 were male. In the study, there was also a control group: N0=80 healthy volunteers (45 were male and 35 female) with the same age as the patients. Blood for analysis was taken at 8 o'clock in the morning, at room temperature of 19-24°C, every three months in a period of 12 months.

Echocardiography and EKG were also performed on all the patients with Toshiba SSH-140A machine, color Doppler probe 3.7Hz, sectorial type, taking into account as key parameters the thickness of the back wall of the left ventricle and the thickness of-Left ventricular internal diameter end diastole (LVPVd) and interventricular septal end diastole (IVSd>12 mm). Together with the examination of Lp(a) concentrations, the lipid profile was also analyzed. The analyzes were done at the Clinical Laboratory Institute at the University Clinical Center of the Faculty of Medicine – Skopje, North Macedonia.

STATISTICAL PROCESSING OF THE MATERIAL: From the statistical methods, arithmetic mean value, standard deviation X±SD were used. The comparative statistics of the lipid parameters between the analyzed groups were analyzed with students ‘t’ dependent and independent samples according to the Mann-Whitney U-test and Wilcoxon - test. The results of the lipid fractions will be shown tabularly (see table 3) with the statistical program SPSS V26.

RESULTS: The obtained values of lipids (Col.Total, TG, HDL-ch, LDL-ch) and lipoprotein (a) in both groups are presented with mean values and standard deviation X-SD. Due to the fact that in the obtained results of Lp(a) in both sexes, in patients with coronary disease, we did not notice any significant difference, we will present them as common for both groups, with CVD with maximum values of 78.00-16,00 mg/dl while in the control group =15.20-4.30 mg/dl, with a statistically significant difference with p<0.000. The same difference was found from the obtained results of lipid concentrations between the two groups with p <0.0001 (as presented in the tables below).

CONCLUSION: The results obtained in the paper proved that high concentrations of Lp(a) > 30 mg/dl are risk factors for the occurrence of Ath of the coronary arteries and that these patients are at a 5-8 times higher risk for the development of Ath of coronary arteries, compared to individuals with normal Lp(a) values, therefore the treatment of high concentrations of Lp(a) should be started at the beginning of their appearance. In conclusion, we can suggest that the adequate treatment of high Lp(a) concentrations and the balancing of the lipid profile can apparently affect the prevention of atherosclerotic processes of the coronary arteries, therefore we prefer that in individuals with a history of CAD and those with coronary disease, the examination of Lp(a) and lipid profile should be one of the initial examinations during the management of patients with CAD.

Keywords: Lipoprotein (a), atherosclerosis, Cardiovascular Arterial Diseases (CAD), lipid profile.

References

Andrea Pasta, Anna Laura Cremonini, et al. PCSK9 inhibitors for treating hypercholesterolemia 2020 Feb; 21(3): 353-363. Expert opin Pharmacoter. 2020 Feb; 21(3): 353-363. https://doi.org/10.1080/14656566.2019.1702970

Berg K., Dahlen G., and Frick M. H. Lp(a) lipoprotein and pre-β1 lipoprotein in patients with coronary heart disease. Clin. Genet. 1974. 6: 230-235. https://doi.org/10.1111/j.1399-0004.1974.tb00657.x

Berg K. A new serum type system in man–the Lp system. Acta Pathol.Microbiol. Scand. (1963), 59: 369-382. https://doi.org/10.1111/j.1699-0463.1963.tb01808.x

Bouchareb R, Mahmut A, Nsaibia MJ et al. Autotaxin derived from lipoprotein(a) and valve interstitial cells promotes inflammation and mineralization of the aortic valve; Circulation, 2015; 132: 677–690. https://doi.org/10.1161/CIRCULATIONAHA.115.016757

Danesh J, Collins R, Peto R. Lipoprotein(a) and Coronary Heart Disease. Meta-Analysis Of Prospective Studies. Circulation. 2000; 102: 1082-1085. https://doi.org/10.1161/01.CIR.102.10.1082

Fless GM, ZumMallen ME, Scanu AM. Isolation of apolipoprotein(a) from lipoprotein(a). J Lipid Res, 1985; 26: 1224-1229. https://doi.org/10.1016/S0022-2275(20)34270-X

Florian Kronenberg, Samia Mora et al. Lipoprotein(a) in atherosclerotic cardiovascular disease and aortic stenosis: a European Atherosclerosis Society consensus statement. European Heart Journal, Volume 43, Issue 39, 14 October 2022, Pages 3925-3946. https://doi.org/10.1093/eurheartj/ehac361

Garg PK, Guan W, Karger AB. Lipoprotein (a) and risk for calcification of the coronary arteries, mitral valve, and thoracic aorta: the multi-ethnic study of atherosclerosis.J Cardiovasc Comput Tomogr. 2021; 15: 154–160. https://doi.org/10.1016/j.jcct.2020.06.002

Ginsberg HN, Stein EA. Effect of alirocumab, a monoclonal proprotein convertase subtilisin/kexin 9 antibody, on lipoprotein(a) concentrations (a pooled analysis of 150 mg every two weeks dosing from phase 2 trials). Am J Cardiol, 2014; 114: 711-715.

https://doi.org/10.1016/j.amjcard.2014.05.060

Jennie Olopaade, Pharm D, RPH. Pietrangelo PCSK9 Inhibitors: What September 1, 2021. [Crossref]

Kaiser Y, Daghem M, Tzolos E, et al. Association of Lipoprotein(a) With Atherosclerotic Plaque Progression. J Am Coll Cardiol. 2022 Jan, 79 (3) 223–233. https://doi.org/10.1016/j.jacc.2021.10.044

Kraft, H. G., Menzel, H. J., Hoppichler, F., Vogel, W., & Utermann, G. (1989). Changes of genetic apolipoprotein phenotypes caused by liver transplantation. Implications for apolipoprotein synthesis. The Journal of clinical investigation, 83(1), 137-142. https://doi.org/10.1172/JCI113849

Krempler, F., Kostner, G. M., Bolzano, K., & Sandhofer, F. (1980). Turnover of lipoprotein (a) in man. The Journal of clinical investigation, 65(6), 1483-1490. https://doi.org/10.1172/JCI109813.

Luc G, Bard JM, Arveiler D, et al. Lipoprotein (a) as a predictor of coronary heart disease: the PRIME Study. Atherosclerosis. 2002; 163: 377-384. https://doi.org/10.1016/S0021-9150(02)00026-6

Maranhão RC, Carvalho PO, Strunz CC, Pileggi F. Lipoprotein (a): structure, pathophysiology and clinical implications. Arq Bras Cardiol. 2014 Jul; 103(1): 76-84. https://doi.org/10.5935/abc.20140101

McLean J.W., Tomlinson J.E. et al. cDNA sequence of human apolipoprotein(a) is homologous to plasminogen. Nature. 1987. 330: 132-137. https://doi.org/10.1093/eurheartj/ehq386

M.Bihari Warga, G.Kostner, and A. Czinner. Lp(a) the risc of Coronarz Heart Disease.European Journal of Epidemiolgy 0392-2990, supl.1:1992, pp.33-35. https://doi.org/10.1007/BF00145347

Nordestgaard BG, Chapman MJ, Ray K, et al. European Atherosclerosis Society Consensus Panel. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J. 2010 Dec; 31(23): 2844-53. https://doi.org/10.1093/eurheartj/ehq386

Nordestgaard BG, Chapman MJ, Ray K et. Al. Lipoprotein(a) as a cardiovascular risk factor: current status. Eur Heart J, 2010, 31; 2844-2853. https://doi.org/10.1093/eurheartj/ehq386

Osnabrugge RLMylotte D, Head SJ et al. Aortic stenosis in the elderly: disease prevalence and number of candidates for transcatheter aortic valve replacement: a meta-analysis and modeling study. J Am Coll Cardiol, 201; 62: 1002–1012. https://doi.org/10.1016/j.jacc.2013.05.015

Rader DJ, Cain W, Zech LA, Usher D, Brewer HB., Jr Variation in lipoprotein(a) concentrations among individuals with the same apolipoprotein (a) isoform is determined by the rate of lipoprotein(a) production. J Clin Invest, 1993; 91: 443-447. https://doi.org/10.1172/JCI116221

Rader DJ, Cain W, Ikewaki K, et al. The inverse association of plasma lipoprotein(a) concentrations with apolipoprotein(a) isoform size is not due to differences in Lp(a) catabolism but to differences in production rate. J Clin Invest, 1994; 93: 2758-2763. https://doi.org/10.1172/JCI117292

Rader DJ, Mann WA, Cain W, et al. The low density lipoprotein receptor is not required for normal catabolism of Lp(a) in humans. J Clin Invest, 1995; 95: 1403-1408. https://doi.org/10.1172/JCI117794

Reyes-Soffer G, Pavlyha M, Ngai C, et al. Effects of PCSK9 Inhibition with Alirocumab on Lipoprotein Metabolism in Healthy Humans. Circulation, 2017; 135: 352-362. https://doi.org/10.1161/CIRCULATIONAHA.116.025253

Scipione CA, Koschinsky ML, Boffa MB. Lipoprotein(a) in clinical practice: New perspectives from basic and translational science. Crit Rev Clin Lab Sci. 2018 Jan; 55(1): 33-54. https://doi.org/10.1080/10408363.2017.1415866

Seman LJ, DeLuca C, Jenner JL, et al. Lipoprotein(a)-cholesterol and coronary heart disease in the Framingham Heart Study. Clin Chem. 1999; 45: 1039-1046. https://doi.org/10.1093/clinchem/45.7.1039

Tsimikas S, Stroes ESG. The dedicated “Lp(a)clinic”: A concept whose time has arrived? Atherosclerosis 2020; 300: 1-9. https://doi.org/10.1016/j.atherosclerosis.2020.03.003

Tsimikas S. Potential Causality and Emerging Medical Therapies for Lp(a) and Its Associated Oxidized Phospholipids in Calcific Aortic Valve Stenosis. Circ Res, 2019; 124: 405-415. https://doi.org/10.1161/CIRCRESAHA.118.313864

Van der Valk FM, Bekkering S, et al.Oxidized phospholipids on lipoprotein(a) elicit arterial wall inflammation and an inflammatory monocyteresponse in humans. Circulation 2016; 134: 611, 624. https://doi.org/10.1161/CIRCULATIONAHA.116.020838

von Eckardstein A, Schulte H, Cullen P, Assmann G. Lipoprotein(a) further increases the risk of coronary events in men with high global cardiovascular risk. J Am Coll Cardiol. 2001; 37: 434-439. https://doi.org/10.1016/s0735-1097(00)01126-8

Watts GF, Chan DC, Somaratne R, et al. Controlled study of the effect of proprotein convertase subtilisin-kexin type 9 inhibition with evolocumab on lipoprotein(a) particle kinetics. Eur Heart J, 2018; 39: 2577-2585. https://doi.org/10.1093/eurheartj/ehy122

Wilson DP, Jacobson TA, Jones PH, et al. Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association. J Clin Lipidol. 2019 May-Jun; 13(3): 374-392. https://doi.org/10.1016/j.jacl.2019.04.010

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Published

2023-05-05

How to Cite

Zylbeari, G., Bexheti, Z., Zylbeari-Masha, E., Zylbeari, A., & Zylbeari, L. (2023). CORRELATION OF LIPOPROTEIN(a) AND CORONARY ARTERY DISEASES. ANGLISTICUM. Journal of the Association-Institute for English Language and American Studies, 12(3), pp.44–52. https://doi.org/10.58885/ijllis.v12i3.44.gz

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Volume 12, Nr.3, March 2023