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Role of inflammation, autotaxin and lipoprotein (a) in degenerative aortic valve stenosis in patients with coronary artery disease

https://doi.org/10.15829/1728-8800-2021-2598

Abstract

Aim. To study the relationship between the concentration of lipoprotein (a) (Lp (a)) and autotaxin (ATX) in patients with and without degenerative aortic valve stenosis (AoS) in the presence of coronary artery disease (CAD).

Material and methods. The study included 461 patients (mean age, 66±11 years, men, 323), 354 of whom had CAD with stenosis ≥50% in at least one coronary artery according to angiography. Degenerative AoS was diagnosed with ultrasound. The control group consisted of 107 patients without CAD and degenerative AoS. Concentrations of Lp (a), ATX, lipids and blood cells were measured for all patients.

Results. CAD without degenerative AoS (group 1) was diagnosed in 307 patients, while 47 patients had CAD and degenerative AoS (group 2). Patients in both groups were older than patients in the control group (66±10, 74±8, and 61±13 years, respectively). The ATX level was lower in group 1 (median [25; 75%]: 495 [406; 583] ng/ml) than in the control group (545 [412; 654] ng/ml) or group 2 (545 [476; 605] ng/ml) (p<0,05 for all). Lp (a) was lower in the control group (14,5 [5,5; 36,0] mg/dl) than in group 1 (24,9 [9,7; 58,4] mg/dl) (p<0,005) and group 2 (23,8 [9,9; 75,7] mg/dL) (p<0,05). According to the logistic regression, an increased ATX level, regardless of age and other risk factors, was associated with degenerative AoS only in patients with CAD, while age and neutrophil to lymphocyte ratio were associated with the development of degenerative AoS both in patients with CAD and the general group.

Conclusion. An elevated Lp (a) level is associated with CAD regardless of the aortic valve involvement, while an increased concentration of ATX and neutrophil to lymphocyte ratio in patients with CAD were associated with degenerative AoS regardless of age and other risk factors.

About the Authors

A. L. Burdeynaya
National Medical Research Center of Cardiology
Russian Federation

Moscow



O. I. Afanasyeva
National Medical Research Center of Cardiology
Russian Federation

Moscow



E. A. Klesareva
National Medical Research Center of Cardiology
Russian Federation

Moscow



N. A. Tmoyan
National Medical Research Center of Cardiology
Russian Federation

Moscow



O. A. Razova
National Medical Research Center of Cardiology
Russian Federation

Moscow



M. I. Afanasyeva
National Medical Research Center of Cardiology
Russian Federation

Moscow



M. V. Ezhov
National Medical Research Center of Cardiology
Russian Federation

Moscow



S. N. Pokrovsky
National Medical Research Center of Cardiology
Russian Federation

Moscow



References

1. Go AS, Mozaffarian D, Roger VL, et al. Executive summary: heart disease and stroke statistics — 2013 update: a report from the American Heart Association. Circulation. 2013;127:143-52. doi:10.1161/CIR.0b013e31828124ad.

2. Khubulava GG, Gulyaev NI, Kravchuk VN, et al. Incidence of degenerative aortic stenosis in the patterns of valvular heart disease. Grudnaya i Serdechno-Sosudistaya Khirurgiya (Russian Journal of Thoracic and Cardiovascular Surgery). 2018;60(1):28-35. (In Russ.) doi:10.24022/0236-2791-2018-60-1-28-35.

3. Otto CM, Kuusisto J, Reichenbach DD, et al. Characterization of the early lesion of ‘degenerative’ valvular aortic stenosis: histologic and immunohistochemical studies. Circulation. 1994;90:844-53. doi:10.1161/01.cir.90.2.844.

4. Carita P, Coppola G, Novo G, et al. Aortic stenosis: insights on pathogenesis and clinical implications. J Geriatr Cardiol. 2016;13(6):489-98. doi:10.11909/j.issn.1671-5411.2016.06.001.

5. Capoulade R, Chan KL, Yeang C, et al. Oxidized Phospholipids, Lipoprotein(a), and Progression of Calcific Aortic Valve Stenosis. J Am Coll Cardiol. 2015;66(11):1236-46. doi: 10.1016/j.jacc.2015.07.020.

6. Teo KK, Corsi DJ, Tam JW, et al. Lipid lowering on progression of mild to moderate aortic stenosis: meta-analysis of the randomized placebo-controlled clinical trials on 2344 patients. Can J Cardiol. 2011;27(6):800-8. doi:10.1016/j.cjca.2011.03.012.

7. 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; 132:67790. doi: 10.1161/CIRCULATIONAHA.115.016757

8. Dahlen GH. Incidence of Lp(a) lipoprotein among populations in “Lipoprotein(a)” ed. Scanu A. M. Academic Press. San Diego. 1990. С.151-75. ISBN-13: 978-0126209907 ISBN-10: 0126209901.

9. Afanasieva OI, Adamova lYu, Benevolenskaya GF, Pokrovsky SN. An immunoenzyme method for determining lipoprotein(a). Bull Exp Biol Med. 1995; 120(10):398-401. (In Russ.) doi: 10.1007/bf02444976.

10. Ellis KL, Boffa MB, Sahebkar A, et al. The renaissance of lipoprotein(a): brave new world for preventive cardiology? Prog Lipid Res. 2017;68:57-82. doi:10.1016/j.plipres.201709.001.

11. Malarstig A, Green FR, Lathrop M, et al. Genetic variants associated with Lp(a) lipoprotein level and coronary disease. N Engl J Med. 2009;361:2518-28. doi:10.1056/NEJMoa0902604.

12. Borrelli MJ, Youssef F, Boffa MB, Koschinsky ML. New Frontiers in Lp(a)-Targeted Therapies. Trends Pharmacol Sci. 2019;40(3):212-25. doi:10.1016/j.tips.2019.01.004.

13. Thanassoulis G, Campbell CY, Owens DS. Genetic associations with valvular calcification and aortic stenosis. N Engl J Med. 2013;368:503-12. doi:10.1056/NEJMoa1109034.

14. Arsenault BJ, Boekholdt SM, Dube MP, et al. Lipoprotein(a) levels, genotype, and incident aortic valve stenosis: a prospective mendelian randomization study and replication in a case-control cohort. Circ Cardiovasc Genet. 2014;7:304-10. doi: 10.1161/CIRCGENETICS.113.000400.

15. Kamstrup PR, Tybj®rg-Hansen A, Nordestgaard BG. Elevated Lipoprotein(a) and Risk of Aortic Valve Stenosis in the General Population. J Am Coll Cardiol. 2014;63:470-7 doi: 10.1016/j.jacc.2013.09.038.

16. Nsaibia MJ, Mahmut А, Boulanger MC. Autotaxin interacts with lipoprotein(a) and oxidized phospholipids in predicting the risk of calcific aortic valve stenosis in patients with coronary artery disease. J Intern Med. 2016;280:509-17 doi: 10.1016/j.jacc.2019.01.070.

17. 17 Tanindi A, Erkan AF, Alhan A, Tore HF. Arterial stiffness and central arterial wave reflection are associated with serum uric acid, total bilirubin, and neutrophil-to-lymphocyte ratio in patients with coronary artery disease. Anatol J Cardiol. 2015;15:396-403. doi:10.5152/akd.2014.5447

18. Song J, Zheng Q, Ma X, et al. Predictive Roles of Neutrophil-to-Lymphocyte Ratio and C-Reactive Protein in Patients with Calcific Aortic Valve Disease. Int Heart J. 2019;60:345-51. doi:10.1536/ihj.18-196.

19. Sproston NR, Ashworth JJ. Role of C-Reactive Protein at Sites of Inflammation and Infection. Front Immunol. 2018;9:754. doi:10.3389/fimmu.2018.00754.

20. Afanasieva OI, Tmoyan NA, Klesareva EA, et al. The Relationship of the Concentration of Lipoprotein(a) and Markers of Inflammation With Multifocal Atherosclerosis in Women. Kardiologiia. 2019;59(10):39-48. (In Russ.) doi:10.18087/cardio.2019.10.n520.


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Burdeynaya A.L., Afanasyeva O.I., Klesareva E.A., Tmoyan N.A., Razova O.A., Afanasyeva M.I., Ezhov M.V., Pokrovsky S.N. Role of inflammation, autotaxin and lipoprotein (a) in degenerative aortic valve stenosis in patients with coronary artery disease. Cardiovascular Therapy and Prevention. 2021;20(2):2598. https://doi.org/10.15829/1728-8800-2021-2598

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ISSN 1728-8800 (Print)
ISSN 2619-0125 (Online)