Lp(a)、NLR、PLR与钙化性主动脉瓣疾病的研究进展
Research Progress of Lipoprotein (a), Neutrophil-Lymphocyte Ratio, Platelet-Lymphocyte Ratio and Calcified Aortic Valve Disease
摘要: 随着全球人口老龄化的日益加重，钙化性主动脉瓣疾病(CAVD)已成为一种常见的心血管疾病。目前尚无药物治疗或延缓疾病的进展，外科主动脉瓣置换术(AVR)是有效治疗手段。CAVD与动脉粥样硬化有着相似的病理生理过程，与脂质代谢异常、慢性炎症密切相关。既往研究证实，脂蛋白(a)、炎症反应在主动脉瓣钙化过程中起着关键作用。本文主要简述了脂蛋白(a)、NLR、PLR与CAVD的相关性及发病机制，为CAVD的预防和治疗提供新的参考依据。
Abstract: Calcified aortic valve disease (CAVD) has become a common cardiovascular disease with the in-creasing aging of the global population. There are currently no drugs to treat or slow the progres-sion of the disease, surgical aortic valve replacement (AVR) is an effective treatment. CAVD has a similar pathophysiological process with atherosclerosis, and is closely related to abnormal lipid metabolism and chronic inflammation. Previous studies have confirmed that lipoprotein (a) and in-flammatory response play key roles in the process of aortic valve calcification. In this paper, the correlation and pathogenesis of CAVD between lipoprotein (a), neutrophil-lymphocyte ratio, plate-let-lymphocyte ratio was briefly reviewed, providing a new reference for the prevention and treat-ment of CAVD.
文章引用：张萍, 张亚萍. Lp(a)、NLR、PLR与钙化性主动脉瓣疾病的研究进展[J]. 临床医学进展, 2022, 12(10): 9104-9110. https://doi.org/10.12677/ACM.2022.12101316

参考文献

[1] Furukawa, K. (2014) Recent Advances in Research on Human Aortic Valve Calcification. Journal of Pharmacological Sciences, 124, 129-137. [Google Scholar] [CrossRef] 
[2] Otto, C. and Prendergast, B. (2014) Aor-tic-Valve Stenosis—From Patients at Risk to Severe Valve Obstruction. The New England Journal of Medicine, 371, 744-756. [Google Scholar] [CrossRef] 
[3] Nishimura, R., Otto, C., Bonow, R., et al. (2017) 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients with Valvular Heart Dis-ease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation, 135, e1159-e1195. [Google Scholar] [CrossRef] 
[4] Yutzey, K., Demer, L., Body, S., et al. (2014) Calcific Aortic Valve Disease: A Consensus Summary from the Alliance of Investigators on Calcific Aortic Valve Disease. Arterioscle-rosis, Thrombosis, and Vascular Biology, 34, 2387-2393. [Google Scholar] [CrossRef] 
[5] Small, A., Kiss, D., Giri, J., et al. (2017) Biomarkers of Cal-cific Aortic Valve Disease. Arteriosclerosis, Thrombosis, and Vascular Biology, 37, 623-632. [Google Scholar] [CrossRef] 
[6] Erqou, S., Kaptoge, S., Perry, P., et al. (2009) Lipoprotein (a) Concentration and the Risk of Coronary Heart Disease, Stroke, and Nonvascular Mortality. JAMA, 302, 412-423. [Google Scholar] [CrossRef] [PubMed]
[7] Jang, A., Han, S., Sohn, I., et al. (2020) Lipoprotein (a) and Cardio-vascular Diseases-Revisited. Circulation Journal, 84, 867-874. [Google Scholar] [CrossRef] 
[8] Schmidt, K., Noureen, A., Kronenberg, F., et al. (2016) Structure, Function, and Genetics of Lipoprotein (a). Journal of Lipid Research, 57, 1339-1359. [Google Scholar] [CrossRef] 
[9] Arsenault, B., Boekholdt, S., Dubé, M., et al. (2014) Lipoprotein (a) Lev-els, Genotype, and Incident Aortic Valve Stenosis: A Prospective Mendelian Randomization Study and Replication in a Case-Control Cohort. Circulation. Cardiovascular Genetics, 7, 304-310. [Google Scholar] [CrossRef] 
[10] Stewart, B.F., Siscovick, D., Lind, B.K., et al. (1997) Clinical Factors Associated with Calcific Aortic Valve Disease fn1fn1This Study Was Supported in Part by Contracts NO1-HC85079 through HC-850086 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. Journal of the American College of Cardiology, 29, 630-634. [Google Scholar] [CrossRef] 
[11] Zheng, K., Arsenault, B., Kaiser, Y., et al. (2019) ApoB/ApoA-I Ratio and Lp(a) Associations with Aortic Valve Stenosis Incidence: Insights from the EPIC-Norfolk Prospective Population Study. Journal of the American Heart Association, 8, e013020. [Google Scholar] [CrossRef] 
[12] Kamstrup, P., Hung, M., Witztum, J., et al. (2017) Oxidized Phospholipids and Risk of Calcific Aortic Valve Disease: The Copenhagen General Population Study. Arteriosclerosis, Thrombosis, and Vascular Biology, 37, 1570-1578. [Google Scholar] [CrossRef] 
[13] 刘硕霖. 脂蛋白(a)与主动脉瓣钙化的相关性研究[D]: [硕士学位论文]. 北京: 北京协和医学院, 2020.
[14] Losi, M., Brevetti, G., Schiano, V., et al. (2010) Aortic Valve Sclerosis in Patients with Peripheral and/or Coronary Arterial Disease. Echocardiography, 27, 608-612. [Google Scholar] [CrossRef] [PubMed]
[15] Szolc, P., Niewiara, Ł., Kawulak, M., et al. (2020) Neu-trophil-Lymphocyte Ratio and Platelet-Lymphocyte Ratio as Predictors of Coronary Microcirculatory Disease Occurrence and Outcome in Patients with Chronic Coronary Syndrome and No Significant Coronary Artery Stenosis. Wiadomosci lekarskie (Warsaw, Poland: 1960), 73, 2598-2606. [Google Scholar] [CrossRef] 
[16] Avci, A., Elnur, A., Göksel, A., et al. (2014) The Relationship be-tween Neutrophil/Lymphocyte Ratio and Calcific Aortic Stenosis. Echocardiography, 31, 1031-1035. [Google Scholar] [CrossRef] [PubMed]
[17] Küçükseymen, S., Çağırcı, G., Güven, R., et al. (2017) Is Neutrophyl to Lymphocyte Ratio Really a Useful Marker for All Grades of Degenerative Aortic Stenosis? Türk Kardiyoloji Derneği Arşivi, 45, 506-513. [Google Scholar] [CrossRef] [PubMed]
[18] Akdag, S., Akyol, A., Asker, M., et al. (2015) Plate-let-to-Lymphocyte Ratio May Predict the Severity of Calcific Aortic Stenosis. Medical Science Monitor: International Medical Journal of Experimental and Clinical Research, 21, 3395-3400. [Google Scholar] [CrossRef] 
[19] Yayla, Ç., Açikgöz, S., Yayla, K., et al. (2016) The Association be-tween Platelet-to-Lymphocyte Ratio and Inflammatory Markers with the Severity of Aortic Stenosis. Biomarkers in Medicine, 10, 367-373. [Google Scholar] [CrossRef] [PubMed]
[20] Edem, E., Reyhanoğlu, H., Küçükukur, M., et al. (2016) Predictive Value of Platelet-to-Lymphocyte Ratio in Severe Degenerative Aortic Valve Stenosis. Journal of Research in Medical Sciences: The Official Journal of Isfahan University of Medical Sciences, 21, 93. [Google Scholar] [CrossRef] [PubMed]
[21] Bian, W., Wang, Z., Sun, C., et al. (2021) Pathogenesis and Mo-lecular Immune Mechanism of Calcified Aortic Valve Disease. Frontiers in Cardiovascular Medicine, 8, Article ID: 765419. [Google Scholar] [CrossRef] [PubMed]
[22] Pasipoularides, A. (2016) Calcific Aortic Valve Disease: Part 1—Molecular Pathogenetic Aspects, Hemodynamics, and Adaptive Feedbacks. Journal of Cardiovascular Transla-tional Research, 9, 102-118. [Google Scholar] [CrossRef] [PubMed]
[23] Izquierdo-Gómez, M., Hernández-Betancor, I., García-Niebla, J., et al. (2017) Valve Calcification in Aortic Stenosis: Etiology and Diagnostic Imaging Techniques. BioMed Research In-ternational, 2017, Article ID: 5178631. [Google Scholar] [CrossRef] [PubMed]
[24] Erhart, G., Lamina, C., Lehtimäki, T., et al. (2018) Genetic Factors Ex-plain a Major Fraction of the 50% Lower Lipoprotein(a) Concentrations in Finns. Arteriosclerosis, Thrombosis, and Vascular Biology, 38, 1230-1241. [Google Scholar] [CrossRef] 
[25] Mahmut, A., Boulanger, M., El Husseini, D., et al. (2014) Elevated Expression of Lipoprotein-Associated Phospholipase A2 in Calcific Aortic Valve Disease: Implications for Valve Mineralization. Journal of the American College of Cardiology, 63, 460-469. [Google Scholar] [CrossRef] [PubMed]
[26] Sun, W., Li, H., Yu, Y., et al. (2009) MEKK3 Is Required for Lysophosphatidic Acid-Induced NF-κB Activation. Cellular Signalling, 21, 1488-1494. [Google Scholar] [CrossRef] [PubMed]
[27] Bouchareb, R., Mahmut, A., Nsaibia, M., et al. (2015) Autotaxin Derived from Lipoprotein (a) and Valve Interstitial Cells Promotes Inflammation and Mineralization of the Aortic Valve. Circulation, 13, 677-690. [Google Scholar] [CrossRef] 
[28] Libby, P. and Ridker, P. (2004) Inflammation and Atherosclerosis: Role of C-Reactive Protein in Risk Assessment. The American Journal of Medicine, 116, 9S-16S. [Google Scholar] [CrossRef] [PubMed]
[29] Miller, J., Weiss, R. and Heistad, D. (2011) Calcific Aortic Valve Stenosis: Methods, Models, and Mechanisms. Circulation Research, 108, 1392-1412. [Google Scholar] [CrossRef] 
[30] Bogdanova, M., Kostina, A., Zihlavnikova Enayati, K., et al. (2018) Inflammation and Mechanical Stress Stimulate Osteogenic Differentiation of Human Aortic Valve Interstitial Cells. Frontiers in Physiology, 9, Article No. 1635. [Google Scholar] [CrossRef] [PubMed]
[31] Açar, G., Kalkan, M., Avci, A., et al. (2015) The Relation of Plate-let-Lymphocyte Ratio and Coronary Collateral Circulation in Patients with Stable Angina Pectoris and Chronic Total Oc-clusion. Clinical and Applied Thrombosis/Hemostasis: Official Journal of the International Academy of Clinical and Ap-plied Thrombosis/Hemostasis, 21, 462-468. [Google Scholar] [CrossRef] [PubMed]
[32] Langer, H., Weber, C., Gawaz, M., et al. (2013) The Platelet—Thrombosis and Beyond. Thrombosis and Haemostasis, 110, 857-858. [Google Scholar] [CrossRef] 
[33] Smyth, S., Mcever, R., Weyrich, A., et al. (2009) Platelet Functions beyond Hemostasis. Journal of Thrombosis and Haemostasis: JTH, 7, 1759-1766. [Google Scholar] [CrossRef] [PubMed]
[34] Blackshear, J., Wysokinska, E., Safford, R., et al. (2013) Indexes of von Willebrand Factor as Biomarkers of Aortic Stenosis Severity (from the Biomarkers of Aortic Stenosis Severity [BASS] Study). The American Journal of Cardiology, 111, 374-381. [Google Scholar] [CrossRef] [PubMed]
[35] Page, C. and Pitchford, S. (2013) Neutrophil and Platelet Com-plexes and Their Relevance to Neutrophil Recruitment and Activation. International Immunopharmacology, 17, 1176-1184. [Google Scholar] [CrossRef] [PubMed]
[36] Rossebø, A., Pedersen, T., Boman, K., et al. (2008) Intensive Lipid Lowering with Simvastatin and Ezetimibe in Aortic Stenosis. The New England Journal of Medicine, 359, 1343-1356. [Google Scholar] [CrossRef] 
[37] Chan, K., Teo, K., Dumesnil, J., et al. (2010) Effect of Lipid Lowering with Rosuvastatin on Progression of Aortic Stenosis: Results of the Aortic Stenosis Progression Obser-vation: Measuring Effects of Rosuvastatin (Astronomer) Trial. Circulation, 121, 306-314. [Google Scholar] [CrossRef] 

为你推荐