The role of polymorphisms in genes that regulate neurohumoral systems in patients with atrial fibrillation
DOI:
https://doi.org/10.14739/2310-1210.2019.3.169201Keywords:
genetic polymorphism, atrial fibrillation, renin-angiotensin-aldosterone system, catecholamines, NO synthaseAbstract
One of the important medical and social present-day problems is atrial fibrillation (AF) which prevalence in the adult population is 2 % for persons under 65 and 9 % for those over 65 years of age and it is a common cause of ischemic stroke. The embolic complications incidence is 2.1 % per year in patients with paroxysmal AF, and 3.0 % per year in patients with persistent AF.
The aim of the study is to analyze the modern literary sources related to the role of gene polymorphisms regulating some neurohumoral systems in group of patients with atrial fibrillation.
A combination of certain genes polymorphisms can contribute to AF risk. Especially important are gene studies of the renin-angiotensin-aldosterone system (RAAS) role in the pathogenesis of AF which are currently being studied with a particular intensity. Recent data show that activation of RAAS plays an important role in the development and recurrence of AF. These studies are of great practical interest as the associative effect of angiotensin converting enzyme (ACE) inhibitors in the prevention of AF has been identified.
AGT gene encodes a plasma protein known as angiotensinogen. This protein is expressed in the liver and is cleaved by the enzymatic renin action in response to lower blood pressure. The resulting product, angiotensin I, is then cleaved by ACE to the physiologically active enzyme angiotensin II. Defects in this gene may also be associated with non-hereditary AF. More than 16 spot mutations in the AGT gene were discovered, most of which resulted in amino acid substitutions.
Conclusions. The analysis of the literature allows to conclude that, first, genetic polymorphisms may influence both the severity of pathological changes in the body and the efficacy of pharmacotherapy, and second, the study of RAAS gene polymorphisms may allow early detection of persons with increased risk of persistent AF recurrence and its prevention.
References
January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Conti, J. B., et al. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Journal of the American College of Cardiology, 64(21), e1–e76. doi: 10.1016/j.jacc.2014.03.022
Vanassche, T., Lauw, M. N., Eikelboom, J. W., Healey, J. S., Hart, R. G., Alings, M., et al. (2015). Risk of ischaemic stroke according to pattern of atrial fibrillation: analysis of 6563 aspirin-treated patients in ACTIVE-A and AVERROES. European heart journal, 36(5), 281–288. doi: 10.1093/eurheartj/ehu307
Popova, E. P., & Fisenko, V. P. (2017). Fibrillyaciya predserdij: mekhanizmy razvitiya i lekarstvennaya terapiya [Atrial fibrillation: mechanisms of development and drug therapy]. E'ksperimental'naya i klinicheskaya farmakologiya, 80(4), 34–44. [in Russian]. doi: 10.30906/0869-2092-2017-80-4-34-44
Kuskaeva, A. V., Nikulina, S. Yu., Chernova, A. A., & Aksyutina, N. V. (2016). Geneticheskie prediktory fibrillyacii predserdij [Genetic predictors of atrial fibrillation]. Racional'naya farmakoterapiya v kardiologii, 12(3), 331–336. [in Russian]. doi: http://dx.doi.org/10.20996/1819-6446-2016-12-3-331-336
Kirchhof, P., Benussi, S., Kotecha, D., Ahlsson, A., Atar, D., Casadei, B., et al. (2016). 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur Heart J, 37(38), 2893–2962. doi: 10.1093/eurheartj/ehw210
Iravanian, S., & Dudley Jr, S. C. (2008). The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias. Heart rhythm, 5(6), S12–S17. doi: 10.1016/j.hrthm.2008.02.025
Ehrlich, J. R., Hohnloser, S. H., & Nattel, S. (2005). Role of angiotensin system and effects of its inhibition in atrial fibrillation: clinical and experimental evidence. European heart journal, 27(5), 512–518. doi: 10.1093/eurheartj/ehi668
Jalife, J. (2014). Mechanisms of persistent atrial fibrillation. Current opinion in cardiology, 29(1), 20–27. doi: 10.1097/HCO.0000000000000027
Topal, N. P., Ozben, B., Hancer, V. S., Tanrikulu, A. M., Diz-Kucukkaya, R., Fak, A. S., et al. (2011). Polymorphisms of the angiotensin-converting enzyme and angiotensinogen gene in patients with atrial fibrillation. Journal of the Renin-Angiotensin-Aldosterone System, 12(4), 549–556. doi: 10.1177/1470320311399605
Wang, Q., Hu, X., Li, S., Wang, X., Wang, J., Zhang, R., et al. (2015). Association of the angiotensinogen M235T polymorphism with recurrence after catheter ablation of acquired atrial fibrillation. Journal of the Renin-Angiotensin-Aldosterone System, 16(4), 888–897. doi: 10.1177/1470320315594315
Boldt, A., Wetzel, U., Weigl, J., Garbade, J., Lauschke, J., Hindricks, G., et al. (2003). Expression of angiotensin II receptors in human left and right atrial tissue in atrial fibrillation with and without underlying mitral valve disease. Journal of the American College of Cardiology, 42(10), 1785–1792.
Mehta, P. K., & Griendling, K. K. (2007). Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. American Journal of Physiology-Cell Physiology, 292(1), C82–C97. doi: 10.1152/ajpcell.00287.2006
Bonnardeaux, A., Davies, E., Jeunemaitre, X., Fery, I., Charru, A., Clauser, E., et al. (1994). Angiotensin II type 1 receptor gene polymorphisms in human essential hypertension. Hypertension, 24(1), 63–69.
Belenkov, Y. N., Privalova, E. V., Kaplunova, V. Y., Stambol'skiĭ, D. V., & Fomin, A. A. (2010). Analysis of morpho-functional parameters of the heart and polymorphisms of Renin-Angiotensin-aldosterone system genes in patients with different variants of the course of hypertrophic cardiomyopathy. Kardiologiia, 50(6), 27–34.
van Geel, P. P., Pinto, Y. M., Buikema, H., & van Gilst, W. H. (1998). Is the A1166C polymorphism of the angiotensin II type 1 receptor involved in cardiovascular disease? European heart journal, 19, G13–7.
Van Geel, P. P., Pinto, Y. M., Voors, A. A., Buikema, H., Oosterga, M., Crijns, H. J., & van Gilst, W. H. (2000). Angiotensin II type 1 receptor A1166C gene polymorphism is associated with an increased response to angiotensin II in human arteries. Hypertension, 35(3), 717–721. doi: 10.1161/01.HYP.35.3.717
Belluzzi, F., Sernesi, L., Preti, P., Salinaro, F., Fonte, M. L., & Perlini, S. (2009). Prevention of recurrent lone atrial fibrillation by the angiotensin-II converting enzyme inhibitor ramipril in normotensive patients. Journal of the American College of Cardiology, 53(1), 24–29. doi: 10.1016/j.jacc.2008.08.071
Tayebjee, M. H., Creta, A., Moder, S., Hunter, R. J., Earley, M. J., Dhinoja, M. B., & Schilling, R. J. (2010). Impact of angiotensin-converting enzyme-inhibitors and angiotensin receptor blockers on long-term outcome of catheter ablation for atrial fibrillation. Europace, 12(11), 1537–1542. doi: 10.1093/europace/euq284
Healey, J. S., Baranchuk, A., Crystal, E., Morillo, C. A., Garfinkle, M., Yusuf, S., & Connolly, S. J. (2005). Prevention of atrial fibrillation with angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: a meta-analysis. Journal of the American College of Cardiology, 45(11), 1832–1839. doi: 10.1016/j.jacc.2004.11.070
Chapurnykh, A. (2012). β-Adrenoblokatory v lechenii aritmii [β-Adrenoblockers in the Treatment of Arrythmias]. Kardiologiya, 52(6), 86–92. [in Russian].
Pacanowski, A. M. (2007). Johnson JA ADRB1 Gene Summary. Pharmacological Reviews, 59(1), 2–4.
Parvez, B., Chopra, N., Rowan, S., Vaglio, J. C., Muhammad, R., Roden, D. M., & Darbar, D. (2012). A common β1-adrenergic receptor polymorphism predicts favorable response to rate-control therapy in atrial fibrillation. Journal of the American College of Cardiology, 59(1), 49–56. doi: 10.1016/j.jacc.2011.08.061
Nia, A. M., Caglayan, E., Gassanov, N., Zimmermann, T., Aslan, O., Hellmich, M., et al. (2010). Beta1-adrenoceptor polymorphism predicts flecainide action in patients with atrial fibrillation. PLoS One, 5(7), e11421. doi: 10.1371/journal.pone.0011421
Nicoulina, S., Shulman, V., Shesternya, P., Chernova, A., Salmina, A., Issachenko, O., et al. (2010). Association of ADRB1 gene polymorphism with atrial fibrillation. Genetic testing and molecular biomarkers, 14(2), 249–253. doi: 10.1089/gtmb.2009.0100
Vecoli, C. (2014). Endothelial nitric oxide synthase gene polymorphisms in cardiovascular disease. In Vitamins & Hormones, 96, 387–406. doi: 10.1016/B978-0-12-800254-4.00015-5
Tovazhnyanskaya, E. L. (2016). E'ndotelial'naya disfunkciya. Klinicheskie aspekty problemy i puti ee resheniya [Endothelial dysfunction. Clinical aspects of the problem and ways to solve it]. Zhurnal nevrologіi іm. B.M. Man'kovs'kogo, 3, 17–21. [in Russian].
Casas, J. P., Cavalleri, G. L., Bautista, L. E., Smeeth, L., Humphries, S. E., & Hingorani, A. D. (2006). Endothelial nitric oxide synthase gene polymorphisms and cardiovascular disease: a HuGE review. American journal of epidemiology, 164(10), 921–935. doi: 10.1093/aje/kwj302
Pal, G. K., Adithan, C., Umamaheswaran, G., Pal, P., Nanda, N., Indumathy, J., & Syamsunder, A. N. (2016). Endothelial nitric oxide synthase gene polymorphisms are associated with cardiovascular risks in prehypertensives. Journal of the American Society of Hypertension, 10(11), 865–872. doi: 10.1016/j.jash.2016.09.001
Hasanzad, M., Imeni, M., & Mohammadhasani, M. R. (2014). Genetic polymorphism of endothelial nitric oxide synthase in coronary artery disease. Intern. Heart Vasc. Dis. J, 2(2), 32–36.
Downloads
How to Cite
Issue
Section
License
Authors who publish with this journal agree to the following terms:- Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
- Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
- Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access)