EFFECT OF PROGRESSION ATRIAL FIBRILLATION THE LEVEL OF MATRIX METALLOPROTEINASE-9
DOI:
https://doi.org/10.11603/2415-8798.2017.2.7840Keywords:
atrial fibrillation, extracellular matrix, matrix metalloproteinase-9, pathological mechanisms.Abstract
Atrial fibrillation (AF) is one of the most common diseases in clinical practice. Experimental and clinical studies showed the existence of relationship between AF and changes in atrial electrical properties.
The aim of the study – to investigate the levels of matrix metalloproteinase-9 (MMP-9) and to evaluate its significance and role in the various stages of the development of idiopathic atrial fibrillation (AF).
Materials and Methods. The study included patients with idiopathic AF. In accordance with the degree of disease progression, patients were divided into 3 groups: paroxysmal, persistent and chronic AF. The control group consisted of practically healthy patients. To determine the serum levels of MMP-9 we used the double-antibody immunoassay with the enzyme label.
Results and Discussion. Each study group consisted of 20 patients; the control group consisted of 40 patients. The level of MMP-9 in the treatment groups was significantly different from the control and amounted to: 170.62 ± 24.65, 202.33 ± 29.18, 252.3 ± 21.87 ng / ml for paroxysmal, persistent and chronic forms of AF and 75 78 ± 14.7 ng / ml in the control group, respectively. As the disease progresses the level of MMP-9 increased (p<0.05).
Conclusions. Increased levels of MMP-9 is likely associated with the development and progression of idiopathic AF.
References
Miyazaki, S., Kuwahara, T. & Kobori, A. (2011). Prevalence, electrophysiological properties, and clinical implications of dissociated pulmonary vein activity following pulmonary vein antrum isolation. Am. J. Cardiol. 108 (8), 1147-1154. doi: 10.1016/j.amjcard.2011.06.015. Epub 2011 Jul 24.
Hijazi, Z., Oldgren, J., Siegbahn, A. & Wallentin, L. (2017). Application of biomarkers for risk stratification in patients with atrial fibrillation. Clinical Chemistry, 63 (1), 152-164.
Liu, C., Fu, H. & Li, J. (2012). Hyperglycemia aggravates atrial interstitial fibrosis, ionic remodeling and vulnerability to atrial fibril- lation in diabetic rabbits. Anadolu Kardiyol. Derg., 12, 543-550.
Martin Aguilar, Xiao Yan, Qi, & Hai Huang (2014). Fibroblast electrical remodeling in heart failure and potential effects on atrial fibrillation. Biophysical Journal, 107, 2444-2455
Kostin, S., Klein, G. & Szalay, Z. (2002). Structural correlate of atrial fibrillation in human patients. Cardiovasc. Res., 54, 361-379.
Veidal, S.S., Nielsen, M.J. & Leeming, D.J. (2012). Phosphodiesterase inhibition mediates matrix metalloproteinase activity and the level of collagen degradation fragments in a liver fibrosis ex vivo rat model. BMC Res. Notes, 5, 686.
Fan, D., Takawale, A. & Lee, J. (2012). Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease. Fibrogenesis Tissue Repair, 5, 15.
Georgescu, S.P., Aronovitz, M.J. & Iovanna, J.L. (2011). Decreased metalloprotease 9 induction, cardiac fibrosis, and higher autophagy after pressure overload in mice lacking the tran- scriptional regulator p8. Am. J. Physiol. Cell Physiol., 301, C1046-C1056.
Spinale, F.G., Coker, M.L. & Heung, L.J. (2000). A matrix metalloproteinase induction/activa- tion system exists in the human left ventricular myocardium and is upregulated in heart failure. Circulation, 102, 1944-1949.
El-Aziz, T.A. & Mohamed, R.H. (2017). Matrix metalloproteinase -9 polymorphism and outcome after acute myocardial infarction. Int. J. Cardiol., 15 (227), 524-528.
Fuster, V., Ryden, L.E. & Cannom, D.S. (2006). ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation. Circulation, 114, 700-752.
Vilen, S.T., Salo, T. & Sorsa, T. (2013). Fluctuating roles of matrix metalloproteinase-9 in oral squamous cell carcinoma. Sci. World J., 2013, 1-11.
Iyer, R.P., Brás, de Castro, L.E. & Patterson, N.L. (2016). Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution. J. Mol Cell Cardiol., 100, 109-117.
Sodha, N.R., Clements, R.T. & Boodhwani, M. (2009). Endostatin and angiostatin are increased in diabetic patients with coronary artery disease and associated with impaired coronary collateral formation. Am. J. Physiol. Heart Circ. Physiol., 296, H428-H434.
Ducharme, A., Frantz, S. & Aikawa, M. (2000). Targeted deletion of matrix metalloproteinase-9 attenuates left ventricular enlargement and collagen accumulation after experimental myocardial infarction. J. Clin. Invest., 106, 55-62.
Wang, W., Wu, P.S. & Yang, X.L. (2010). Role of matrix metalloproteinase and tissue inhibitor of metalloproteinase in atrial structural remodeling in patients with atrial fibrillation. Nan Fang Yi Ke Da Xue Xue Bao, 30, 1160-1162.
Kato, K., Fujimaki, T. & Yoshida, T. (2009). Impact of matrix metalloproteinase-2 levels on long-term outcome following pharmacological or electrical cardioversion in patients with atrial fibrillation. Europace, 11, 332-337.
Dorian, P., & Mangat, I. Quality of life variables in the selection of rate versus rhythm control in patients with atrial fibril- lation: observations from the Canadian Trial of Atrial Fibrillation. Card Electrophysiol. Rev., 7, 276-279.
Santos, M.C., de Souza, A.P., & Gerlach, R.F. (2004). Inhibition of human pulpal gelatinases (MMP-2 and MMP-9) by zinc oxide cements. J. Oral Rehabil., 31, 660-664.
Anne, W., Willems, R. & Roskams, T. (2005). Matrix metalloproteinases and atrial remodeling in patients with mitral valve disease and atrial fibrillation. Cardiovasc. Res., 67, 655-666.
Chiang, C.E., Naditch-Brule, L. & Murin, J. (2012). Distribution and risk profile of paroxysmal, persistent, and permanent atrial fibrillation in routine clinical practice: insight from the real-life global survey evaluating patients with atrial fibrillation international registry. Circ. Arrhythm. Electrophysiol., 5, 632-639.
M. Morishima, E. Iwata, C. Nakada (2016). Atrial fibrillation-mediated upregulation of miR-30d regulates myocardial electrical remodeling of the G-protein-gated K(+) channel, IK. Ach. Circ. J., 25; 80 (6), 1346-1355. doi: 10.1253/circj.CJ-15-1276.
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