Relationship between the Expression Level of Calcium Handling Proteins of the Sarcoplasmic Reticulum of Cardiomyocytes and the Structural and Functional State of the Patient Hearts with Permanent Atrial Fibrillation
Tóm tắt
The relationship between the expression level of Ca2+-ATPase (SERCA2a) and calsequestrin (CASQ2) and the structural and functional characteristics of the heart of patients with permanent atrial fibrillation was studied. The study included 40 patients with persistent atrial fibrillation. Patients underwent radiofrequency ablation (RFA), during which a biopsy of myocardial tissue was taken from the left ventricle. Intracardiac hemodynamic parameters were recorded from standard echocardiographic positions. The content of SERCA2a and CASQ2 proteins in the myocardium was determined by immunoblotting. Correlation was found between the level of SERCA2a and CASQ2 in the myocardium and the size of the left atrium. Patients with higher values of end-diastolic and end-systolic heart volumes had high levels of SERCA2a. Lower rates of early (peak E) and late (peak A) diastolic filling of the left ventricle were associated with high SERCA2a expression. The level of expression of the calcium handling proteins Ca2+-ATPase and calsequestrin was associated with the structural and functional parameters of the heart of patients with permanent atrial fibrillation.
Tài liệu tham khảo
Bokeria, L.A., Filatov, A.G. Kovalev, S.A., and Kovalev, A.S., Treatment of atrial fibrillation: data from randomized trials, Vestn. Eksp. Klin. Khir., 2012, vol. 5, no. 2, p. 448.
Borisova, E.V., Plekhanov, I.G., and Popov, S.V., Quality of life of patients after the creation of a complete atrioventricular block and implantation of a frequency-adaptive pacemaker, Sib. Med. Zh., 2013, vol. 28, no. 2, p. 74.
Proietti, M., Farcomeni, A., Romiti, G.F., et al., Association between clinical risk scores and mortality in atrial fibrillation: Systematic review and network meta-regression of 669.000 patients, Eur. J. Prevent. Cardiol., 2020, vol. 27, no. 6, p. 633.
Frommeyer, G., Eckardt, L., and Milberg, P., Calcium handling and ventricular tachyarrhythmias, Wien. Med. Wochenschr., 2012, vol. 162, nos. 13–14, p. 283.
Schlotthauer, K. and Bers, D.M., Sarcoplasmic reticulum Ca2+ release causes myocyte depolarization. Underlying mechanism and threshold for triggered action potentials, Circ. Res., 2000, vol. 87, no. 9, p. 774.
Molina, C.E., Abu-Taha, I.H., Wang, Q., et al., Profibrotic, electrical, and calcium-handling remodeling of the atria in heart failure patients with and without atrial fibrillation, Front. Physiol. 2018, vol. 9, p. 1383.
Voigt, N., Heijman, J., Wang, Q., et al., Cellular and molecular mechanisms of atrial arrhythmogenesis in patients with paroxysmal atrial fibrillation, Circulation, 2014, vol. 129, no. 2, p. 145.
Kuken, B.N., Aikemu, A.N., Xiang, S.Y., and Wulasihan, M.H., Effect of SERCA2a overexpression in the pericardium mediated by the AAV1 gene transfer on rapid atrial pacing in rabbits, Genet. Mol. Res., 2015, vol. 14, no. 4, p. 13625.
Sun, J. and Ailiman, M., Regulation of calcium pump through Notch/Jagged/Hes signaling pathway in canine model of chronic atrial fibrillation, Int. J. Clin. Exp. Pathol., 2019, vol. 12, no. 11, p. 4034.
Wang, H., Zhou, X.H., Li, Z.Q., et al., Prevention of atrial fibrillation by using sarcoplasmic reticulum calcium ATPase pump overexpression in a rabbit model of rapid atrial pacing, Med. Sci. Monit., 2017, vol. 23, p. 3952.
Kuum, M., Kaasik, A., Joubert, F., et al., Energetic state is a strong regulator of sarcoplasmic reticulum Ca2+ loss in cardiac muscle: different efficiencies of different energy sources, Cardiovasc. Res., 2009, vol. 83, no. 1, p. 89.
Faggioni, M. and Knollmann, B.C., Calsequestrin 2 and arrhythmias, Am. J. Physiol.: Heart Circ. Physiol., 2012, vol. 302, no. 6, p. H1250.
Gergs, U., Fahrion, C.M., Bock, P., et al., Evidence for a functional role of calsequestrin 2 in mouse atrium, Acta Physiol. (Oxford), 2017, vol. 219, no. 3, p. 669.
Faggioni, M., Savio-Galimberti, E., Venkataraman, R., et al., Suppression of spontaneous ca elevations prevents atrial fibrillation in calsequestrin 2-null hearts, Circ.: Arrhythmia Electrophysiol., 2014, vol. 7, no. 2, p. 313.
Glukhov, A.V., Kalyanasundaram, A., Lou, Q., et al., Calsequestrin 2 deletion causes sinoatrial node dysfunction and atrial arrhythmias associated with altered sarcoplasmic reticulum calcium cycling and degenerative fibrosis within the mouse atrial pacemaker complex, Eur. Heart J., 2015, vol. 36, no. 11, p. 686.
Dobrev, D. and Wehrens, X.H.T., Calcium-mediated cellular triggered activity in atrial fibrillation, J. Physiol-., 2017, vol. 595, no. 12, p. 4001.
Lugenbiel, P., Wenz, F., Govorov, K., et al., Atrial fibrillation complicated by heart failure induces distinct remodeling of calcium cycling proteins, PLoS One, 2015, vol. 10, no. 3, p. e0116395.
Brandenburg, S., Arakel, E.C., Schwappach, B., and Lehnart, S.E., The molecular and functional identities of atrial cardiomyocytes in health and disease, Biochim. Biophys. Acta, Mol. Cell Res., 2016, vol. 1863, no. 7, p. 1882.
Denham, N.C., Pearman, C.M., Caldwell, J.L., et al., Calcium in the pathophysiology of atrial fibrillation and heart failure, Front. Physiol., 2018, vol. 9, p. 1380.
Kalifa, J., Maixent, J.M., Chalvidan, T., et al., Energetic metabolism during acute stretch-related atrial fibrillation, Mol. Cell. Biochem., 2008, vol. 317, nos. 1–2, p. 69.
Tu, T., Zhou, S., Liu, Z., et al., Quantitative proteomics of changes in energy metabolism-related proteins in atrial tissue from valvular disease patients with permanent atrial fibrillation, Circ. J., 2014, vol. 78, no. 4, p. 993.
Zhang, G.X., Obata, K., Takeshita, D., et al., Evaluation of left ventricular mechanical work and energetics of normal hearts in SERCA2a transgenic rats, J. Physi-ol. Sci., 2012, vol. 62, no. 3, p. 221.
Terentyev, D., Viatchenko-Karpinski, S., Györke, I., et al., Calsequestrin determines the functional size and stability of cardiac intracellular calcium stores: mechanism for hereditary arrhythmia, Proc. Natl. Acad. Sci. U.S.A., 2003, vol. 100, no. 20, p. 11759.
Kubalova, Z., Györke, I., Terentyeva, R., et al., Modulation of cytosolic and intra-sarcoplasmic reticulum calcium waves by calsequestrin in rat cardiac myocytes, J. Physiol., 2004, vol. 561, no. 2, p. 515.
Liu, B., Ho, H.T., Brunello, L., et al., Ablation of HRC alleviates cardiac arrhythmia and improves abnormal Ca handling in CASQ2 knockout mice prone to CPVT, Cardiovasc. Res., 2015, vol. 108, no. 2, p. 299.
Lou, Q., Belevych, A.E., Radwański, P.B., et al., Alternating membrane potential/calcium interplay underlies repetitive focal activity in a genetic model of calcium-dependent atrial arrhythmias, J. Physiol., 2015, vol. 593, no. 6, p. 1443.
Belenkov, Yu.N. and Agmanova, E.T., Diastolic heart function in patients with chronic heart failure and methods for diagnosing its disorders using tissue myocardial dopplerography, Kardiologiya, 2003, no. 11, p. 58.
Nagueh, S.F., Smiseth, O.A., Appleton, C.P., et al., Recommendations for the evaluation of left ventricular diastolic function by echocardiography: an update from the American society of echocardiography and the European association of cardiovascular imaging, J. Am. Soc. Echocardiogr., 2016, vol. 29, no. 4, p. 277.