The Relationship Between Prolidase Activity and Atrial Electromechanical Changes in Patients with Paroxysmal Atrial Fibrillation

Author(s): Mustafa Begenc Tascanov*.

Journal Name: Combinatorial Chemistry & High Throughput Screening

Volume 22 , Issue 1 , 2019

Become EABM
Become Reviewer

Abstract:

Background: Tissue fibrosis increases in the structure of the atrial tissue of atrial fibrillation patients. Prolidase enzyme regulates collagen synthesis. There may be an association between electrocardiography (ECG) findings and prolidase activity.

Objective: This study investigated the association between atrial conduction time and prolidase activity, a collagen synthesis enzyme, and P-wave dispersion (PWD) in patients with Paroxysmal Atrial Fibrillation (PAF).

Methods: Exclusion criteria included the age of <18 years, heart failure, diabetes, hypertension, hyperlipidemia, malignancy, cerebrovascular disease, chronic respiratory distress, osteoporosis, rheumatoid arthritis, renal disease, cirrhosis, and other types of arrhythmia. Patients diagnosed with PAF within 48 hours were considered to have a definite diagnosis. PWD was calculated using a 12-lead ECG, and inter- and intraatrial electromechanical delay (EMD) was assessed using tissue Doppler imaging and conventional echocardiography. Serum prolidase levels were measured in both groups.

Results: A total of 43 patients with PAF (20 female, 23 male; mean age, 46.8 ± 5.7 years) and 42 healthy volunteers (21 female, 21 male; mean age, 43.9 ± 5.1 years) were included in the study.

Inter- and intraatrial EMD, PWD, minimum P-wave (Pmin), and maximum P-wave (Pmax) measurements were significantly higher (39.7 ± 2.7, 35.7 ± 2.3, p < 0.001; 13.2 ± 2.6, 8.5 ± 1.9, p < 0.001; 47.1 ± 11, 24.1 ± 7.1, p < 0.001; 69.8 ± 8.8, 66.7 ± 10.2, p < 0.130; 114.8 ± 13, 93.6 ± 8.6, p < 0.001, respectively) and serum prolidase levels were significantly lower in patients with PAF compared to healthy controls (3.96 ± 1.2, 8.5 ± 3.56, p < 0.001). In patients with PAF, correlation analysis showed a negative correlation between prolidase levels and intra- and interatrial EMD, PWD, and Pmax (r = -0.41, p < 0.05; r = -0.54, p < 0.05; r = -0.62, p < 0.05; r = -0.49, p < 0.05, respectively). Interatrial EMD showed a significant positive correlation with intraatrial EMD, Pmax, and PWD in patients with PAF (r = 0.90, p < 0.05; r = 0.574, p < 0.05; r = 0.43, p < 0.05, respectively). Additionally, the level of high-sensitivity C-reactive protein (hs-CRP) was significantly higher in patients with PAF (6.6 ± 8, 1.8 ± 1.6, p < 0.001).

Conclusion: The decreased plasma prolidase activity in patients with PAF may explain the irregularity of the collagen metabolism of different extracellular components and may indicate the onset of atrial remodeling. Changes in PWD, interatrial EMD, and serum prolidase level may predict PAF before diagnosis.

Keywords: Paroxysmal atrial fibrillation, prolidase, fibrosis, collagen synthesis, serum prolidase level, diagnosis.

[1]
Reddy, V.; Taha, W.; Kundumadam, S.; Khan, M. Atrial fibrillation and hyperthyroidism: A literature review. Indian Heart J., 2017, 69(49), 545-550.
[2]
Liu, G.Z.; Hou, T.T.; Yuan, Y.; Hang, P.Z.; Zhao, J.J.; Sun, L.; Zhao, G.Q.; Zhao, J.; Dong, J.M.; Wang, X.B. Fenofibrate inhibits atrial metabolic remodelling in atrial fibrillation through PPAR‐α/sirtuin 1/PGC‐1α pathway. Br. J. Pharmacol., 2016, 173(6), 1095-1109.
[3]
Feinberg, W.M.; Cornell, E.S.; Nightingale, S.D.; Pearce, L.A.; Tracy, R.P.; Hart, R.G.; Bovill, E.G. Relationship between prothrombin activation fragment F1. 2 and international normalized ratio in patients with atrial fibrillation. Stroke, 1997, 28(6), 1101-1106.
[4]
Chugh, S.S.; Havmoeller, R.; Narayanan, K.; Singh, D.; Rienstra, M.; Benjamin, E.J.; Gillum, R.F.; Kim, Y.H.; McAnulty, J.H.; Zheng, Z.J. Worldwide epidemiology of atrial fibrillation: A Global Burden of Disease 2010 Study. Circulation, 2014, 129(8), 837-847.
[5]
Sankaranarayanan, R.G.; Kirkwood, R.; Visweswariah, D.J. How does chronic atrial fibrillation ınfluence mortality in the modern treatment era? Curr. Cardiol. Rev., 2015, 11(3), 190-198.
[6]
Nattel, S.; Dobrev, D. Electrophysiological and molecular mechanisms of paroxysmal atrial fibrillation. Nat. Rev. Cardiol., 2016, 13(10), 575.
[7]
Frommeyer, G.; Schmidt, M.; Clauß, C.; Kaese, S.; Stypmann, J.; Pott, C.; Eckardt, L.; Milberg, P. Further insights into the underlying electrophysiological mechanisms for reduction of atrial fibrillation by ranolazine in an experimental model of chronic heart failure. Eur. J. Heart Fail., 2012, 14(12), 1322-1331.
[8]
Zegkos, T.; Efthimiadis, G.K.; Parcharidou, D.G.; Gossios, T.D.; Giannakoulas, G.; Ntelios, D.; Ziakas, A.; Paraskevaidis, S.; Karvounis, H.I. Atrial fibrillation in hypertrophic cardiomyopathy: A turning point towards increased morbidity and mortality. Hellenic J. Cardiol., 2017, 58(5), 331-339.
[9]
Kirchhof, P.; Benussi, S.; Kotecha, D.; Ahlsson, A.; Atar, D.; Casadei, B.; Castella, M.; Diener, H.C.; Heidbuchel, H.; Hendriks, J. 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS. Eur. Heart J., 2016, 37(38), 2893-2962.
[10]
Palka, J.A.; Phang, J.M. Prolidase activity in fibroblasts is regulated by interaction of extracellular matrix with cell surface integrin receptors. J. Cell. Biochem., 1997, 67(2), 166-175.
[11]
Bergmann, M.; Fruton, J.S. On proteolytic enzymes, XII. Regarding the specificity of aminopeptidase and carboxypeptidase. A new type of enzyme in the intestinal tract. J. Biol. Chem., 1937, 117, 189-202.
[12]
Zanaboni, G.; Dyne, K.M.; Rossi, A.; Monafo, V.; Getta, G. Prolidase deficiency: Biochemical study of erythrocyte and skin fibroblast prolidase activity in Italian patients. Haematologica, 1994, 79(1), 13-18.
[13]
Myara, I.; Myara, A.; Mangeot, M.; Fabre, M.; Charpentier, C.; Lemonnier, A. Plasma prolidase activity: A possible index of collagen catabolism in chronic liver disease. Clin. Chem., 1984, 30(2), 211-215.
[14]
Erbağcı, A.B.; Araz, M.; Erbağcı, A.; Tarakçıoğlu, M.; Namıduru, E.S. Serum prolidase activity as a marker of osteoporosis in type 2 diabetes mellitus. Clin. Biochem., 2002, 35(4), 263-268.
[15]
Altindag, O.; Erel, O.; Aksoy, N.; Selek, S.; Celik, H.; Karaoglanoglu, M. Increased oxidative stress and its relation with collagen metabolism in knee osteoarthritis. Rheumatol. Int., 2007, 27(4), 339-344.
[16]
Gejyo, F.; Kishore, B.; Arakawa, M. Prolidase and prolinase activities in the erythrocytes of patients with chronic uremia. Nephron, 1983, 35(1), 58-61.
[17]
Demirbag, R.; Yıldız, A.; Gur, M.; Yilmaz, R.; Elçi, K.; Aksoy, N. Serum prolidase activity in patients with hypertension and its relation with left ventricular hypertrophy. Clin. Biochem., 2007, 40(13-14), 1020-1025.
[18]
Aktürk, E.; Aşkın, L.; Nacar, H.; Taşolar, M.H.; Türkmen, S.; Çetin, M.; Bozkurt, M. Association of serum prolidase activity in patients with isolated coronary artery ectasia. Anatol. J. Cardiol., 2018, 19(2), 110.
[19]
Bishop, J.E. Regulation of cardiovascular collagen deposition by mechanical forces. Mol. Med. Today, 1998, 4(2), 69-75.
[20]
Boos, C.J.; Anderson, R.A.; Lip, G.Y. Is atrial fibrillation an inflammatory disorder. Eur. Heart J., 2005, 27(2), 136-149.
[21]
Selcuk, M.T.; Selcuk, H.; Maden, O.; Temizhan, A.; Aksu, T.; Doğan, M.; Sasmaz, A. Relationship between inflammation and atrial fibrillation in patients with isolated rheumatic mitral stenosis. J. Heart Valve Dis., 2007, 16(5), 468-474.
[22]
Boldt, A.; Wetzel, U.; Lauschke, J.; Weigi, J.; Gummert, J.; Hindricks, G.; Kottkamp, H.; Dhein, S. Fibrosis in left atrial tissue of patients with atrial fibrillation with and without underlying mitral valve disease. Heart, 2004, 90(4), 400-405.
[23]
Casaclang-Verzosa, G.; Gersh, B.J.; Tsang, T.S. Structural and functional remodeling of the left atrium: clinical and therapeutic implications for atrial fibrillation. J. Am. Coll. Cardiol., 2008, 51(1), 1-11.
[24]
Quiñones, M.A.; Otto, C.M.; Stoddard, M.; Waggoner, A.; Zoghbi, W.A. Recommendations for quantification of Doppler echocardiography: A report from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of Echocardiography. J. Am. Soc. Echocardiogr., 2002, 15(2), 167-184.
[25]
Özer, N.; Yavuz, B.; Can, I.; Atalar, E.; Aksöyek, S.; Övünç, K.; Özmen, F.; Kes, S. Doppler tissue evaluation of intra-atrial and interatrial electromechanical delay and comparison with P-wave dispersion in patients with mitral stenosis. J. Am. Soc. Echocardiogr., 2005, 18(9), 945-948.
[26]
Frustaci, A.; Chimenti, C.; Bellocci, F.; Morgante, E.; Russo, M.A.; Maseri, A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation, 1997, 96(4), 1180-1184.
[27]
Surażyński, A.; Sienkiewicz, P.; Wołczyński, S.; Pałka, J. Differential effects of echistatin and thrombin on collagen production and prolidase activity in human dermal fibroblasts and their possible implication in β1-integrin-mediated signaling. Pharmacol. Res., 2005, 51(3), 217-221.
[28]
Rabus, M.; Demirbag, R.; Yildiz, A.; Tezcan, O.; Yilmaz, R.; Ocak, A.R.; Alp, M.; Erel, O.; Aksoy, N.; Yakut, C. Association of prolidase activity, oxidative parameters, and presence of atrial fibrillation in patients with mitral stenosis. Arch. Med. Res., 2008, 39(5), 519-524.
[29]
Sezen, Y.; Bas, M.; Altıparmak, H.; Yildiz, A.; Buyukhatipoglu, H.; Faruk Dag, O.; Kaya, Z.; Aksoy, N. Serum prolidase activity in idiopathic and ischemic cardiomyopathy patients. J. Clin. Lab. Anal., 2010, 24(4), 213-218.


Rights & PermissionsPrintExport Cite as


Article Details

VOLUME: 22
ISSUE: 1
Year: 2019
Page: [69 - 75]
Pages: 7
DOI: 10.2174/1386207322666190306143317
Price: $58

Article Metrics

PDF: 22
HTML: 2
EPUB: 1
PRC: 1