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Assessment of proarrhythmic ventricular electrophysiological remodeling in patients with rheumatoid arthritis

Untersuchung des proarrhythmischen ventrikulären elektrophysiologischen Remodelings bei Patienten mit rheumatoider Arthritis

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Abstract

Introduction

Rheumatoid arthritis (RA) is related to cardiovascular disease and results in increased mortality rates. Ischemia, autonomic nervous system dysfunction, impaired cardiac ionic currents, and genetic predisposition may be the underlying mechanisms. Proarrhythmic ventricular electrophysiological remodeling detected on the basis of Tp‑e interval, Tp-e/QT, and Tp-e/QTc ratios plays a key role in the prognosis. Our aim was to assess proarrhythmic ventricular electrophysiological remodeling in patients with RA, a well-known chronic inflammatory disorder.

Materials and methods

A total of 163 patients with RA and 47 patients as a control group were included in this retrospective study. Proarrhythmic ventricular electrophysiological remodeling markers were evaluated in both groups along with baseline demographic and clinical variables. Patients using medication or with chronic disorders that can affect ventricular repolarization markers were excluded.

Results

The patients with RA had prolonged Tp‑e interval (66 ms [44–80]; 80 ms [78–96], p < 0.001) and increased Tp-e/QT ratio (0.18 [0.12–0.22]; 0.22 [0.20–0.24], p < 0.001) and Tp-e/QTc ratio (0.16 [0.11–0.19]; 0.20 [0.17–0.22], p < 0.001) compared to the control group.

Conclusion

The Tp‑e interval and Tp-e/QT ratio, which may help to clarify the pathophysiological mechanisms of ventricular arrhythmias, were increased in patients with RA.

Zusammenfassung

Hintergrund

Die rheumatoide Arthritis (RA) ist mit Herz-Kreislauf-Erkrankungen vergesellschaftet und führt zu einer erhöhten Mortalitätsrate. Ischämie, eine Funktionsstörung des autonomen Nervensystems, beeinträchtigte kardiale Ionenströme und genetische Prädisposition sind möglicherweise die zugrunde liegenden Mechanismen. Proarrhythmisches ventrikuläres elektrophysiologisches Remodeling, das auf der Grundlage des Tp-e-Intervalls, des Tp-e/QT- und des Tp-e/QTc-Verhältnisses diagnostiziert wird, spielt eine wesentliche Rolle für die Prognose. Ziel der vorliegenden Arbeit war es, das proarrhythmische ventrikuläre elektrophysiologische Remodeling bei Patienten mit RA als einer bekannten chronischen entzündlichen Erkrankung zu untersuchen.

Material und Methoden

In diese retrospektive Studie wurden 163 Patienten mit RA und 47 Patienten als Kontrollgruppe einbezogen. Marker für das proarrhythmische ventrikuläre elektrophysiologische Remodeling wurden in beiden Gruppen zusammen mit demografischen und klinischen Ausgangsparametern untersucht. Patienten, die Medikamente nehmen, oder mit chronischen Krankheiten, die ventrikuläre Repolarisationsmarker beeinflussen können, wurden aus der Studie ausgeschlossen.

Ergebnisse

Die RA-Patienten wiesen im Vergleich mit der Kontrollgruppe ein verlängertes Tp-e-Intervall auf (66 ms [44–80]; 80 ms [78–96], p < 0,001) und ein erhöhtes Tp-e/QT-Verhältnis (0,18 [0,12–0,22]; 0,22 [0,20–0,24]; p < 0,001) sowie Tp-e/QTc-Verhältnis (0,16 [0,11–0,19]; 0,20 [0,17–0,22], p < 0,001).

Schlussfolgerung

Das Tp-e-Intervall und das Tp-e/QT-Verhältnis, die dazu beitragen können, die pathophysiologischen Mechanismen ventrikulärer Arrhythmien zu entschlüsseln, waren bei Patienten mit RA erhöht.

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References

  1. Lawrence RC, Helmick CG, Arnett FC et al (1998) Estimates of the prevalence of arthritis and selected musculoskeletal disorders in the United States. Arthritis Rheum 41:778–799

    Article  CAS  Google Scholar 

  2. Gabriel SE (2001) The epidemiology of rheumatoid arthritis. Rheum Dis Clin North Am 27:269–281

    Article  CAS  Google Scholar 

  3. Koopman WJ, Moreland LW (2005) Arthritis and allied conditions. A textbook of rheumatology, 15th edn. Lippincott Williams & Wilkins, Philadelphia

    Google Scholar 

  4. Bacon PA, Townend JN (2001) Nails in the coffin: increasing evidence for the role of rheumatic disease in the cardiovascular mortality of rheumatoid arthritis [editorial. Arthritis Rheum 44:2707–2710

    Article  CAS  Google Scholar 

  5. Vandenbroucke JP, Hazevoet HM, Cats A (1984) Survival and cause of death in rheumatoid arthritis: a 25-year prospective followup. J Rheumatol 11:158–161

    CAS  PubMed  Google Scholar 

  6. Patel KHK, Jones TN, Sattler S, Mason JC, Ng FS (2020) Proarrhythmic electrophysiological and structural remodeling in rheumatoid arthritis. Am J Physiol Heart Circ Physiol 319(5):H1008–H1020

    Article  CAS  Google Scholar 

  7. Danesh J, Whincup P, Walker M et al (2000) Low grade inflammation and coronary heart disease: prospective study and updated metaanalyses. BMJ 321:199–204

    Article  CAS  Google Scholar 

  8. Szmitko PE, Wang CH, Weisel RD et al (2003) New markers of inflammation and endothelial cell activation: Part I. Circulation 108:1917–1923

    Article  Google Scholar 

  9. Rost NS, Wolf PA, Kase CS et al (2001) Plasma concentration of C‑reactive protein and risk of ischemic stroke and transient ischemic attack: the Framingham study. Stroke 32:2575–2579

    Article  CAS  Google Scholar 

  10. Evrengül H, Dursunoglu D, Cobankara V, Polat B, Seleci D, Kabukçu S et al (2004) Heart rate variability in patients with rheumatoid arthritis. Rheumatol Int 24:198–202

    Article  Google Scholar 

  11. Janse van Rensburg DC, Ker JA, Grant CC, Fletcher L (2012) Autonomic impairment in rheumatoid arthritis. Int J Rheum Dis 15:419–426

    Article  Google Scholar 

  12. Mountantonakis S, Deo R (2012) Biomarkers in atrial fibrillation, ventricular arrhythmias, and sudden cardiac death. Cardiovasc Ther 30:74–80

    Article  Google Scholar 

  13. Antzelevitch C, Sicouri S, Di Diego JM, Burashnikov A, Viskin S, Shimizu W et al (2007) Does Tpeak-Tend provide an index of transmural dispersion of repolarization? Heart Rhythm 4:1114–1116

    Article  Google Scholar 

  14. Smetana P, Schmidt A, Zabel M, Hnatkova K, Franz M, Huber K et al (2011) Assessment of repolarization heterogeneity for prediction of mortality in cardiovascular disease: peak to the end of the T wave interval and nondipolar repolarization components. J Electrocardiol 44:301–308

    Article  Google Scholar 

  15. Gupta P, Patel C, Patel H, Narayanaswamy S, Malhotra B, Green JT et al (2008) T(p-e)/QT ratio as an index of arrhythmogenesis. J Electrocardiol 41:567–574

    Article  Google Scholar 

  16. Arnett FC, Edwothy SM, Bloch DA, Meshane DJ, Fries JF, Cooper NS (1988) The American Rheumatism Association 1987 criteria for the classification of rheumatoid arthritis. Arthritis Rheum 31:315–324

    Article  CAS  Google Scholar 

  17. Goldenberg I, Moss AJ, Zareba W (2006) QT interval: how to measure it and what is “normal”. J Cardiovasc Electrophysiol 17:333–336

    Article  Google Scholar 

  18. Klingenberg R, Lüscher TF (2015) Rheumatoid arthritis and coronary atherosclerosis: two cousins engaging in a dangerous liaison. Eur Heart J 36:3423–3425

    Article  CAS  Google Scholar 

  19. Libby P (2008) Role of inflammation in atherosclerosis associated with rheumatoid arthritis. Am J Med 121:S21–S31

    Article  CAS  Google Scholar 

  20. Meune C, Touze E, Trinquart L, Allanore Y (2009) Trends in cardiovascular mortality in patients with rheumatoid arthritis over 50 years: a systematic review and meta-analysis of cohort studies. Rheumatology 48(10):1309–1313

    Article  Google Scholar 

  21. Maradit-Kremers H, Crowson CS, Nicola PJ, Ballman KV, Ballman KV, Roger VL, Jacobsen SJ, Gabriel SE (2005) Increased unrecognized coronary heart disease and sudden death in rheumatoid arthritis. A population-based cohort study. Arthritis Rheum 52:402–411

    Article  Google Scholar 

  22. Lazzerini PE, Capecchi PL, Acampa M, Galeazzi M, Laghi-Pasini F (2014) Arrhythmic risk in rheumatoid arthritis: the driving role of Systemic inflammation. Autoimmun Rev 13:936–944

    Article  Google Scholar 

  23. Sgreccia A, Morelli S, Ferrante L, Perrone C, De Marzio P, De Vincentiis G et al (1998) QT interval and QT dispersion in systemic sclerosis(scleroderma). J Inter Med 243:127–132

    CAS  Google Scholar 

  24. Adlan AM, Panoulas VF, Smith JP, Fisher JP, Kitas GD (2015) Association between correctedQT interval and inflammatory cytokines in rheumatoid arthritis. J Rheumatol 42:421–428

    Article  CAS  Google Scholar 

  25. Acar GR, Akkoyun M, Nacar AB, Dirnak I, Yıldırım Çetin G, Nur Yıldırım M et al (2014) Evaluation of Tp‑e interval and Tp-e/QT ratio in patients with rheumatoid arthritis. Turk Kardiyol Dern Ars 42:29–34

    Article  Google Scholar 

  26. Panoulas VF, Toms TE, Douglas KM, Sandoo A, Metsios GS, Stavropoulos-Kalinoglou A, Kitas GD (2014) Prolonged QTc interval predicts all-cause mortality inpatients with rheumatoid arthritis: an association driven by high inflammatory burden. Baillieres Clin Rheumatol 53:131–137

    Google Scholar 

  27. Zhang Y, Post WS, Blasco-Colmenares E et al (2011) Electrocardiographic QT interval and mortality: ameta-analysis. Epidemiology 22:660–670

    Article  Google Scholar 

  28. Kors JA, Ritsema van Eck HJ, van Herpen G (2008) The meaning of theTp-Te interval and its diagnostic value. J Electrocardiol 41:575–580

    Article  Google Scholar 

  29. Acar GR, Yorgun H, İnci MF, Akkoyun M, Bakan B, Nacar AB et al (2014) Evaluation of Tp‑e interval and Tp-e/QT ratio in patients withankylosing spondylitis. Mod Rheumatol 24(2):327–330

    Article  Google Scholar 

  30. Akcay A, Acar G, Sayarlioglu M, Sokmen A, Kaya H, Ispiroglu M et al (2009) QT dispersion and transmural dispersion of repolarization inpatients with familial Mediterranean fever. Mod Rheumatol 19:550–555

    Article  Google Scholar 

  31. Yayla C, Yayla ME, Yayla KG, Ilgen U, Akboğa MK, Düzgün N (2016) The assessment of Tp‑e interval and Tp-e/QT ratio inpatients with systemic sclerosis. Arch Rheumatol 31(2):139–144

    Article  Google Scholar 

  32. Erikssen G, Liestol K, Gullestad L, Haugaa KH, Bendz B, Amlie JP (2012) The terminal part of the QT interval (T peak to T end): a predictor of mortality after acute myocardial infarction. Ann Noninvasive Electrocardiol 17:85–94

    Article  Google Scholar 

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Correspondence to Mehmet Engin Tezcan M.D..

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N. Aladag, A. Guner, C. Arslan, A.K. Kalkan, S. Kahraman, H.Z. Agus, N. Sen, M.E. Tezcan, B.S. Yildiz and M. Yildiz declare that they have no competing interests.

All procedures performed in studies involving human participants or on human tissue were in accordance with the ethical standards of the institutional and/or national research committee and with the 1975 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all individual participants included in the study.

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Aladag, N., Guner, A., Arslan, C. et al. Assessment of proarrhythmic ventricular electrophysiological remodeling in patients with rheumatoid arthritis. Herz 47, 465–470 (2022). https://doi.org/10.1007/s00059-021-05072-9

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  • DOI: https://doi.org/10.1007/s00059-021-05072-9

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