Evaluation of Ventricular Repolarization Markers and Fragmented QRS in Patients with Bipolar Disorder

Öz

Aim: Bipolar disorder (BD) is one of the chronic psychiatric diseases. It has been reported that cardiovascular diseases are seen twice as often in patients with BD. Fragmented QRS (fQRS) has been found to be associated with myocardial scarring and is used as a marker of arrhythmia and mortality. Ventricular repolarization (VR) is often evaluated using QT interval and T wave measurement data. In our study, we aimed to evaluate fQRS, QTc interval, QT dispersion (QTd), Tp-e interval, Tp-e/QT ratio results and VR, together with blood biochemistry parameter results of cases with BD. Material and Method: Our research was conducted with 51 people diagnosed with bipolar disorder and 52 healthy people as the control group. fQRS, QTc interval, QT dispersion (QTd), Tp-e interval, Tp-e/QT ratio were measured using 12-lead electrocardiography (ECG). The results of the data obtained from ECG and blood biochemistry parameter levels were used to compare the healthy and patient groups. Results: Tp-e interval (p=0.018) and Tpe/QT ratio (p=0.036) were found to be statistically significantly higher and total cholesterol level (p=0.006) lower in patients with bipolar disorder compared to the control group. Conclusion: An increased Tpe/QT ratio, along with a prolonged Tp-e interval, may be a useful marker of ventricular arrhythmia risk in individuals with fQRS BD.

Anahtar Kelimeler

• bipolar disorder
• ventricular repolarization
• electrocardiography
• fragmented QRS

Kaynakça

1. 1. Mitchell AJ, Malone D. Physical health and schizophrenia. Curr Opin Psychiatry. 2006;19(4):432–7.
2. 2. Hennekens CH. Increasing global burden of cardiovascular disease in general populations and patients with schizophrenia. J Clin Psychiatry. 2007;68(4):4–7.
3. 3. Riordan HJ, Antonini P, Murphy MF. Atypical antipsychotics and metabol ic syndrome in patients with schizophrenia: risk factors, monitoring, and healthcare implications. Am Health Drug Benefits. 2011;4(5):292–302.
4. 4. Lang UE, Borgwardt S. Molecular mechanisms of depression: perspectives on new treatment strategies. Cell Physiol Biochem. 2013;31(6):761–77.
5. 5. Chaddha A, Robinson EA, Kline-Rogers E, Alexandris-Souphis T, Rubenfire M. Mental health and cardiovascular disease. Am J Med. 2016;129(11):1145–8.
6. 6. Lichtman JH, Froelicher ES, Blumenthal JA, Carney RM, Doering LV, Frasure-Smith N, et al. Depression as a risk factor for poor prognosis among patients with acute coronary syndrome: systematic review and recommendations: a scientific statement from the American Heart Association. Circulation. 2014;129(12):1350–69.
7. 7. Alstrom CH. Mortality in mental hospitals with especial regard to tuberculosis. Acta Psychiatr Neurol Scand. 1942;24.
8. 8. Odegard O. Mortality in Norwegian mental hospitals. Acta Genet. 1951;2:141–73.

9. 9. Straus SMJM, Bleumink GS, Dieleman JP, van der Lei J, Stricker BHC, Sturkenboom MCJM. The incidence of sudden cardiac death in general population. J Clin Epidemiol. 2004;57(1):98102.
10. 10. Sachs G, Bowden C, Calabrese JR, Ketter T, Thompson T, White R, et al. Effects of lamotrigine and lithium on body weight during maintenance treatment of bipolar I disorder. Bipolar Disord. 2006;8(2):175–81.
11. 11. Hermida OG, Fontela T, Ghiglione M, Uttenthal LO. Effect of lithium on plasma glucose, insulin and glucagon in normal and streptozotocin-diabetic rats: role of glucagon in the hyperglycaemic response. Br J Pharmacol. 1994;111(3):861–5.
12. 12. Dinesen H, Gram L, Andersen T, Dam M. Weight gain during treatment with valproate. Acta Neurol Scand. 1984;70(2):659.
13. 13. Pylvanen V, Knip M, Pakarinen A, Kotila M, Turkka J, Isojarvi JI. Serum insulin and leptin levels in valproate-associated obesity. Epilepsia. 2002;43(5):514–7.
14. 14. Huang TL, Chen JF. Serum lipid profiles and schizophrenia: effects of conventional or atypical antipsychotic drugs in Taiwan. Schizophr Res. 2005;80(1):55–9.
15. 15. Henderson DC, Cagliero E, Gray C, Nasrallah RA, Hayden DL, Schoenfeld DA, et al. Clozapine, diabetes mellitus, weight gain, and lipid abnormalities: a five-year naturalistic study. Am J Psychiatry. 2000;157(6):975–81.
16. 16. Osser DN, Najarian DM, Dufresne RL. Olanzapine increases weight and serum triglyceride levels. J Clin Psychiatry. 1999;60(11):767–70.
17. 17. Michalets EL, Smith LK, Van Tassel ED. Torsade de pointes resulting from the addition of droperidol to an existing cytochrome P450 drug interaction. Ann Pharmacother. 1998;32(7-8):761–65.
18. 18. Lawrence KR, Nasraway SA. Conduction disturbances associated with administration of butyrophenone antipsychotics in the critically ill: a review of the literature. Pharmacotherapy. 1977;17(3):531–7.
19. 19. Krahenbuhl S, Sauter B, Kupferschimidt H, Krause M, Wyss PA, Meier PJ. Case Report: reversible QT prolongation with torsade de pointes in a patient with pimozide intoxication. Am J Med Sci. 1995;309(6):315–6.
20. 20. Gupta P, Patel C, Patel H, Narayanaswamy S, Malhotra B, Green JT, et al. T(p-e)/QT ratio as an index of arrhythmo- genesis. J Electrocardiol. 2008;41(6):567–74.
21. 21. Tanriverdi Z, Besli F, Gungoren F. The evaluation of Tp-e interval after transcatheter aortic valve implantation. J Electrocardiol. 2018;51(4):573.
22. 22. Yilmaz CF, Elboga G, Altunbas G, Vuruşkan E, Uğur BK, Sucu M. Evaluation of ventricular repolarization features with Tpe, Tp-e/QTc, JTc and JTd during electroconvulsive therapy. J Electrocardiol. 2018;51(3):440–2.
23. 23. Wenzel-Seifert K, Wittmann M, Haen E. QTc prolongation by psychotropic drugs and the risk of Torsade de Pointes. Deutsches Ärzteblatt International. 2011;108(41):687.
24. 24. Das MK, Saha C, El Masry H, Peng J, Dandamudi G, Mahenthiran J, et al. Fragmented QRS on a 12-lead ECG. a predictor of mortality and cardiac events in patients with coronary artery disease. Heart Rhythm. 2007;4(11):1385–92.
25. 25. Das MK, Khan B, Jacob S, Kumar A, Mahenthiran, J. Significance of a fragmented QRS complex versus a Q wave in patients with coronary artery disease. Circulation. 2006;113(21):2495–501.
26. 26. Havranek EP, Emsermann CD, Froshaug DN, Masoudi FA, Krantz MJ, Hanratty R, et al. Thresholds in the relationship between mortality and left ventricular hypertrophy defined by electrocardiography. J Electrocardiol. 2008;41(4):342–50.
27. 27. Rosen BD, Edvardsen T, Lai S, Castillo E, Pan L, Jerosch-Herold M, et al. Left ventricular concentric remodeling is associated with decreased global and regional systolic function: the multiethnic study of atherosclerosis. Circulation. 2005;112(7):98491.
28. 28. Allen JK, Blumenthal RS, Margolis S, Young DR, Miller E, Kelly K. Nurse case management of hypercholesterolemia in patients with coronary heart disease: Results of a randomized clinical trial. Am Heart J. 2002;144(4):678–86.
29. 29. Pfeffer MA, Sacks FM, Moyé LA, East C, Goldman S, Nash DT, et al. Influence of baseline lipids on effectiveness of pravastatin in the CARE Trial. Cholesterol And Recurrent Events. J Am Coll Cardiol. 1999;33(1):125–30.
30. 30. Shari S Bassuk, Nader Rifai, Paul M Ridker. Highsensitivity C-reactive protein: Clinical importance. Curr Probl Cardiol. 2004;29(8):439–93.
31. 31. Karaçağlar Emir. ST yükselmesiz akut koroner sendromlarda niasin tedavisinin Hs-CRP üzerine etkisi. 2011.
32. 32. Xia Y, Liang Y, Kongstad O, Liao Q, Holm M, Olsson B, et al. In vivo validation of the coincidence of the peak and end of the T wave with full repolarization of the epicardium and endocardium in swine. Heart Rhythm. 2005;2(2):162–9.
33. 33. Funk MC, Beach SR, Bostwick JR, Celano C, Hasnain M, Pandurangi A, et al. QTc prolongation and psychotropic medications. Am J Psychiatry. 2020;177(3):273–4.