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Case Report Torsade de Pointes Triggered by Early Ventricular Escape Beats in a Patient with Complete Atrioventricular Block Erkan Yildirim, 1 Baris Bugan, 2 Suat Gormel, 1 Uygar Cagdas Yuksel, 1 Murat Celik, 1 Yalcin Gokoglan, 1 Serdar Firtina, 1 Sinan Iscen, 1 Emre Yalcinkaya, 1 Ugur Kucuk, 1 and Hasan Kutsi Kabul 1 1 Department of Cardiology, Gulhane Military Medical Academy, 06010 Ankara, Turkey 2 Cardiology Service, Girne Military Hospital, 99300 Girne, Northern Cyprus, Mersin 10, Turkey Correspondence should be addressed to Baris Bugan; [email protected] Received 14 November 2015; Accepted 8 March 2016 Academic Editor: Christopher S. Snyder Copyright © 2016 Erkan Yildirim et al. is is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Torsade de pointes is an uncommon and malignant form of polymorphic ventricular tachycardia and associated with a prolonged QT interval, which may be congenital or acquired. Complete atrioventricular block may cause QT interval prolongation and torsade de pointes. In this paper, we present a case with complete atrioventricular block complicated with frequent episodes of torsade de pointes triggered by early premature ventricular contractions despite normal QT intervals. 1. Introduction Syncope is a frequent symptom in patients with com- plete atrioventricular block (CAVB) [1]. In the majority of cases, low cardiac output caused by decreased heart rate is responsible for the symptoms. However in some cases bradycardia associated QT prolongation may lead to malign ventricular tachyarrhythmias causing syncope [1, 2]. We, herein, reported a case with CAVB complicated with frequent episodes of torsade de pointes (TdP) triggered by early pre- mature ventricular contractions (PVCs) despite normal QT intervals. 2. Case Report A 73-year-old woman was admitted to our clinic for fainting and syncope. She had several episodes of syncope in the last few hours. She was on oral antidiabetics for diabetes mellitus and ramipril for hypertension. Her past medical history was otherwise normal. On initial physical examination, she was bradycardic (36 bpm), but alert and fully oriented. Her blood pressure was 100/70 mmHg. e physical examination was otherwise normal. Her initial electrocardiogram (ECG) showed CAVB with a rate of 38bpm and with frequent PVCs (Figure 1). Her blood chemistry was normal. Bedside echocardiogram revealed no structural heart disease. While being monitored in the coronary intensive care unit she suddenly developed TdP leading to syncope which required DC cardioversion for termination (Figure 2). She had several other episodes of sustained and nonsustained TdP until transvenous temporary pacemaker was in effect. All TdP episodes were triggered by an early PVC which hit the descending portion of the T wave on ECG (Figure 3). Increas- ing the heart rate by temporary cardiac pacing completely abolished the PVCs and TdP episodes. Coronary angiogram showed noncritical atherosclerotic plaques and ventricular tachycardia (VT) was not induced with electrophysiology study. e patient was further treated with a dual permanent pacemaker. e 6-month follow-up was uneventful. 3. Discussion e term TdP refers to a VT characterized by QRS complexes of changing amplitude that appear to twist around the isoelectric line and occur at rates of 200 to 250/min. TdP during bradyarrhythmias has been reported to be associated with gender, degree of QT prolongation and duration of Hindawi Publishing Corporation Case Reports in Cardiology Volume 2016, Article ID 7919642, 3 pages http://dx.doi.org/10.1155/2016/7919642

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  • Case ReportTorsade de Pointes Triggered by Early Ventricular Escape Beatsin a Patient with Complete Atrioventricular Block

    Erkan Yildirim,1 Baris Bugan,2 Suat Gormel,1 Uygar Cagdas Yuksel,1

    Murat Celik,1 Yalcin Gokoglan,1 Serdar Firtina,1 Sinan Iscen,1 Emre Yalcinkaya,1

    Ugur Kucuk,1 and Hasan Kutsi Kabul1

    1Department of Cardiology, Gulhane Military Medical Academy, 06010 Ankara, Turkey2Cardiology Service, Girne Military Hospital, 99300 Girne, Northern Cyprus, Mersin 10, Turkey

    Correspondence should be addressed to Baris Bugan; [email protected]

    Received 14 November 2015; Accepted 8 March 2016

    Academic Editor: Christopher S. Snyder

    Copyright © 2016 Erkan Yildirim et al.This is an open access article distributed under the Creative Commons Attribution License,which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

    Torsade de pointes is an uncommon and malignant form of polymorphic ventricular tachycardia and associated with a prolongedQT interval, whichmay be congenital or acquired. Complete atrioventricular blockmay causeQT interval prolongation and torsadede pointes. In this paper, we present a case with complete atrioventricular block complicated with frequent episodes of torsade depointes triggered by early premature ventricular contractions despite normal QT intervals.

    1. Introduction

    Syncope is a frequent symptom in patients with com-plete atrioventricular block (CAVB) [1]. In the majority ofcases, low cardiac output caused by decreased heart rateis responsible for the symptoms. However in some casesbradycardia associated QT prolongation may lead to malignventricular tachyarrhythmias causing syncope [1, 2]. We,herein, reported a case with CAVB complicated with frequentepisodes of torsade de pointes (TdP) triggered by early pre-mature ventricular contractions (PVCs) despite normal QTintervals.

    2. Case Report

    A 73-year-old woman was admitted to our clinic for faintingand syncope. She had several episodes of syncope in the lastfew hours. She was on oral antidiabetics for diabetes mellitusand ramipril for hypertension. Her past medical historywas otherwise normal. On initial physical examination, shewas bradycardic (36 bpm), but alert and fully oriented. Herblood pressure was 100/70mmHg. The physical examinationwas otherwise normal. Her initial electrocardiogram (ECG)showed CAVB with a rate of 38 bpm and with frequent

    PVCs (Figure 1). Her blood chemistry was normal. Bedsideechocardiogram revealed no structural heart disease. Whilebeing monitored in the coronary intensive care unit shesuddenly developed TdP leading to syncope which requiredDC cardioversion for termination (Figure 2). She had severalother episodes of sustained and nonsustained TdP untiltransvenous temporary pacemaker was in effect. All TdPepisodes were triggered by an early PVC which hit thedescending portion of the Twave on ECG (Figure 3). Increas-ing the heart rate by temporary cardiac pacing completelyabolished the PVCs and TdP episodes. Coronary angiogramshowed noncritical atherosclerotic plaques and ventriculartachycardia (VT) was not induced with electrophysiologystudy. The patient was further treated with a dual permanentpacemaker. The 6-month follow-up was uneventful.

    3. Discussion

    The term TdP refers to a VT characterized by QRS complexesof changing amplitude that appear to twist around theisoelectric line and occur at rates of 200 to 250/min. TdPduring bradyarrhythmias has been reported to be associatedwith gender, degree of QT prolongation and duration of

    Hindawi Publishing CorporationCase Reports in CardiologyVolume 2016, Article ID 7919642, 3 pageshttp://dx.doi.org/10.1155/2016/7919642

  • 2 Case Reports in Cardiology

    Figure 1: ECG showed CAVB with frequent PVCs. ECG: electrocardiogram, PVCs: premature ventricular contractions.

    Figure 2: Bedside monitor showed TdP. TdP: torsade de pointes.

    bradyarrhythmia. Between 5% and 30% of patients withCAVB have been reported to develop TdP [1]. Althoughmany predisposing factors have been cited for TdP, the mostcommon causes are congenital syndromes, severe bradycar-dia, potassium depletion, and use of medication such as classIA, IC, or III antiarrhythmic drugs [1, 2].

    In patients with bradycardia-induced TdP, a numberof ECG parameters during bradycardia are correlated withincreased risk of TdP including QT interval, T wave mor-phology, and T peak to T end (Tp-Te) [2, 3]. Although ECGparameters can be reasonable predictors of TdP in brad-yarrhythmias, there are limited data on cellular or geneticmechanisms of bradycardia-induced TdP [4, 5].

    CAVB may lead to downregulation of potassium chan-nels, QT interval prolongation, and TdP [6]. However, QTcand serum potassium levels were within normal limits inthis case. Genetic factors and female gender might have animportant role as risk factors for this patient. In addition,electrocardiogram showed us VPCs in which R waves super-imposed on T waves as “R-on-T” phenomenon (Figure 3).We believed that these early beats were triggering TdP.

    The “R-on-T” phenomenon was first described by Smirkin 1949. He described the early beats as precursors forventricular fibrillation and sudden death [7].

    Fries et al. [8] reported the incidence of “R-on-T” phe-nomenon in patients with implantable cardioverter defibril-lators. The study showed that 15% of VPCs initiated VT. Ofthe VPCs that led to VT, 16% occurred on the ascendinglimb, 23% on top, and 61% on the descending limb of the Twave. VPCs leading to TdP were more likely to occur on thedescending limb of the preceding T wave as seen in our case(Figure 3) [8].

    In conclusion, acquired CAVB may sometimes induceTdP and the episodes of TdP result in syncope, cardiacarrest, and even death due to degeneration into ventric-ular fibrillation. PVCs especially “R-on-T” phenomenonshould alert physicians as precursors for ventricular fibril-lation and sudden death. Early recognition and implanta-tion of cardiac pacemaker can be lifesaving. Meanwhile allattempts should be made for findings of any underlyingcauses.

  • Case Reports in Cardiology 3

    Figure 3: A TdP episode triggered by an early PVC which hit the descending portion of the T wave on ECG. ECG: electrocardiogram, TdP:torsade de pointes.

    Competing Interests

    The authors declare that they have no competing interests.

    References

    [1] G. Jensen, B. Sigurd, and E. Sandoe, “Adams-stokes seizures dueto ventricular tachydysrhythmias in patients with heart block:prevalence and problems of management,” Chest, vol. 67, no. 1,pp. 43–48, 1975.

    [2] T. Kurita, T. Ohe, N. Marui et al., “Bradycardia-induced abnor-mal QT prolongation in patients with complete atrioventricularblock with torsades de pointes,” The American Journal ofCardiology, vol. 69, no. 6, pp. 628–633, 1992.

    [3] I. Topilski, O. Rogowski, R. Rosso et al., “Themorphology of theQT interval predicts torsade de pointes during acquired brad-yarrhythmias,” Journal of the American College of Cardiology,vol. 49, no. 3, pp. 320–328, 2007.

    [4] H. Yoshida,M.Horie, H. Otani, T. Kawashima, Y. Onishi, and S.Sasayama, “Bradycardia-induced long QT syndrome caused bya de novomissense mutation in the S2-S3 inner loop of HERG,”American Journal of Medical Genetics, vol. 98, no. 4, pp. 348–352, 2001.

    [5] P. Chevalier, C. Bellocq, G. Millat et al., “Torsades de pointescomplicating atrioventricular block: evidence for a geneticpredisposition,” Heart Rhythm, vol. 4, no. 2, pp. 170–174, 2007.

    [6] P. G. A. Volders, K. R. Sipido, M. A. Vos et al., “Downregulationof delayed rectifier K+ currents in dogs with chronic completeatrioventricular block and acquired torsades de pointes,” Circu-lation, vol. 100, no. 24, pp. 2455–2461, 1999.

    [7] F. H. Smirk, “R waves interrupting T waves,” British HeartJournal, vol. 11, no. 1, pp. 23–36, 1949.

    [8] R. Fries, M. Steuer, H.-J. Schäfers, and M. Böhm, “The R-on-T phenomenon in patients with implantable cardioverter-defibrillators,”American Journal of Cardiology, vol. 91, no. 6, pp.752–755, 2003.

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