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 Table of Contents  
INTERESTING CASE REPORT
Year : 2018  |  Volume : 2  |  Issue : 3  |  Page : 174-178

Tachycardia-induced cardiomyopathy in a teenage boy


Department of Medicine, MGM Medical College, Aurangabad, Maharashtra, India

Date of Web Publication10-Dec-2018

Correspondence Address:
Dr. Rajesh Krishnachandra Shah
Shrikrishna Hospital' 223, Samarthnagar, Aurangabad, 431 - 001, Bihar
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jiae.jiae_83_17

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  Abstract 

Tachycardiomyopathy or tachycardia-induced cardiomyopathy (TIC) is a relatively rare but completely or partially treatable condition, where there is an impairment of left ventricular (LV) function secondary to chronic, continuous, or intermittent tachycardia, which presents as heart failure. It has been shown that the rate control by means such as cardioversion, negative chronotropic agents, and surgical- or catheter-based atrioventricular nodal ablation, depending on the etiology, resulted in significant improvement of systolic function. The diagnosis of TIC is entertained following the observation of improvement in LV systolic function, after necessary therapy to control the arrhythmia or heart rate. It is necessary that the clinicians should have a high index of suspicion while dealing with LV systolic dysfunction or dilated cardiomyopathy and should control the arrhythmia stringently. This case report describes a 14-year-old boy presenting with breathlessness of 18–24-month duration who had features of dilated cardiomyopathy on echocardiography. Impaired LV systolic function was due to fascicular ventricular tachycardia and he recovered completely after catheter-based ablation within a period of 5–6 months.

Keywords: Ablation therapy, cardiomegaly, cardiomyopathy, fascicular ventricular tachycardia, tachycardia-induced cardiomyopathy, tachycardiomyopathy


How to cite this article:
Shah RK. Tachycardia-induced cardiomyopathy in a teenage boy. J Indian Acad Echocardiogr Cardiovasc Imaging 2018;2:174-8

How to cite this URL:
Shah RK. Tachycardia-induced cardiomyopathy in a teenage boy. J Indian Acad Echocardiogr Cardiovasc Imaging [serial online] 2018 [cited 2019 Jan 16];2:174-8. Available from: http://www.jiaecho.org/text.asp?2018/2/3/174/247034




  Introduction Top


Tachycardia-induced cardiomyopathy (TIC) is a relatively rare condition, requiring high index of suspicion to treat the cause, as it is a completely or sometimes a partially treatable condition.


  Clinical Presentation Top


A 14-year-old boy presented on May 5, 2017, with breathlessness Grade II on and off fatigue and uneasiness since 1½–2 years.

On presentation, his pulse was 150/min and regular, with a systolic blood pressure of 80 mmHg. His heart sounds were normal and there were no clinical signs of heart failure. There was no history of any significant problem such as rheumatic heart disease. He was not involved in any active sports due to breathlessness.

His electrocardiogram (ECG) at presentation showed a heart rate of 151/min, with right bundle branch block (RBBB) and left anterior hemiblock with a narrow QRS complex, suggestive of fascicular ventricular tachycardia (FVT) [Figure 1].
Figure 1: Electrocardiogram on admission

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Echocardiography done immediately showed dilated chambers of the heart with the left ventricular (LV) internal diameter measuring 54 mm. The right ventricular (RV) basal diameter was 40 mm with poor LV and RV systolic function and an LV ejection fraction (LVEF) of 20%. On the first echocardiography, global longitudinal strain (GLS) was not performed [Videos 1-3 and [Figure 2]. The dilemma here was whether it was dilated cardiomyopathy causing arrhythmia or repeated arrhythmia causing dilated cardiomyopathy.
Figure 2: Right ventricular measurements on May 5th

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As he was hemodynamically stable, he was given tablet Metoprolol 25 mg and tablet torsemide 5 mg. The repeat ECG done in the intensive care unit (ICU) showed sinus rhythm with a heart rate of 70/min, LV hypertrophy, and global “T” wave inversion [Figure 3]. Repeat echocardiogram in the ICU, on May 7, 2017, showed the same changes, with LVEF of 20% and RV dysfunction.
Figure 3: Electrocardiogram on May 6th

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He was advised electrophysiology (EP) studies, which he underwent after 1 month. The echocardiogram before EP studies, i.e., on June 7, 2017, which was done at a different center showed a report mentioning LVEF of 45%, thus showing improvement within 1 month of control of tachycardia. The EP study confirmed the presence of FVT, and he underwent radiofrequency ablation for it.

Echocardiogram done after 2½ months, i.e., on June 25, 2017, showed mild improvement in LV Function, with LFEF of 46% and GLS of 11% [Videos 4-6 and [Figure 4] and [Figure 5].
Figure 4: Left ventricle size on July 25 2017

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Figure 5: Global longitudinal strain on July 25, 2017

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The LVEF by Simpson's method was done which showed EF of 46% [Figure 6] and [Figure 7]. The fractional area change (FAC) of the RV was 7.3% [Figure 8] and [Figure 9].
Figure 6: Simpson's end diastolic volume on July 25 2017

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Figure 7: Simpson's end systolic volume on July 25 2017

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Figure 8: Right ventricular fractional area change, end diastolic area on July 25, 2017

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Figure 9: Right ventricular fractional area change, end systolic area on July 25, 2017

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Echocardiogram done 5½ months later, i.e., on October 11, 2017, showed near normal LVEF of 53.3% and GLS of 14.5% [Videos 7-9 and [Figure 10] and [Figure 11]]. The summary of the changes seen is shown in [Table 1].
Figure 10: Left ventricular size on October 11, 2017

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Figure 11: Global longitudinal strain on October 11, 2017

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Table 1: Summary of Measurements in serial Echocardiograms

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The LVEF by Simpson's method showed LVEF of 53.3% [Figure 12] and [Figure 13]. The RV function also improved with a FAC of 33.8 [Figure 14] and [Figure 15].
Figure 12: Simpson's end diastolic volume on October 11, 2017

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Figure 13: Simpson's end systolic volume on October 11, 2017

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Figure 14: Right ventricular fractional area change, end systolic area on October 11, 2017

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Figure 15: Right ventricular fractional area change, end diastolic area on October 11, 2017

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  Discussion Top


Whipple et al. first described experimental TIC in 1962.[1] The condition was first coined by Gallagher.[2]

The term TIC or tachycardiomyopathy refers to impairment in LV function secondary to chronic tachycardia, which is partially or completely reversible once the tachyarrhythmia is controlled. TIC can occur both in experimental animals and in patients with tachyarrhythmia. It has been shown that the rate control by means of cardioversion, negative chronotropic agents, and surgical- or catheter-based atrioventricular (AV) node ablation, depending on the etiology, resulted in significant improvement of systolic function.[3]

TIC can occur with any type of chronic or frequently recurring atrial, AV, and VT. TIC can occur at any age. It has been reported in infants, children,[4] adolescents,[5] and adults.[6],[7]

FVT is also known as idiopathic VT, as it occurs in the absence of structural heart disease; it is the most common type of idiopathic VT arising from the LV and is seen in 10% of the VT. It is a reentrant type of tachycardia. It is nonresponsive to adenosine, vagal maneuvers, and lidocaine but responds best to verapamil. It usually occurs in young healthy patients between the ages of 15–40 years.[8] The distinguishing features of FVT are:[8]

  • It is a monomorphic VT and has AV dissociation, fusion, and captured beats, which help differentiate it from supra-VT with RBBB
  • The QRS duration is between 100 and 140 ms; thus, it is a narrow complex tachycardia as against the other types of VT
  • It has an RBBB pattern.


The exact incidence of TIC is not known. In patients with atrial fibrillation, approximately 25%–75% of those with LV dysfunction had some degree of TIC.[9],[10],[11],[12],[13]

Tachycardiomyopathy can be seen with very frequent premature ventricular contractions, VT of outflow tract of the RV, and fascicular tachycardia.[14],[15]

Pathophysiology

Underlying histologic changes are characterized by cardiomyocyte lengthening and hyperplasia, extracellular matrix changes, myocardial fibrosis, myofibril misalignment, loss of sarcomere register, and apoptosis.[16],[17]

The mechanisms of tachycardiomyopathy are not fully defined but include subclinical ischemia, abnormalities in energy metabolism, redox stress, and calcium overload.[3] In addition to poor LV systolic function, patients with TIC have a smaller LV end-diastolic dimension compared to patients with idiopathic dilated cardiomyopathy.[17],[18]

This profound cardiac dilatation is typically accompanied by RV and LV wall thinning, markedly elevated ventricular filling pressures, and decreased contractile state with severe impairment of systolic function.[19],[20],[21],[22]

Certain important facts about tachycardia-induced cardiomyopathy

  1. Tachycardiomyopathy usually develops at heart rates above 100/min; faster the rate, higher the chances of development of TIC
  2. It is more common with ventricular rather than atrial arrhythmias, and it develops faster with ventricular arrhythmias
  3. Incessant ectopic atrial tachycardia is a less common cause of tachycardiomyopathy. It accounts for 5% of cases of tachycardiomyopathy in adults and 14% in children[23]
  4. It is more common and faster with continuous tachycardia than intermittent tachycardia
  5. The time of onset cannot be predicted
  6. The maximum recovery is usually within the 1st month, but recovery can occur up to 1 year
  7. The presence of mitral regurgitation (MR) begets MR, facilitating development of TIC
  8. Recurrence of arrhythmia induces LV systolic dysfunction faster.



  Conclusion Top


TIC is a relatively rare condition, requiring a high index of suspicion to treat the cause, as it is a completely or sometimes a partially treatable condition.

The diagnosis of TIC is not always simple, but the treating physician should have a high index of suspicion and should start therapy if the patient suffers from congestive heart failure with tachyarrhythmias. This is because LV dysfunction may recover after adequate treatment and it is the only way to make a definite diagnosis of tachycardiomyopathy.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Whipple GH, Sheffield LT, Woodman EG. Reversible congestive heart failure due to chronic rapid stimulation of the normal heart. Pro N Engl Cardiovasc Soc 1962;20:39-40.  Back to cited text no. 1
    
2.
Gallagher JJ. Tachycardia and cardiomyopathy: the chicken-egg dilemma revisited. J Am Coll Cardiol. 1985; 6:1172–1173.  Back to cited text no. 2
    
3.
Mohamed HA. Tachycardia-induced Cardiomyopathy (Tachycardiomyopathy). Libyan J Med 2007;2:26–9.  Back to cited text no. 3
    
4.
Juneja R, Shah S, Naik N, Kothari SS, Saxena A, Talwar KK. Management of cardiomyopathy resulting from incessant supraventricular tachycardia in infants and children. India Heart J 2002;54:176-80.  Back to cited text no. 4
    
5.
Walker NL, Cobbe SM, Birnie DH. Tachycardiomyopathy: A diagnosis not to be missed. Heart 2004;90.  Back to cited text no. 5
    
6.
Calo L, Sciarra L, Scioli R, Lamberti F, Loricchio ML, Pandozi C, et al. Recovery of cardiac function after ablation of atrial tachycardia arising from the tricuspid annulus. Ital Heart J 2005;6:652-7.  Back to cited text no. 6
    
7.
Salemi VM, Arteaga E, Mady C. Recovery of systolic and diastolic function after ablation of incessant supraventricular tachycardia. Eur J Heart fail 2005;7:1177-9.  Back to cited text no. 7
    
8.
Edhouse J, Morris F. ABC of clinical electrocardiography: Broad complex tachycardia-Part II. BMJ 2002;324:776-9.  Back to cited text no. 8
    
9.
Geelen P, Goethals M, de Bruyne B, Brugada P. A prospective hemodynamic evaluation of patients with chronic fibrillation undergoing radiofrequency catheter ablation of the atrioventricular junction. Am J Cardiol 1997;80:1606-9.  Back to cited text no. 9
    
10.
Fenelon G, Wijns W, Andries E, Brugada P. Tachycardiomyopathy: mechanisms and clinical applications. Pacing Clin Electrophysiol. 1996;19:95-106.  Back to cited text no. 10
    
11.
Rodrigues LM, Smeets JL, Xie B. Improvement in left ventricular function by ablation of atrioventricular nodal conduction in selected patients with lone atrial fibrillation. Am J Cardio 1993;72:1137-41.  Back to cited text no. 11
    
12.
Redfield MM, Kay GN, Jenkins LS, Mianulli M, Jensen DN, Ellenbogen KA. Tachycardia-related cardiomyopathy: A common cause of ventricular dysfunction in patients with atrial fibrillation referred for atrioventricular ablation. Mayo Clin Proc 2000;75:790-5.  Back to cited text no. 12
    
13.
Grogan M, Smith HC, Gersh BJ, Wood DL. Left ventricular dysfunction due to atrial fibrillation in patients initially believed to have idiopathic dilated cardiomyopathy. Am J Cardiol 1992;69:1570-3.  Back to cited text no. 13
    
14.
Vijgen J, Hill P, Biblo LA, Carlson MD. Tachycardia-induced cardiomyopathy secondary to right ventricular outflow tract ventricular tachycardia: improvement of left ventricular systolic function after radiofrequency catheter ablation of the arrhythmiaJ Cardiovasc Electrophysiol 1997;8:445-50.  Back to cited text no. 14
    
15.
Shinbane JS, Wood MA, Jensen DN, Ellenbogen KA, Fitzpatrick AP, Scheinman MM, et al. Tachycardia-induced cardiomyopathy: a review of animal models and clinical study. J Am Coll Cardiol 1997;29:709-15.  Back to cited text no. 15
    
16.
Fenelon G1, Wijns W, Andries E, Brugada P. Tachycardiomyopathy: mechanisms and clinical implications. Pacing Clin Electrophysiol. 1996 Jan;19:95-106.  Back to cited text no. 16
    
17.
Ellis ER, Josephson ME. “Heart failure and tachycardia-induced cardiomyopathy”. Current Heart Failure Reports 2013;10:296-306.  Back to cited text no. 17
    
18.
Gopinathannair R, Etheridge SP, Marchlinski FE, Spinale FG, Lakkireddy D, Olshansky B. “Arrhythmia-Induced Cardiomyopathies: Mechanisms, Recognition, and Management”. Journal of the American College of Cardiology. 2015;66:1714-28.  Back to cited text no. 18
    
19.
Patel HJ, Pilla JJ, Polidori DJ, Pusca SV, Plappert TA, Sutton MS, et al. Ten weeks of rapid ventricular pacing creates a long-term model of left ventricular dysfunction. J Thorac Cardiovasc Surg 2000;119:834-41.  Back to cited text no. 19
    
20.
Tanaka R, Spinale FG, Crawford FA, Zile MR. Effect of chronic supraventricular tachycardia on left ventricular function and structure in newborn pigs. J Am Coll Cardiol 1992;20:1650-60.  Back to cited text no. 20
    
21.
Zellner JL, Spinale FG, Eble DM, Hewett KW, Crawford FA., Jr. Alterations in myocyte shape and basement attachment with tachycardia-induced heart failure. Circ Res 1991;69:590-600.  Back to cited text no. 21
    
22.
Ohio M, Cheng CP, Little WC. Mechanisms of altered patterns of left ventricular filling during the development of congestive heart failure. Circulation 1994;89:2241-50.  Back to cited text no. 22
    
23.
Tracy CM. Arrhythmia-induced cardiomyopathy 2016. p. 1-20. Available from: https://www.uptodate.com/contents/arrhythmia-induced-cardiomyopathy. [Last cited on 2017 Dec 14].  Back to cited text no. 23
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10], [Figure 11], [Figure 12], [Figure 13], [Figure 14], [Figure 15]
 
 
    Tables

  [Table 1]



 

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