In order to bring you the best possible user experience, this site uses Javascript. If you are seeing this message, it is likely that the Javascript option in your browser is disabled. For optimal viewing of this site, please ensure that Javascript is enabled for your browser.
Did you know that your browser is out of date? To get the best experience using our website we recommend that you upgrade to a newer version. Learn more.

We use cookies to optimise the design of this website and make continuous improvement. By continuing your visit, you consent to the use of cookies. Learn more

Tachycardia-induced cardiomyopathy

An article from the E-Journal of the ESC Council for Cardiology Practice

Tachycardia-induced cardiomyopathy is a reversible cause of heart failure and dilated cardiomyopathy. Tachycardia-induced cardiomyopathy should be considered in all patients with a dilated cardiomyopathy of uncertain origin and who have tachycardia or atrial fibrillation with a fast ventricular rate. Abolishing tachycardia with drugs or catheter ablation often results in clinical improvement and ventricular function recovery.

Arrhythmias


Background

Congestive heart failure is one of the major health care problems in western countries. Its prevalence is increasing and, together with diabetes and atrial fibrillation, it is considered one of the three cardiovascular epidemics of the third millennium, emphasising the importance of diagnosing potentially reversible etiologies of heart failure.
Tachycardia induced cardiomyopathy (TIC) is defined as systolic and/or diastolic ventricular dysfunction resulting from a prolonged elevated heart rate which is reversible upon control of the arrhythmia or the heart rate. TIC has been reported in both experimental models and in patients with incessant or very frequent tachyarrhythmia. Experimental animal models with sustained rapid pacing can produce severe biventricular systolic dysfunction. Whipple et al. established the first experimental model for biventricular systolic dysfunction in 1962 (1) and his model has since been used for many further studies on this topic. In the clinical setting, TIC is usually seen in patients with no previous structural heart disease, although it may be responsible for ventricular dysfunction aggravation in those with underlying heart disease (2).  Data from several studies and from case reports have shown that rate control by cardioversion, negative chronotropic agents, catheter ablation or antitachycardia pacing results in improvement of the ventricular systolic function.

I - Pathophysiology

The normal heart rate in humans is between 55 and 95 beats per minute (3). The sustained heart rate limit above which TIC will appear is not well established. However, a prolonged heart rate above 100 beats per minute may be relevant (4) and deserves attention. TIC may manifest months to years after the onset of the responsible tachycardia, but because TIC is a rate dependent cardiomyopathy, those patients with higher tachycardia rates develop TIC earlier (5,6). Time to onset of ventricular dysfunction is also dependent on the presence of an underlying structural heart disease. Other factors include the type and duration of tachyarrhythmia, the patient’s age, drugs, and coexisting medical conditions (7).
High ventricular rates initially result in cardiac dilatation and mitral regurgitation, which are typically associated with elevated ventricular filling pressures, decreased contractility, right and left ventricular wall thinning, and, eventually, heart failure with neurohormonal activation. Cardiac output is usually reduced, and systemic vascular resistances are typically elevated (8). In experimental models, some of these changes can be seen as early as 24-48 hours after rapid cardiac pacing with continuing deterioration in ventricular function for up to 3-5 weeks.
Abnormal calcium handling, reduced cellular energy storing, and abnormal energy use have been proposed as the underlying mechanisms responsible for this syndrome. These mechanisms determine myocardial remodeling. Cellular changes include loss of myocytes, cellular elongation, myofibril misalignment, and loss of sarcomere register, which may be due to derangement of the extracellular matrix (9).

Table 1 : Described arrhythmias associated with tachycardiomyopathy

  • Supraventricular causes

Atrial tachycardia
Atrial flutter
Atrual fibrillation
Atrioventricular nodal reentry tachycardia
Atrioventricular tachycardia
Permanent junctional reciprocating tachycardia
Atrial pacing at high rates

  • Ventricular causes

Premature ventricular complexes
Right ventricular outflow tachycardia (VT)
Idiopathic left ventricular tachycardia
Bundle-branch reentry VT
Ventricular pacing at high rates

 
II - Clinical features and diagnosis

TIC may present itself at any age and has been reported as a result of various tachyarrhythmia mechanisms (TABLE I [10-14]). Supraventricular tachycardias are more frequently involved than ventricular arrhythmias (fig. 1).

Figure 1. Incessant supraventricular tachycardia due to atrioventricular reentry by a concealed accessory pathway in a young male. The tachycardia is terminated following adenosine infusion but with almost immediate spontaneous reinitiation

However, more recently TIC has also been described as a result of frequent ventricular ectopic beats. This has been explained by the asynergic and inefficient left ventricular contraction of the ectopic beats, which is similar to that reported in patients with left bundle branch block or right ventricular pacing. The resulting abnormal left ventricular torsion may cause disruption and further progression of asynergic left ventricular wall motion.
The diagnosis of TIC requires awareness about this condition, as the underlying arrhythmia may not always be apparent. It should be suspected in patients with structural heart disease and heart failure who suffer from chronic or frequently recurring tachyarrhythmias and in all patients with no other obvious explanation for ventricular dysfunction. The diagnosis of TIC in this latter setting can be only confirmed after cardiac function restoration following tachycardia or heart rate control (fig. 2).  (15,16).
Figure 2. Chest xray images of the same patient of figure 1 wich were taken on admission (left panel) and 3 months after (right panel) successful ablation of the accessory pathway. Significant resolution of cardiomegaly is apparent.


 

III- Treatment

Heart rate normalisation, either with rate or rhythm control, is the cornerstone of therapy in TIC. Most of the data available come from patients with atrial fibrillation. In this setting, normalisation of heart rate using any of the two methods (rate or rhythm control) improves systolic function. However, in other clinical scenarios, TIC treatment should be directed to termination of the responsible arrhythmia and to treating heart failure. This approach may include antiarrhythmic drug therapy and DC cardioversion, although, due to the serious potential consequences of this syndrome, a definitive cure to the arrhythmia as can be obtained with a catheter ablation, should be pursued whenever possible (17). Atrioventricular junction conduction ablation followed by pacemaker implantation is also an option for those patients in whom a definitive cure cannot be obtained by other means. However, it has recently been suggested that even heart rate control using this latter approach is inferior in terms of left ventricular ejection fraction recovery to catheter ablation of the arrhythmia substrate (fig. 3) (18) .

Figure 3. Ejection fraction improvement following pulmonary vein isolation and AV nodal ablation in patients with heart failure. (18)

IV - Prognosis

Ventricular dysfunction recovery in TIC patients following sinus rhythm restoration is variable. It depends on the rate and duration of the responsible arrhythmia. Both experimental models and some reports in humans (18-21), showed the greatest left ventricular ejection fraction recovery 1 month after arrhythmia cessation and a more gradual recovery reaching a complete normalisation up to one year thereafter, in some cases. Nevertheless, the impact of recurrent or new tachyarrhythmias on left ventricular function has been poorly assessed. This has been studied in a group of patients with TIC who were followed for 12 years (22) and those who had recurrent tachycardia had a rapidly declining left ventricular function, heart failure, and a high incidence of sudden cardiac death. 

Tachycardia-induced cardiomyopathy is a reversible cause of heart failure and dilated cardiomyopathy. Tachycardia-induced cardiomyopathy should be considered in all patients with a dilated cardiomyopathy of uncertain origin and who have tachycardias or atrial fibrillation with a fast ventricular rate. Abolishing tachycardia with drugs or catheter ablation often results in clinical improvement and ventricular function recovery.

Q and A

16 Jan. 2009 :

Question
Dr. Savaş Celebi
Ankara-Türkiye :

How can we discriminate tachycardia induced cardiomyopathy from those secondary tachycardias just following cardiomyopathy? For example TIC after atrial fibrillation vs atrial fibrillation due to cardiomyopathy?
 
Answer
Prof. Jose L. Merino

You can suspect TIC (or a component of TIC in a patient already with ventricular dysfunction due to other causes) when the patient presents with an almost incessant heart rate above 130 bpm and there is no apparent cause (infection, shock, etc) for it. Nevertheless, sometimes distinction between TIC and other causes of ventricular dysfunction can be very tricky and only possible after HR control. 

References


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.

2. V. Ramesh Iyer, MD. Ventricular Dysfunction: Tachycardia induced Cardiomyopathy. Indian Pacing and Electrophysiology Journal 2008 : Suppl. 1: S122-S129

3. Mark E. Josephson. Clinical cardiac electrophysiology. 3th ed. Philadelphia (PA): Lippincott Williams & Williams; 2002

4. Ernesto Umana, MD, C. Arturo Solares, MD, Martin A. Alpert, MD. Tachycardia-Induced Cardiomyopathy. Am J Med. 2003; 114:51–55.

5. Quiniou G, Chevalier JM, Barbou F, Bire F, Clementy J. Tachycardia-induced cardiomyopathy, unusual and reversible cause of left ventricular dysfunction: Report of 9 cases. Ann Cardiol Angeiol 2000; 49(5):301–308.

6. Shinbane JS,Wood MA, Jensen DN, Ellenbogen KA, Fitzpatrick AP, Scheinman MM. Tachycardia-induced cardiomyopathy: A review of animal models and clinical studies. J Am Coll Cardiol 1997; 29(4):709–715.

7. Fenelon G,Wijns W,Andries E, Brugada P. Tachycardiomyopathy: mechanisms and clinical applications. Pacing Clin Electrophysiol: 1996; 19:95-106.

8. 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.

9. Wilson J, Douglas P, Hickey W, et al. Experimental congestive heartfailure produced by rapid ventricular pacing in the dog: cardiac effects. Circulation. 1987;75:857–867.

10.  Yu YH, Bilezikian JP. Tachycardia-induced cardiomyopathy secondary to thyrotoxicosis: A young man with previously unrecognized Graves' disease. Thyroid 2000; 10(10):923–927.
11.  Chugh SS, Shen WK, Luria DM, Smith HC. First evidence of premature ventricular complex-induced cardiomyopathy: A potentially reversible cause of heart failure. J Cardiovasc Electrophysiol 2000; 11(3):328–329.

12.  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 arrhythmia. J Cardiovasc Electrophysiol 1997; 8(4):445–450.

13.  Singh B, Kaul U, Talwar KK, Wasir HS. Reversibility of "tachycardia-induced cardiomyopathy" following the cure of idiopathic left ventricular tachycardia using radiofrequency energy. Pacing Clin Electrophysiol 1996; 19(9):1391–1392.
14.  Ott P, Kelly PA, Mann DE, Damle RS, Reiter MJ, Lindefeld J.Tachycardia-induced cardiomyopathy in a cardiac transplant recipient: Treatment with radiofrequency catheter ablation. J Cardiovasc Electrophysiol 1995; 6(5):391–395.

15.  Redfeam DP, Hill JD, Keal R, Toff WD, Stafford PJ. Left ventricular dysfunction resulting from frequent unifocal ventricular ectopics with resolution following radiofrequency ablation. Europace 2003; 5:247–250.
16.  Leonardo Calo, Ermenegildo De Ruvo, Antonella Sette, Luigi Sciarra, Roberto Scioli, Francesco Sebastiani, Marco Topai, Renzo Iulianella, et al. Tachycardia-induced cardiomyopathy: mechanisms of heart failure and clinical implications. Journal of Cardiovascular Medicine 2007; 8: 3
17.  Wood MA, Brown-Mahoney C, Kay GN, Ellenbogen KA. Clinical outcomes after ablation and pacing therapy for atrial fibrillation. A meta analysis. Circulation 2000; 101:1138–1144.

18. Mohammed N. Khan, M.D., Pierre Jaïs, M.D., Jennifer Cummings,M.D.,Luigi Di Biase, M.D., Prashanthan Sanders, M.D., David O. Martin, M.D., et al. Pulmonary-Vein Isolation for Atrial Fibrillation in Patients with Heart failure. PABA- CHF. N Engl J Med 2008; 359: 1778-85

19.  Spinale FG, Holzgrefe HH, Mukherjee R, Arthur SR, Child MJ, Powell JR. Left ventricle and myocyte structure and function after early recovery from tachycardia-induced cardiomyopathy. Am J Physiol 1995; 268: 836–847.

20.  Yamamoto K, Burnett JC Jr, Meyer LM, Sinclair L, Stevens TL, Redfield MM. Ventricular remodeling during development and recovery from modified tachycardia-induced cardiomyopathy model. Am J Physiol 1996; 271: 1529–1534.

21.  Kessler G, Rosenblatt S, Friedman J, Kaplinsky E. Recurrent dilated cardiomyopathy reversed with conversion of atrial fibrillation. Am Heart J 1997; 133:384-6.

22.  Cruz F, Cheriex E, Smeets J, Atie J, Peres AK, Penn OC, Brugada P, Wellens HJ. Reversibility of tachycardia-induced cardiomyopathy after cure of incessant supraventricular tachycardia. J Am Coll Cardiol 1990; 16:739-744.

23.  Pamela Nerheim, MD; Sally Birger-Botkin, RN; Lubna Piracha, DO; Brian Olshansky, MD. Heart Failure and Sudden Death in Patients With Tachycardia-Induced Cardiomyopathy and Recurrent Tachycardia. Circulation. 2004; 110: 247-252

VolumeNumber:

Vol7 N°16

Notes to editor


Dr Jose L. Merino, FESC, Member of the Europace 2009 Programme
Arrhythmia Research Unit, Hospital Universitario La Paz, Madrid, Spain.
jlmerino@secardiologia.es

The content of this article reflects the personal opinion of the author/s and is not necessarily the official position of the European Society of Cardiology.