Tachycardia induced cardiomyopathy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and Keywords: chronotropic cardiomyopathy; tachycardiomyopathy; tachycardia mediated cardiomyopathy

Overview

Tachycardia induced cardiomyopathy is a decline in left ventricular function and left ventricular dilation as a result of chronic or frequently recurring paroxysmal tachycardia. The tachycardia can either be an atrial tachycardia or a ventricular tachycarrhythmia. Depending upon the duration of the tachycardia, the condition is either completely or partially reversible.

Historical Perspective

The relationship between tachycardia and a reversible decline in left ventricular dysfunction was first described by Phillips and Levine in 1949 [1].

Pathophysiology

Animal models demonstrate that sustained atrial or ventricular pacing results in dilation of all four cardiac chambers with thinning of the left and right ventricular walls. Both diastolic and systolic dysfunction develops in all four chambers as well [2]. The left ventricular wall thins, the cardiac output drops and the systemic vascular resistance (SVR)rises. Chronic tachcardia is associated with a prolongation of myocytelength [3]. Later in the course of the disease, mitral regurgiation may develop due to dilation of the mitral valve anulus.

As a result of the reduced cardiac output, there is activation of the neurohormonal axis with elevations of the following hormones:

Although the precise mechanism is not known, it has been speculated that the underlying mechanism of disease involves a depletion of myocardial energetics[4][5]. There also appear to be abnormalities in calcium handling and calcium channel activity that may explain the reduction in cardiac contractility[6] These abnormalities can persist up to 4 weeks after discontinuation of the tachycardia.

Causes

The following tachyarrhythmias have all been associated with the development of tachycardia induced cardiomyopathy:

Disorders that Tachycardia Induced Cardiomyopathy Must be distinguished From

Patients with atrial fibrillation and a very low left ventricular ejection fraction can be presumptively diagnosed as having an primary idiopathic dilated cardiomyopathy with secondary atrial fibrillation. Following aggressive rate control (pharmacologic and conversion of rhythm) in 10 patients initially diagnosed as having an idiopathic dilated cardiomyopathy, there was an improvement in left ventricular function at 30 months [7].

Epidemiology and Demographics

Tachycardia induced cardiomyopathy occurs in patients of all ages [8][9][10][11]

Estimates of the incidence of tachycardia induced cardiomyopathy among patients with atrial fibrillation vary widely from 25% to 75% in small series [12][13][14][15][16].

Risk Factors

The rate and duration of the elevation in heart rate necessary to cause a cardiomyopathy is unclear and is likely dependent on a number of other factors. It has been speculated that the rate, type, duration of the rhythm as well as the patient's age, and co-morbidities all play a role[17].

Natural History, Complications, and Prognosis

Depending upon the duration of the tachycardia, the condition is either completely or partially reversible after some time.[18] The pace of recovery of left ventricual dysfunctionis similar to that of hibernating myocardium [19]. It may take one year for instance for left ventricular function to recover [20][21]

Diagnosis

Resumption of normal or near normal left ventricular function following resolution of the tachycardia establishes the diagnosis. The diagnosis should be suspected if a patient was known to have normal LV function who sustains a decline in the setting of recurrent, paroxysmal or a chronic tachyarrhythmia. Holter monitoring can be useful to gauge the patients heart rate throughout 24 hours as the heart rate may vary tremendously with exercise and rest.

Treatment

The primary treatment for a tachycardia induced cardiomyopathy is correct the underlying tachycardia. This may include the use of:

Supportive agents such as ACE inhibitors / angiotensin receptor blockers are of benefit to try to prevent remodeling of the left ventricle.

References

  1. Phillips E, Levine SA. Auricular fibrillation without other evidence of heart disease: a cause of reversible heart failure. Am J Med 1949; 7:478-89.
  2. 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.
  3. 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.
  4. Spinale F, Tanaka R, Crawford F, Zile MR. Changes in myocardial blood flow during development of and recovery from tachycardia induced cardiomyopathy. Circulation 1992; 85:717-729.
  5. Shinabane 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; 29:709-15.
  6. O=Brien PJ, Ianuzzo CD, Moe GW, Stopps TP, Armstrong PW. Rapid ventricular pacing of dogs to heart failure: biochemical and physiological studies. Can J Physiol Pharmacol 1990; 68:34-9.
  7. 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.
  8. 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(3-4):176-80.
  9. 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(3-4):176-80.
  10. Calo L, Sciarra L, Scioli R, Lamberti F, Loricchio ML, Pandozi C, Santini M. Recovery of cardiac function after ablation of atrial tachycardia arising from the tricuspid annulus. Ital Heart J. 2005; 6(8):652-7.
  11. Salemi VM, Arteaga E, Mady C. Recovery of systolic and diastolic function after ablation of incessant supraventricular tachycardia. Eur J Heart fail. 2005 Dec; 7(7):1177-9.
  12. 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.
  13. Fenelon G,Wijns W,Andries E, Brugada P. Tachycardiomyopathy: mechanisms and clinical applications. Pacing Clin Electrophysiol 1996; 19:95-106.
  14. 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; 72:1137-1141.
  15. Redfield MM, Kay GN, Jenkins LS, Mianulli M, Jensen DN, Ellenbogen KA. Tachycardiarelated cardiomyopathy: a common cause of ventricular dysfunction in patients with atrial fibrillation referred for atrioventricular ablation. Mayo Clin Proc 2000; 75:790-795.
  16. 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.
  17. Fenelon G,Wijns W,Andries E, Brugada P. Tachycardiomyopathy: mechanisms and clinical applications. Pacing Clin Electrophysiol 1996; 19:95-106.
  18. Calo L, Sciarra L, Scioli R, Lamberti F, Loricchio ML, Pandozi C, Santini M. (2005). "Recovery of cardiac function after ablation of atrial tachycardia arising from the tricuspid annulus". Ital Heart J. 6 (8): 652–7. PMID 16161499.
  19. Rahimatoola SH. From coronary artery disease to heart failure: role of the hibernating myocardium. Am J Cardiol 1995; 75:16-22E.
  20. Fenelon G,Wijns W,Andries E, Brugada P. Tachycardiomyopathy: mechanisms and clinical applications. Pacing Clin Electrophysiol 1996; 19:95-106.
  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.


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