Tachycardia induced cardiomyopathy

Synonyms and Keywords: chronotropic cardiomyopathy, tachycardiomyopathy

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.

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. 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. 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:


 * Plasma cathecholamines
 * Atrial natriuretic peptide
 * Renin
 * Aldosterone

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

Epidemiology and Demographics
Tachycardia induced cardiomyopathy occurs in patients of all ages

Estimates of the incidence of tachycardia induced cardiomyopathy among patients with atrial fibrillation vary widely from 25% to 75% in small series.

Causes
Atrial fibrillation, atrial flutter, AV nodal reentry tachycardia, and ventricular tachycardia 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.

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.

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.

Treatment
The primary treatment for a tachycardia induced cardiomyopathy is correct the underlying tachycardia. This may include the use of:
 * Negative chronotropic agents such as beta blockers
 * Cardioversion
 * AV node ablation
 * Treatment of the underlying condition such as hyperthyroidism or atrial fibriallation

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

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