Tachycardia-Related Cardiomyopathy in Patients with Atrial Fibrillation

Abstract

During atrial fibrillation, an uncontrolled ventricular response may result in extensive changes in ventricular function and structure referred to as tachycardia-related cardiomyopathy [1–3]. These consequenses of tachyarrhythmia are crucial since it may be reversible with tachycardia rate or rhythm control. A detailed review of the present knowledge regarding tachycardia-related cardiomyopathy and therapy for rate control was published by the authors in 1998 [4]. Our present understanding of tachycardiainduced cardiomyopathy relies mainly on experiments in animal models. Sustained rapid atrial or ventricular pacing can produce severe biventricular systolic and diastolic dysfunction in animals. The heart failure is characterized by elevated ventricular filling pressures, impairment of left and right ventricular systolic function, increased left and right end-systolic and end-diastolic volumes, reduction of cardiac output, and elevation of systemic vascular resistance. The mechanisms responsible for the hemodynamic and structural changes associated with pacing-induced cardiomyopathy have not been fully elucidated. However, a potential role for abnormal calcium channel activity is likely. Myocyte action potentials show reduced membrane resting potential and upstroke velocity as well as prolonged duration at 90% repolarization. Action potential prolongation could be due to an absolute reduction in L-type calcium current flow into the myocyte, caused by reduced open probability of the channel. Once heart failure has developed in the clinical setting, additional adrenergic activation may initiate an important vicious cycle with further enhancement of ventricular response leading to further reduction of cardiac output and amplification of heart failure. Control of fast ventricular response is immediately beneficial in tachycardia-related cardiomyopathy. In animal models after termination of pacing, mean arterial pressures, cardiac output and systemic vascular resistance approach control levels within 48 hours. Left ventricular ejection fraction normalizes completely after 1–2 weeks. In clinical studies, a marked improvement in left ventricular function generally starts after 1 month of cessation of the tachycardia and may continue for another 6–8 months. Therefore, treatment of tachycardia should be the primary goal in those patients. Methods of rate control include drug therapy, complete AV junction ablation and AV node modification. In patients with structural heart disease, more aggressive therapeutic options like complete AV node ablation can be appropriate since in these patients the progression to congestive heart failure may be fast. Impairment of left ventricular function due to atrial fibrillation has been reported in all age groups, in structurally normal hearts, and in various types of structural heart disease. However, the prevalence of tachycardia-related cardiomyopathy is still matter of speculation and commonly considered to be very low. In a recently published substudy of the Ablate and Pace Trial, the prevalence of tachycardiarelated cardiomyopathy was determined in patients who were referred for complete AV junction ablation and consecutive pacemaker implantation for therapy of atrial fibrillation [5]. The authors examined patients who had reduced ejection fraction before atrioventricular ablation and determined how many of them had tachycardia-related cardiomyopathy, as evidenced by a normalization of their systolic function 3 and 12 months after ventricular rate control by AV junction ablation and right ventricular pacing. In this study, sixty-three out of a total of 161 patients had systolic dysfunction. Forty-eight of these patients had at least one follow-up echocardiographic study, and thus, were subject to study. It was found that 16 of the 48 patients had a marked improvement in the ejection fraction to a value higher than 45% following ventricular rate control by AV junction ablation. And although patients eligible for AV ablation are at high risk for tachycardia-related cardiomyopathy because many of them have not been able to obtain heart