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Circulation. 2004;110:897-903
Published online before print August 9, 2004, doi: 10.1161/01.CIR.0000139336.69955.AB
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(Circulation. 2004;110:897-903.)
© 2004 American Heart Association, Inc.


Original Articles

Remodeling of Sinus Node Function in Patients With Congestive Heart Failure

Reduction in Sinus Node Reserve

Prashanthan Sanders, MBBS, PhD; Peter M. Kistler, MBBS; Joseph B. Morton, MBBS, PhD; Steven J. Spence, ACCT; Jonathan M. Kalman, MBBS, PhD

From the Department of Cardiology, Royal Melbourne Hospital, and the Department of Medicine, University of Melbourne, Melbourne, Australia.

Correspondence to Professor Jonathan M. Kalman, Department of Cardiology, Royal Melbourne Hospital, Melbourne, Australia 3050. E-mail jon.kalman{at}mh.org.au

Received March 14, 2004; revision received May 4, 2004; accepted May 6, 2004.

Background— Experimental and clinical studies have demonstrated diffuse atrial remodeling in congestive heart failure (CHF). We hypothesized that patients with CHF would demonstrate derangement of sinus node function.

Methods and Results— Eighteen patients with symptomatic CHF (left ventricular ejection fraction, 26±5%) and 18 age-matched control subjects were studied. Under autonomic blockade, the following were evaluated: intrinsic sinus cycle length, corrected sinus node recovery time (CSNRT), sinoatrial conduction time, number and duration of fractionated electograms or double potentials along the crista terminalis, and location of the earliest sinus activity. Electroanatomic mapping was performed to evaluate the location and nature of the sinus node complex, to characterize sinoatrial propagation, and to evaluate conduction abnormalities and voltage amplitude along the crista terminalis. Patients with CHF demonstrated the following findings compared with age-matched control subjects: prolongation of the intrinsic sinus cycle length (P=0.005), prolongation of CSNRT (P<0.0001), caudal localization of sinus activity both during sinus rhythm (P=0.03) and after pacing (P=0.002), prolongation of sinoatrial conduction time (P=0.02), greater number (P<0.0001) and duration (P<0.0001) of fractionated electrograms or double potentials along the crista terminalis, loss of voltage amplitude along the crista terminalis (P=0.02), and abnormal and circuitous propagation of the sinus impulse.

Conclusions— This study demonstrates that patients with CHF have significant sinus node remodeling characterized by anatomic and structural changes along the crista terminalis with a reduction in functional sinus node reserve. This finding may have implications for the development of clinical bradycardia in CHF and for the use of negatively chronotropic agents and pacing in this condition.


Key Words: atrium • electrophysiology • heart failure • sinoatrial node • remodeling


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