Details

Autor(en) / Beteiligte

• Kistler, Peter M
• Sanders, Prashanthan
• Fynn, Simon P
• Stevenson, Irene H
• Spence, Steven J
• Vohra, Jitendra K
• Sparks, Paul B
• Kalman, Jonathan M

Titel

Electrophysiologic and electroanatomic changes in the human atrium associated with age

Ist Teil von

• Journal of the American College of Cardiology, 2004-07, Vol.44 (1), p.109-116

Ort / Verlag

New York, NY: Elsevier Inc

Erscheinungsjahr

2004

Quelle

MEDLINE

Beschreibungen/Notizen

• The purpose of this study was to characterize the pattern of atrial remodeling seen with human aging. Atrial fibrillation (AF) occurs in 3% to 4% of the population over 65 years of age. It is associated with thromboembolic complications, worsening heart failure, and increased mortality, yet the electrical and structural remodeling that occurs with human aging remains unknown. Thirteen patients (66.4 ± 1.7 years) ≥60 years (group A), 13 patients (50 ± 2.1 years) age 31 to 59 years (group B), and 15 patients (24.7 ± 1.0 years) ≤30 years (group C) underwent conventional electrophysiologic studies and electroanatomic mapping. We measured atrial refractoriness (ERP) at the distal coronary sinus (CS); low and high lateral right atrium (LRA) and the high septal right atrium at 600, 500, and 400 ms; maximum corrected sinus node recovery time (CSNRT); P-wave duration (PWD); conduction time (CT) along the CS and LRA; and discrete double potentials (DP) along the crista. Aging was associated with an increase in atrial ERP, prolonged CT along the CS, increased PWD and CSNRT. There was no significant change in dispersion of refractoriness or rate adaptation. Electroanatomic mapping revealed diffuse areas of low voltage with regional conduction slowing. Both techniques demonstrated a greater number of DPs and fractionated signals along the crista terminalis with aging. Aging is associated with regional conduction slowing, anatomically determined conduction delay at the crista, and structural changes that include areas of low voltage. In addition, impairment of sinus node function and an increase in atrial ERP occurred with aging. This electrical and structural remodeling may explain the increased propensity to AF with aging.