title: Determinants of LV diastolic function during atrial fibrillation: beat-to-beat analysis in acute dog experiments.
abstract: Left ventricular (LV) diastolic function during atrial fibrillation (AF) remains poorly understood due to the complex interaction of factors and beat-to-beat variability. The purpose of the present study was to elucidate the physiological determinants of beat-to-beat changes in LV diastolic function during AF. The RR intervals preceding a given cardiac beat were measured from the right ventricular electrogram in 12 healthy open-chest mongrel dogs during AF. Doppler echocardiography and LV pressure and volume beat-to-beat analyses were performed. The LV filling time (FT) and early diastolic mitral inflow velocity-time integral (E(vti)) were measured using the pulsed Doppler method. The LV end-diastolic volume (EDV), peak systolic LV pressure (LVP), minimum value of the first derivative of LV pressure curve (dP/dt(min)), and the time constant of LV pressure decay (tau) were evaluated with the use of a conductance catheter for 100 consecutive cardiac cycles. Beat-to-beat analysis revealed a cascade of important causal relations. LV-FT showed a significant positive linear relationship with E(vti) (r = 0.87). Importantly, there was a significant positive linear relationship between the RR interval and LV-EDV in the same cardiac beat (r = 0.53). Consequently, there was a positive linear relationship between LV-EDV and subsequent peak systolic LVP (r = 0.82). Furthermore, there were significant positive linear and negative curvilinear relationships between peak systolic LVP and dP/dt(min) (r = 0.95) and tau (r = -0.85), respectively, in the same cardiac beat. In addition, there was a significant negative curvilinear relationship between dP/dt(min) and tau (r = -0.86). We have concluded that the determinants of LV diastolic function in individual beats during AF depend strongly on the peak systolic LVP. This suggests that the major benefit of slower ventricular rate appears related to lengthening of LV filling interval, promoting subsequent higher peak systolic LVP and greater LV relaxation.
authors.affiliation: Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, OH 44195, USA. toomy@clin.med.tokushima-u.ac.jp
authors.forename: Tomotsugu
authors.initials: T
authors.lastname: Tabata
authors.forename: Richard A
authors.initials: RA
authors.lastname: Grimm
authors.forename: Junko
authors.initials: J
authors.lastname: Asada
authors.forename: Zoran B
authors.initials: ZB
authors.lastname: Popovic
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Yamada
authors.forename: Neil L
authors.initials: NL
authors.lastname: Greenberg
authors.forename: Don W
authors.initials: DW
authors.lastname: Wallick
authors.forename: Youhua
authors.initials: Y
authors.lastname: Zhang
authors.forename: Shaowei
authors.initials: S
authors.lastname: Zhuang
authors.forename: Kent A
authors.initials: KA
authors.lastname: Mowrey
authors.forename: James D
authors.initials: JD
authors.lastname: Thomas
authors.forename: Todor N
authors.initials: TN
authors.lastname: Mazgalev
mesh_terms: D000818:Animals; D001281:Atrial Fibrillation / Q000503:physiopathology*; D001810:Blood Volume; D003971:Diastole; D004285:Dogs; D015150:Echocardiography, Doppler; D006339:Heart Rate; D011312:Pressure; D013599:Systole; D016277:Ventricular Function, Left