Diastolic mitral annular velocity during the development of heart failure.
OBJECTIVE
We sought to investigate the mechanism of reduced diastolic mitral annular velocity with diastolic dysfunction, despite elevated left atrial (LA) pressure.


BACKGROUND
The peak rate of left ventricular (LV) early diastolic filling (E) and velocity of the mitral annulus due to long-axis lengthening (E(M)) are reduced in mild diastolic dysfunction. With more severe dysfunction, E increases in response to increased LA pressures. In contrast, E(M) decreases, despite increased LA pressure.


METHODS
We studied eight dogs instrumented to measure LA pressure, LV pressure, and internal dimensions during the progressive development of heart failure (HF) produced by rapid pacing.


RESULTS
Early diastolic filling decreased after four days of pacing from 114 +/- 32 to 88 +/- 22 ml/s (p < 0.05), but with more severe HF, it progressively increased to 155 +/- 32 ml/s (p < 0.05). In contrast, E(M) progressively decreased from 44 +/- 12 mm/s during the control period to 24 +/- 8 mm/s after four weeks (p < 0.05). Although E(M) was related to the time constant of LV relaxation (tau) (R(2) = 0.85), E was not. The latter occurred coincident with termination of the early diastolic LA to LV pressure gradient during all conditions. In contrast, with increasing HF, E(M) was progressively delayed after LA to LV pressure crossover by 37 +/- 12 ms (p < 0.05). The time from E to E(M) was related to tau (R(2) = 0.97).


CONCLUSIONS
With slowed relaxation during the development of HF, E(M) is reduced and delayed so that it occurs after early, rapid filling. Thus, with slowed relaxation, E(M) does not respond to the early diastolic LA to LV pressure gradient, because it occurs when LV pressure is greater than or equal to LA pressure.
Hasegawa
Hiroshi
H
Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157-1045, USA.
Little
William C
WC
Ohno
Michiya
M
Brucks
Steffen
S
Morimoto
Atsushi
A
Cheng
Heng-Jie
HJ
Cheng
Che-Ping
CP
D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology*; D003971:Diastole / Q000502:physiology*; D004195:Disease Models, Animal; D004285:Dogs; D006325:Heart Atria / Q000503:physiopathology*; D006333:Heart Failure / Q000209:etiology* / Q000503:physiopathology*; D008944:Mitral Valve Insufficiency / Q000150:complications* / Q000503:physiopathology*; D009200:Myocardial Contraction / Q000502:physiology; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000150:complications* / Q000503:physiopathology*