Background-We examined the hypothesis that retardation of apical filling as
measured by color M-mode Doppler echocardiography in the diseased left ven
tricle (LV) reflects a decrease in the intraventricular mitral-to-apical
Methods and Results-In 9 open-chest anesthetized dogs, micromanometers were
placed near the mitral tip and in the apical region. From the color M-mode
Doppler images, the time delay (TB) between peak velocity at the mitral ti
p and the apical region was determined as an index of LV flow propagation.
Acute ischemic LV failure was induced by coronary microembolization. Induct
ion of ischemia caused a marked increase in LV end-diastolic pressure and a
decrease in LV ejection fraction. The time constant of LV isovolumic apica
l pressure decay (tau) increased from 31+/-8 to 49+/-16 ms (P<0.001). The p
eak early diastolic mitral-to-apical pressure gradient (Delta PLVmitral-ape
x) decreased from 1.9+/-0.9 to 0.7+/-0.5 mm Hg (P<0.01), and TD increased f
rom 5+/-3 to 57+/-26 ms (P<0.001). The slowing of flow propagation was limi
ted to the apical portion of the LV cavity. The TD correlated with Delta PL
Vmitral-apex (r=-0.94, P<0.01) and with tau (r=0.92, P<0.01). Before ischem
ia, the mitral-to-apical flow propagation velocity far exceeded the velocit
y of the individual blood cells, whereas during ischemia, flow propagation
velocity approximated the blood
Conclusions-Retardation of apical filling acute ischemic failure was attrib
uted to a decrease in the mitral-to-apical driving pressure, reflecting slo
wing of LV relaxation. The slowing of flow propagation appeared to represen
t a shift in apical filling from a pattern of column motion to a pattern do
minated by convection.