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J Am Coll Cardiol, 2003; 41:1590-1597, doi:10.1016/S0735-1097(03)00260-2
© 2003 by the American College of Cardiology Foundation
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Diastolic mitral annular velocityduring the development of heart failure

Hiroshi Hasegawa, MD, PhD*, William C. Little, MD*,*, Michiya Ohno, MD, PhD*, Steffen Brucks, MD*, Atsushi Morimoto, MD, PhD*, Heng-Jie Cheng, MD, PhD* and Che-Ping Cheng, MD, PhD*

* Cardiology Section, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA



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Figure 1 Plots of the peak left ventricar (LV) filling rate (E) and peak rate of longitudinal expansion (EM) to the peak early diastolic left atrial (LA) to LV pressure gradient during transient caval occlusions before and after heart failure (HF) was produced by four weeks of rapid pacing. Under normal conditions, both E and EM are strongly related to the pressure gradient, indicated by the slopes of the linear regression lines. The dependence of E on the pressure gradient is not altered by HF. In contrast, the dependence of EM on the pressure gradient is markedly reduced after HF.

 


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Figure 2 Analog recordings in a conscious animal before (normal) and after producing progressive heart failure (HF) with four weeks of rapid pacing. Shown are left atrial (LA) and left ventricular (LV) pressures (PLA/PLV), LV volume (VLV), and three LV internal dimensions: anteroposterior (DAP), septolateral (DSL), and long axis (DLA). Under normal conditions, the increase in LV volume during early diastolic filling occurs as all three dimensions expand symmetrically. Most of the increase in LV volume and expansion occurs before the crossover of PLV and PLA (dotted line). In contrast, after HF, the expansion of the long axis is delayed (arrows), occurring after PLA is greater than or equal to PLV, and most of the early diastolic increase in LV volume and expansion of the short-axis dimensions (DSL and DAP) is complete.

 


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Figure 3 Analog recordings of left ventricular (LV) and left atrial (LA) pressures (P), the rate of change of LV volume (dV/dt), and the long-axis dimensions of the LV (dDLA/dt) during the progressive development of pacing-induced heart failure (HF) in a conscious animal. The peak diastolic filling rate (E) declined with mild HF (four days) but progressively increased with more severe HF. In contrast, the peak expansion rate of DLA (EM) progressively declined with increasing HF. Under all circumstances, E coincided with the crossover of LA and LV pressures (dotted line). In contrast, the peak long-axis lengthening (EM) was progressively delayed, relative to E and LA/LV pressure crossover, with increasingly severe HF. Thus, starting after four days of pacing, EM occurred when LV pressure ≥LA pressure.

 


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Figure 4 The peak early diastolic left ventricular (LV) filling rate (E) and peak lengthening rate of the LV anteroposterior dimension (EAP) and septolateral dimension (ESL) were closely related to the peak early diastolic left atrial (LA) to LV pressure gradient during the development of heart failure (HF). In contrast, the peak long-axis lengthening rate (EM) progressively declined, despite the increase in the LA to LV pressure gradient during the development of HF.

 


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Figure 5 During the development of heart failure (HF), the peak early diastolic left ventricular (LV) filling rate (E) and peak lengthening rate of the LV anteroposterior dimension (EAP) and septolateral dimension (ESL) occurred nearly simultaneously with the crossover of LV and left atrial (LA) pressures. In contrast, the peak long-axis lengthening rate (EM) occurred progressively later during the development of HF.

 


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Figure 6 The peak early diastolic left ventricular (LV) filling rate (E) was not related to the time constant of LV pressure fall. In contrast, the peak long-axis lengthening rate (EM) and the time from E to EM were closely related to the time constant.

 





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