第1个回答 2011-06-12
LV end-systolic elastance (ELV in mm Hg/mL) is an index
of contractility that is load independent.29 It is determined
invasively as follows: ELVLV end-systolic pressure/(end
systolic volumeV0), where V0 represents the volume (x axis)
intercept of the end-systolic pressure-volume relationship.
The noninvasive calculation is possible by 2 methods. In 1
method, V0 is ignored (VO is less than end-systolic volume),
ie, LV end-systolic pressure/end systolic volume. In the other,
systolic and diastolic blood pressures, EF, stroke volume,
preejection, and ejection periods are needed. Its normal
resting value is 2.31 mm Hg/mL. Therefore, the EA/ELV
ratio is normally 1.00.36. EA and ELV increase proportionately
with age in normal men, and their ratio remains
unchanged.30 Normal women show a higher increase in ELV
with age, so the ratio decreases slightly.31
In hypertensive men, EA and ELV are greater than in normal
control subject, but their ratio remains normal. Hypertensive
women develop a disproportionately greater increase in ELV,
so their ratio is significantly lower than normal subjects.32 In
patients with systolic heart failure, EA increases as a result of
increased peripheral vascular resistance, whereas ELV is decreased.
Thus, the EA/ELV ratio increases with reduced myocardial
efficiency.33 In DHF, both EA and ELV increase, and in
3 studies,34–36 the EA/ELV ratio was similar in DHF patients
compared with those with hypertension but not heart failure.
Therefore, the consensus from the published literature supports
the notion that abnormal ventricular-arterial coupling at
rest is not the culprit for developing DHF. However, 1 study
noted a reduced vasodilator reserve with exercise37; additional
data are needed during exercise for reliable
conclusions.
第3个回答 2011-06-02
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我也不太懂,但网上翻出来是这样的。