1VT ,RAD,LAD,EPS,SNS,SCD,DC,VA,TdP,ICD,PVCs,PCV,MVO2,FG,PLT,PVC,LVH,MI,GP,VLP,LVOT
VT:vein thrombosis 静脉血栓
RAD:右房内径 right atrium diameter
LAD:左房内径 left atrium diameter...EPS:
SNS: 骶神经刺激
SCD:sudden cardiac death 心源性猝死
DC:树突状细胞
VA:Virtual Application 椎动脉
TdP:远红外线治疗灯;特定电磁波
PVCS:盆腔静脉淤血症pelvic venous congestion syndrome,
PCV:红细胞比积测定
MVO2:
FG:纤维蛋白原
PLT:血小板
PVC室性早搏
LVH: left ventricular hypertrophy 左心室肥大
MI:心梗
GP:膜糖蛋白;环境基因组计划
VLP:心室晚电位ventricular late potential;类病毒颗粒
LVOT:左心室流出道
RAD:右房内径 right atrium diameter
LAD:左房内径 left atrium diameter...EPS:
SNS: 骶神经刺激
SCD:sudden cardiac death 心源性猝死
DC:树突状细胞
VA:Virtual Application 椎动脉
TdP:远红外线治疗灯;特定电磁波
PVCS:盆腔静脉淤血症pelvic venous congestion syndrome,
PCV:红细胞比积测定
MVO2:
FG:纤维蛋白原
PLT:血小板
PVC室性早搏
LVH: left ventricular hypertrophy 左心室肥大
MI:心梗
GP:膜糖蛋白;环境基因组计划
VLP:心室晚电位ventricular late potential;类病毒颗粒
LVOT:左心室流出道
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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.
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2个回答 2011-06-11
我猜2楼是正确的
第3个回答 2011-06-02
1VT,RAD,小伙子,每股收益,视点、SCD、DC、VA,计划书,ICD,PVC,成品,付费,MVO2、PLT、PVC、LVH、心肌梗塞、车牌,LVOT大奖赛,
我也不太懂,但网上翻出来是这样的。
我也不太懂,但网上翻出来是这样的。