Takaoka H, Takeuchi M, Odake M, Hata K, Hayashi Y, Mori M, Yokoyama M
1st Department of Medicine, Kobe University School of Medicine, Japan.
Cardiovasc Res. 1994 Aug;28(8):1251-7. doi: 10.1093/cvr/28.8.1251.
The aim was to characterise the impaired myocardial mechanoenergetics in patients with heart failure due to old myocardial infarction by using the oxygen consumption versus left ventricular pressure--volume area (PVA) relationship.
The VO2-PVA relationship was assessed in 15 patients: group N consisted of seven patients with vasospastic angina pectoris whose left ventricular ejection fractions were normal [72 (SD 8)%], and group F consisted of eight patients with old myocardial infarction whose left ventricular ejection fractions were reduced [45(11)%]. Left ventricular volume and pressure were measured by the conductance catheter method. VO2 was measured by thermodilution.
Linear VO2-PVA relationships with dextran infusions were obtained in both groups (median r = 0.92 v 0.90). There was no difference in the slope between the two groups. There was a positive correlation between Emax and VO2 at median PVA (VO2,PVA0.8) in group N. Emax, an index of left ventricular contractility, was significantly smaller in group F than in group N, at 5.1(2.1) v 3.2(1.1) mm Hg.ml-1.m2; p < 0.05). On the other hand, the VO2 intercept in group F was comparable to that in group N, at 0.71(0.63) v 0.40(0.29) J x beat-1.100 g LV-1; NS). In addition, the ratio of VO2,PVA0.8 to Emax was significantly larger in group F than in group N: 0.55(0.14) v 0.89(0.37) J x beat-1.100 g LV-1.mm Hg-1.ml.m-2 (p < 0.05).
These results suggest that the VO2 for non-mechanical work in group F is disproportionately high relative to the reduced contractility. An abnormality of excitation-contraction coupling rather than of crossbridge cycling may be responsible for the impaired mechanoenergetics in patients with heart failure due to old myocardial infarction.
通过利用氧耗量与左心室压力-容积面积（PVA）的关系，对陈旧性心肌梗死所致心力衰竭患者受损的心肌机械能量学进行特征描述。
对15例患者的VO₂-PVA关系进行评估：N组由7例左心室射血分数正常的变异性心绞痛患者组成[72（标准差8）%]，F组由8例左心室射血分数降低的陈旧性心肌梗死患者组成[45（11）%]。采用电导导管法测量左心室容积和压力。通过热稀释法测量VO₂。
两组在输注右旋糖酐时均获得了线性VO₂-PVA关系（中位数r = 0.92对0.90）。两组之间斜率无差异。N组在中位数PVA（VO₂，PVA0.8）时Emax与VO₂呈正相关。Emax是左心室收缩性的指标，F组的Emax明显小于N组，分别为5.1（2.1）对3.2（1.1）mmHg·ml⁻¹·m²；p<0.05）。另一方面，F组的VO₂截距与N组相当，分别为0.71（0.63）对0.40（0.29）J·次⁻¹·100g左心室；无显著性差异）。此外，F组VO₂，PVA0.8与Emax的比值明显大于N组：0.55（0.14）对0.89（0.37）J·次⁻¹·100g左心室⁻¹·mmHg⁻¹·ml·m⁻²（p<0.05）。
这些结果表明，相对于收缩性降低，F组中非机械功的VO₂过高。兴奋-收缩偶联异常而非横桥循环异常可能是陈旧性心肌梗死所致心力衰竭患者机械能量学受损的原因。
