Kolh P, Lambermont B, Ghuysen A, D'Orio V, Gerard P, Morimont P, Tchana-Sato V, Piérard L, Dogné J M, Limet R
Hemodynamic Research Center (HemoLiège), University of Liège, Liège, Belgium.
Int Angiol. 2003 Jun;22(2):148-58.
Myocardial revascularisation being frequently performed during acute myocardial ischemia, in a hostile hemodynamic environment, we evaluated left ventriculo-arterial (VA) coupling, left ventricular (LV) mechanical efficiency, and the mechanical properties of the systemic vasculature during acute myocardial ischemia.
In 6 pigs, vascular properties [characteristic impedance (R(1)), peripheral resistance (R(2)), compliance (C), inductance (L), arterial elastance (E(a))] were estimated with a windkessel model. LV function was assessed by the slope (E(es)) of end-systolic pressure-volume relationship (ESPVR), and stroke work (SW) - end-diastolic volume (EDV) relation. Pressure-volume area (PVA) was referred to as myocardial oxygen consumption. VA coupling was defined as E(es)/E(a), and mechanical efficiency as SW/PVA. After baseline recordings, the left anterior descending coronary artery was ligated and hemodynamic measures obtained every 30 minutes for 3 hours. Data are expressed as mean (SEM).
Coronary occlusion induced an ESPVR rightward shift, and decreased E(es) from 3.67 (0.33) to 1.92 (0.20) mmHg/ml and the slope of the SW - EDV relationship from 72.3 (3.4) to 40.4 (4.5) mmHg (p<0.001), while E(a) increased from 3.33 (0.56) to 4.65 (0.29) mmHg/ml (p<0.005). This was responsible for a dramatic alteration of VA coupling from 1.22 (0.11) to 0.44 (0.07), (p<0.001). While R2 increased from 1.72 (0.30) to 2.38 (0.16) mmHg x s x ml(-1) (p<0.05) and C decreased from 0.78 (0.16) to 0.46 (0.08) ml/mmHg (p<0.05), R(1) and L were unchanged. Coronary occlusion decreased SW from 4056 (223) to 2580 (122) mmHg.ml (p<0.001), while PVA and SW/PVA decreased from 5575 (514) to 4813 (317) mmHg x ml (NS), and from 0.76 (0.04) to 0.57 (0.03) (p<0.001), respectively.
Acute myocardial ischemia severely altered left ventriculo-arterial coupling and LV mechanical efficiency. Impaired left VA coupling was due to a combination of augmented arterial elastance, secondary to early vasoconstriction later associated with decreased arterial compliance, and decreased LV contractility.
在急性心肌缺血且血流动力学环境恶劣的情况下，心肌血运重建术常被实施，我们评估了急性心肌缺血期间左心室 - 动脉（VA）耦合、左心室（LV）机械效率以及体循环血管的力学特性。
在6头猪中，用风箱模型估算血管特性[特征阻抗（R(1)）、外周阻力（R(2)）、顺应性（C）、电感（L）、动脉弹性（E(a)）]。通过收缩末期压力 - 容积关系（ESPVR）的斜率（E(es)）以及每搏功（SW） - 舒张末期容积（EDV）关系评估左心室功能。压力 - 容积面积（PVA）被视为心肌耗氧量。VA耦合定义为E(es)/E(a)，机械效率定义为SW/PVA。在基线记录后，结扎左前降支冠状动脉，每30分钟进行一次血流动力学测量，持续3小时。数据以平均值（标准误）表示。
冠状动脉闭塞导致ESPVR右移，E(es)从3.67（0.33）降至1.92（0.20）mmHg/ml，SW - EDV关系的斜率从72.3（3.4）降至40.4（4.5）mmHg（p<0.001），而E(a)从3.33（0.56）升至4.65（0.29）mmHg/ml（p<0.005）。这导致VA耦合从1.22（0.11）急剧改变为0.44（0.07），（p<0.001）。虽然R2从1.72（0.30）升至2.38（0.16）mmHg·s·ml(-1)（p<0.05）且C从0.78（0.16）降至0.46（0.08）ml/mmHg（p<0.05），但R(1)和L未改变。冠状动脉闭塞使SW从4056（223）降至2580（122）mmHg·ml（p<0.001），而PVA和SW/PVA分别从5575（514）降至4813（317）mmHg·ml（无显著性差异）以及从0.76（0.04）降至0.57（0.03）（p<0.001）。
急性心肌缺血严重改变了左心室 - 动脉耦合和左心室机械效率。左VA耦合受损是由于动脉弹性增加（继发于早期血管收缩，随后与动脉顺应性降低相关）以及左心室收缩力降低共同作用的结果。
