Foster R E, Johnson D B, Barilla F, Blackwell G G, Orr R, Roney M, Stanley A W, Pohost G M, Dell'Italia L J
Birmingham Veteran Affairs Medical Center, University of Alabama at Birmingham, the Department of Medicine, 35294, USA.
Am Heart J. 1998 Aug;136(2):269-75. doi: 10.1053/hj.1998.v136.89405.
We evaluated global and segmental left ventricular (LV) mass and LV mass/volume ratio in patients with LV dysfunction receiving angiotensin-converting enzyme (ACE) inhibitor therapy after acute myocardial infarction (MI).
ACE inhibitors attenuate LV dilatation and compensatory hypertrophy after acute MI in animal models. However, LV remodeling in patients after acute MI has been largely defined on the basis of changes in chamber volume alone.
Twenty-nine patients with LV ejection fraction <40% received the ACE inhibitor ramipril (range 2.5 to 20 mg/day) within 5 days of their first Q-wave MI. Magnetic resonance imaging was performed at baseline and at 3 months, providing global and regional LV volumes and mass from summated serial short-axis slices. Mean arterial blood pressure was unchanged from baseline to 3-month follow-up (89 +/- 10 to 92 +/- 17 mm Hg). LV mass decreased (90 +/- 25 to 77 +/- 21 gm/m2, p < 0.0005) as LV end-diastolic volumes increased (65 +/- 13 to 73 +/- 22 ml/m2, p < 0.01). Global LV mass to volume ratio decreased from 1.40 +/- 0.28 to 1.08 +/- 0.18 gm/ml (p < 0.0001), as did circumferential wall thickness to volume ratio of noninfarcted myocardium at the base of the LV (0.06 +/- 0.02 to 0.05 +/- 0.02 mm/ml, p < 0.001). LV ejection fraction increased from 35 +/- 6 to 40 +/- 9% (p < 0.001) in the presence of an increase in calculated end-systolic wall stress (185 +/- 57 to 227 +/- 54 gm/cm2, p < 0.01).
ACE inhibitor therapy was associated with improved LV function in the face of a decrease in mass to volume ratio of the LV as well as a decrease in wall thickness to volume ratio of noninfarcted myocardium. Whether ACE inhibitor therapy had direct or indirect effects on these changes in LV mass and function are open questions that require further investigation.
我们评估了急性心肌梗死（MI）后接受血管紧张素转换酶（ACE）抑制剂治疗的左心室功能不全患者的整体和节段性左心室（LV）质量以及LV质量/容积比。
在动物模型中，ACE抑制剂可减轻急性MI后的左心室扩张和代偿性肥厚。然而，急性MI后患者的左心室重构在很大程度上仅基于心室容积的变化来定义。
29例左心室射血分数<40%的患者在首次Q波MI后5天内接受了ACE抑制剂雷米普利（剂量范围为2.5至20mg/天）治疗。在基线和3个月时进行磁共振成像，通过连续短轴切片总和获得整体和局部左心室容积及质量。从基线到3个月随访，平均动脉血压无变化（89±10至92±17mmHg）。随着左心室舒张末期容积增加（65±13至73±22ml/m²，p<0.01），左心室质量下降（90±25至77±21gm/m²，p<0.0005）。整体左心室质量与容积比从1.40±0.28降至1.08±0.18gm/ml（p<0.0001），左心室底部非梗死心肌的圆周壁厚度与容积比也下降（0.06±0.02至0.05±0.02mm/ml，p<0.001）。在计算的收缩末期壁应力增加的情况下（185±57至227±54gm/cm²，p<0.01），左心室射血分数从35±6增加至40±9%（p<0.001）。
ACE抑制剂治疗与左心室功能改善相关，同时左心室质量与容积比以及非梗死心肌的壁厚度与容积比降低。ACE抑制剂治疗对左心室质量和功能的这些变化是直接还是间接影响，仍是有待进一步研究的开放性问题。
