Kramer C M, Ferrari V A, Rogers W J, Theobald T M, Nance M L, Axel L, Reichek N
Department of Medicine, Medical College of Pennsylvania, Pittsburgh, USA.
J Am Coll Cardiol. 1996 Jan;27(1):211-7. doi: 10.1016/0735-1097(95)00429-7.
We hypothesized that angiotensin-converting enzyme inhibitors would limit dysfunction in the first 8 weeks after transmural infarction in adjacent noninfarcted regions, as well as attenuate left ventricular remodeling.
Angiotensin-converting enzyme inhibition limits ventricular dilation and hypertrophy and improves survival after anterior infarction, but its effect on regional function during remodeling is not well characterized.
Thirteen sheep underwent coronary ligation to create an anteroapical infarction. At postinfarction day 2, eight sheep were randomized to therapy with the angiotensin-converting enzyme inhibitor ramipril, and five sheep received no therapy. Animals were studied with magnetic resonance myocardial tagging before and 8 weeks after infarction. Left ventricular volume, mass and ejection fraction were measured, as were changes in percent circumferential shortening within the subendocardium and subepicardium of infarcted and noninfarcted myocardium, both adjacent to and remote from the infarction.
Angiotensin-converting enzyme inhibition limited the increase in end-diastolic volume from a mean (+/- SD) of +1.5 +/- 0.7 ml/kg in control animals to +0.5 +/- 0.8 ml/kg in the treated group (p < 0.04). Segmental function within infarcted and remote noninfarcted tissue did not differ between groups. However, angiotensin-converting enzyme inhibition limited the decline in function in the adjacent noninfarcted region 8 weeks after infarction. Percent circumferential shortening in the subendocardium decreased by -13 +/- 5% in the control group compared with -5 +/- 5% in the treated group (p < 0.03).
In concert with a reduction in left ventricular remodeling after anterior infarction, angiotensin-converting enzyme inhibition limits the decline in function in the adjacent noninfarcted region. Dysfunction in adjacent noninfarcted regions may be an important determinant of left ventricular remodeling after infarction.
我们推测血管紧张素转换酶抑制剂可限制透壁性心肌梗死后最初8周内相邻非梗死区域的功能障碍,并减轻左心室重构。
血管紧张素转换酶抑制可限制心室扩张和肥厚,并改善前壁心肌梗死后的生存率,但其对重构过程中局部功能的影响尚未得到充分描述。
13只绵羊接受冠状动脉结扎以造成前尖部心肌梗死。在心肌梗死后第2天,8只绵羊被随机分配接受血管紧张素转换酶抑制剂雷米普利治疗,5只绵羊未接受治疗。在梗死前和梗死后8周用磁共振心肌标记对动物进行研究。测量左心室容积、质量和射血分数,以及梗死心肌和非梗死心肌的心内膜下和心外膜下圆周缩短百分比的变化,包括梗死灶邻近和远离梗死灶的区域。
血管紧张素转换酶抑制将舒张末期容积的增加从对照组动物的平均(±标准差)+1.5±0.7 ml/kg限制到治疗组的+0.5±0.8 ml/kg(p<0.04)。梗死组织和远处非梗死组织的节段性功能在两组之间没有差异。然而,血管紧张素转换酶抑制限制了梗死后8周相邻非梗死区域功能的下降。对照组心内膜下圆周缩短百分比下降了-13±5%,而治疗组为-5±5%(p<0.03)。
与前壁心肌梗死后左心室重构的减少相一致,血管紧张素转换酶抑制限制了相邻非梗死区域功能的下降。相邻非梗死区域的功能障碍可能是心肌梗死后左心室重构的一个重要决定因素。