Left ventricular function during the early and late stages of scar formation following experimental myocardial infarction.
Left ventricular function during the early and late stages of scar formation following experimental myocardial infarction.
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实验性心肌梗死后疤痕形成早期和晚期的左心室功能。
DOI：
10.1016/0002-8703(70)90424-2
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发表时间：
1970
影响因子：
4.8
通讯作者：
T. Regan
中科院分区：
文献类型：
--
作者：
A. Weisse;R. S. Saffa;G. E. Levinson;W. W. Jacobson;T. Regan
为了评价心肌梗死（MI）后左心室（LV）功能的变化，对麻醉闭胸犬进行了研究，观察了左冠状动脉主干任一分支导管电极上形成血栓诱发急性非大面积MI后的存活情况。在MI后3至4周（早期瘢痕形成）和MI后6至8周（晚期瘢痕形成）对7只犬进行了研究。10只心率和主动脉压与MI组相似的正常犬作为对照。在静息状态和血管紧张素后负荷期间评估左心室功能。在疤痕形成的早期和晚期，梗死心室具有正常的舒张末期容积和正常的等容速度-力长度关系，但静息舒张末期压升高。MI后左室射血率功能（每搏功率、平均射血率和平均环周纤维缩短率）降低，6 - 8周差异具有统计学意义。两个梗死组之间无显著差异。随着后负荷的增加，当每搏功与左室舒张末期压作图时，心肌梗死后左室功能出现下降，但与舒张末期周长作图时，左室功能没有下降。因此，尽管其长度-张力（Frank-Starling）特征和等容速度-力-长度（收缩力）关系没有改变，但愈合的梗死心室在射血期间缩短速度降低，LV舒张末期压增加，在没有心脏失代偿证据的情况下，可能反映了顺应性降低。
To evaluate changes in left ventricular (LV) function after myocardial infarction (MI), anesthetized closed-chest dogs were studied following survival from acute nonmassive MI induced by thrombus formed on a catheter electrode in either branch of the left main coronary artery. Seven dogs were studied 3 to 4 weeks after MI (early scar formation) and 12 dogs 6 to 8 weeks after MI (late scar formation). Ten normal dogs with heart rates and aortic pressures similar to the MI groups served as controls. LV function was evaluated at rest and during afterloading with angiotensin.In both the early and late stages of scar formation, the infarcted ventricles had normal end-diastolic volumes and normal isovolumetric velocity-force length relationships but elevated resting end-diastolic pressures. LV ejection-rate functions (stroke power, mean rate of ejection, and mean rate of circumferential fiber shortening) were reduced after MI, the differences becoming statistically significant by 6 to 8 weeks. There were no significant differences found between the two infarct groups. With augmented afterloading, LV function after MI appeared depressed when stroke work was plotted against LV end-diastolic pressure but not when plotted against end-diastolic circumference. Thus, although its length-tension (Frank-Starling) characteristics and isovolumetric velocity-force-length (contractility) relationships were not altered, the healing infarcted ventricle exhibited reduced velocity of shortening during ejection and increased LV end-diastolic pressure which, in the absence of evidence of cardiac decompensation, probably reflects a reduced compliance.