EARLY DILATION OF THE INFARCTED SEGMENT IN ACUTE TRANSMURAL MYOCARDIAL-INFARCTION - ROLE OF INFARCT EXPANSION IN ACUTE LEFT-VENTRICULAR ENLARGEMENT
EARLY DILATION OF THE INFARCTED SEGMENT IN ACUTE TRANSMURAL MYOCARDIAL-INFARCTION - ROLE OF INFARCT EXPANSION IN ACUTE LEFT-VENTRICULAR ENLARGEMENT
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DOI：
10.1016/s0735-1097(84)80203-x
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发表时间：
1984-01-01
影响因子：
24
通讯作者：
BULKLEY, BH
中科院分区：
文献类型：
--
作者：
ERLEBACHER, JA;WEISS, JL;BULKLEY, BH
心肌梗死后左心室扩大是一个不良的预后征兆，其机制尚未明确。早期左心室扩张可能是由于弗兰克-斯塔林效应，导致未梗塞节段的长度增加，以响应收缩性肌肉质量的减少。与这种适应性生理机制相反，左心室扩张也可能是由梗塞心肌节段拉伸和变薄（即梗塞扩张）的病理过程引起的。为了确定这两种机制对初始透壁前壁心肌梗死后左心室扩张的相对贡献，我们从心肌梗塞症状出现后 72 小时内的 27 名患者和 13 名健康对照受试者中获取了二维超声心动图。在乳头肌水平的短轴超声心动图视图中，使用基于微处理器的图形系统测量舒张末期心内膜前段和后段长度。乳头肌用作划分前段和后段的内部标志。心肌梗塞患者的前段（梗塞）长度为 11.6±。 2.2 厘米（平均值.+-.SD），而在对照受试者中，眼前节长度为 8.6.+-. 1.2 厘米（P < 0.001）。患者的后段（未梗塞）长度与对照受试者的后段长度没有显着差异（分别为 5.4 .+-. 1.2 和 5.3 .+-. 1.0 厘米）。透壁前壁心肌梗塞后前 3 天内可测量到的左心室扩张是由于梗塞节段而非正常未梗塞节段的扩张所致。因此，梗塞扩张似乎是这些患者早期左心室扩大的主要原因。这种左心室扩大的机制可能对心室力学、梗塞面积估计和早期治疗干预具有重要意义。
Left ventricular enlargement after myocardial infarction is a poor prognostic sign, the mechanism of which has not been well defined. Early left ventricular dilation may be due to the Frank-Starling effect, which results in an increase in the length of uninfarcted segments in response to a reduction in contractile muscle mass. In contrast to this adaptive physiologic mechanism, left ventricular dilation may alternatively be caused by a pathologic process that stretches and thins the infarcted myocardial segment (that is, infarct expansion). To determine the relative contributions of these 2 mechanisms to left ventricular dilation after an initial transmural anterior myocardial infarction, 2-dimensional echocardiograms were obtained from 27 patients within 72 h of the onset of symptoms of myocardial infarction and from 13 healthy control subjects. In the minor-axis echocardiographic view at the level of the papillary muscles, anterior and posterior endocardial segment lengths at end-diastole were measured with a microprocessor-based graphic system. The papillary muscles were used as internal landmarks to demarcate the anterior and posterior segments. Anterior (infarcted) segment length in patients with myocardial infarction was 11.6 .+-. 2.2 cm (mean .+-. SD), whereas in control subjects, anterior segment length was 8.6 .+-. 1.2 cm (P < 0.001). Posterior (uninfarcted) segment length in the patients was not significantly different from posterior segment length in the control subjects (5.4 .+-. 1.2 vs. 5.3 .+-. 1.0 cm, respectively). Measurable left ventricular dilation during the first 3 days after transmural anterior myocardial infarction is due to dilation of the infarcted segment and not of the normal uninfarcted segment. Thus, infarct expansion appears to be the major cause of early left ventricular enlargement in these patients. This mechanism of left ventricular enlargement may have significant implications for ventricular mechanics, infarct size estimation and early therapeutic intervention.