LATE EFFECTS OF ACUTE INFARCT DILATION ON HEART SIZE - A 2 DIMENSIONAL ECHOCARDIOGRAPHIC STUDY
LATE EFFECTS OF ACUTE INFARCT DILATION ON HEART SIZE - A 2 DIMENSIONAL ECHOCARDIOGRAPHIC STUDY
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DOI：
10.1016/0002-9149(82)90035-2
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发表时间：
1982-01-01
影响因子：
2.8
通讯作者：
BULKLEY, BH
中科院分区：
文献类型：
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作者：
ERLEBACHER, JA;WEISS, JL;BULKLEY, BH
梗塞区扩张（梗塞扩张）已被证明是透壁前壁心肌梗塞几天内局部左心室扩张的原因。此后该过程是否稳定、持续或消退，以及未梗塞的心肌是否受到影响尚不清楚。为了探讨这一点，我们在前壁透壁心肌梗死后 10 至 21 天开始，在 3 至 30 个月（平均 13 个月）内对 13 名患者进行了 2 至 6 次（平均 4 次）连续二维超声心动图研究。使用乳头肌作为左心室内部标志，根据节段长度与时间的回归线的斜率评估每位患者的前节段和后节段扩张。研究患者被分为有梗塞扩展的患者（七名患者）和没有梗塞扩展的患者（六名患者）。梗塞扩展被定义为梗塞后10至21天的前段长度超过由13名年龄和性别匹配的正常对照受试者确定的正常上限。梗死后 10 至 21 天，7 名扩张患者的平均眼前节长度比正常对照组长 65%。 7 例梗塞扩张的患者在梗塞前段（p < 0.01）和未梗塞后段（p < 0.05）的长期观察中均显示出显着且持续的扩张。眼前段长度平均增加 1.1 厘米（8%），后段长度平均增加 0.9 厘米（19%）。这意味着观察期间左心室整体周长平均增加了 11%。六名没有梗塞扩张的患者显示前段或后段长度没有显着变化（平均值±平均值的标准误差[SEM]分别为-0.7±0.3和0.2±0.3mm/mo）。七名梗塞扩大的患者中，有六名因呼吸困难或心绞痛或两者兼有而导致功能受限；没有梗塞扩张的患者没有心脏功能受限。因此，透壁性心肌梗塞后3周内发生的梗塞扩张似乎是左心室扩张的主要原因，并且与功能状态受损相关。此外，由于梗塞扩张导致的心室大小的显着增加似乎预示着由于梗塞区和未梗塞段的延长而导致的慢性进行性心室扩大。
Dilation of the infarct zone (infarct expansion) has been shown to be a cause of regional left ventricular dilation within days of transmural anterior myocardial infarction. Whether this process stabilizes, continues or regresses thereafter, and whether uninfarcted myocardium is affected is unknown. To explore this, two to six (mean four) serial two dimensional echocardiographic studies were obtained over a 3 to 30 month period (mean 13) in 13 patients beginning 10 to 21 days after anterior transmural myocardial infarction. With use of the papillary muscles as internal left ventricular landmarks, anterior and posterior segmental dilation in each patient was assessed from the slope of the regression line of segment length versus time. Study patients were classified into those with (seven patients) and those without (six patients) infarct expansion. Infarct expansion was defined as an anterior segment length 10 to 21 days after infarction that exceeded the upper limit of normal determined from 13 age-and sex-matched normal control subjects. Ten to 21 days after infarction, the average anterior segment length in the seven patients with expansion was 65 percent greater than that in normal control subjects. The seven patients with infarct expansion showed significant and continuing dilation during long-term observation of both the infarcted anterior (p < 0.01) and the uninfarcted posterior (p < 0.05) segments. The average increase in anterior segment length was 1.1 cm (8 percent) and in posterior segment length 0.9 cm (19 percent). This represents an average increase in overall left ventricular circumference of 11 percent during the observation period. The six patients without infarct expansion showed no significant change in anterior or posterior segment length (mean ± standard error of the mean [SEM] −0.7 ± 0.3 and 0.2 ± 0.3 mm/mo, respectively). Six of the seven patients with infarct expansion were functionally limited by dyspnea or angina, or both; no patient without infarct expansion had functional cardiac limitation.Thus, infarct expansion occurring within 3 weeks of transmural myocardial infarction appears to be the main contributor to left ventricular dilation, and is associated with impaired functional status. Moreover, a significant increase in ventricular size due to infarct expansion appears to predict chronic progressive ventricular enlargement due to lengthening of both the infarcted zone and the uninfarcted segment.