心肌梗死的大小和梗死周围水肿不是急性心肌梗死后舒张功能损害的主要决定因素。

Martin G Sundqvist, Dinos Verouhis, Peder Sörensson, Loghman Henareh, Jonas Persson, Nawzad Saleh, Magnus Settergren, Nils Witt, Felix Böhm, John Pernow, Per Tornvall, Martin Ugander
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摘要

研究急性心肌梗死(MI)急性期心肌梗死大小(IS)、心肌水肿与舒张功能障碍的关系,以及随访中舒张功能障碍的发展。进一步的目的是使用机制模型和常规参数来研究舒张功能。患者在首次急性前路心肌梗死后4-7天(急性)和6个月内接受心血管磁共振(CMR)成像和超声心动图检查,包括参数化舒张充盈法进行机制分析(n = 74)。使用CMR IS对超声心动图舒张参数进行线性回归建模,包括和不包括危险心肌(MAR),并使用似然比检验进行模型比较。6个月随访时的舒张参数采用终值IS建模。除减速时间(R2 = 0.24, p 2 = 0.13, p = 0.01)和机械刚度参数(R2 = 0.21, p 2增加0.08,p = 0.02)外,大多数参数与急性IS无关。在6个月的随访中,最终IS仅与粘弹性能量损失相关(R2 = 0.22, p = 0.001)。在急性心肌梗死中,IS和MAR都与舒张功能有关,但只是在有限的程度上。在梗死后6个月,IS的增加与粘弹性能量损失的减少有关,尽管在一定程度上也是如此。IS和舒张功能障碍之间的关系似乎是由简单的缺血或梗死的空间范围之外的机制介导的。
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The size of myocardial infarction and peri-infarction edema are not major determinants of diastolic impairment after acute myocardial infarction.

To study the relationship between myocardial infarction size (IS), myocardial edema, and diastolic dysfunction after acute myocardial infarction (MI) both in the acute phase, and in the development of diastolic dysfunction in the follow-up setting. A further purpose is to study diastolic function using a mechanistic model as well as conventional parameters. Patients underwent cardiovascular magnetic resonance (CMR) imaging and echocardiography including mechanistic analysis using the parameterized diastolic filling method within 4-7 days (acute) and 6 months after a first acute anterior MI (n = 74). Linear regression modeling of echocardiographic diastolic parameters using CMR IS with and without inclusion of the myocardium at risk (MAR) and model comparisons with likelihood ratio tests were performed. Diastolic parameters at 6 months follow-up were modelled using final IS. For most parameters there was no association with acute IS, except for deceleration time (R2 = 0.24, p < 0.001), left atrial volume index (R2 = 0.13, p = 0.01) and the mechanistic stiffness parameter (R2 = 0.21, p < 0.001). Adding MAR improved only the e' model (adjusted R2 increase: 0.08, p = 0.02). At 6 months follow-up, final IS was only associated with viscoelastic energy loss (R2 = 0.22, p = 0.001). In acute MI, both IS and MAR are related to diastolic function but only to a limited extent. At 6 months after infarction, increasing IS is related to less viscoelastic energy loss, albeit also to a limited extent. The relationship between IS and diastolic dysfunction seems to be mediated by mechanisms beyond simply the spatial extent of ischemia or infarction.

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