Sundqvist Martin G, Verouhis Dinos, Sörensson Peder, Henareh Loghman, Persson Jonas, Saleh Nawzad, Settergren Magnus, Witt Nils, Böhm Felix, Pernow John, Tornvall Per, Ugander Martin
Cardiology Unit, Södersjukhuset, Stockholm, Sweden.
Department of Clinical Science and Education, Karolinska Institutet, Södersjukhuset,, Stockholm, Sweden.
Int J Cardiovasc Imaging. 2025 Jan;41(1):103-112. doi: 10.1007/s10554-024-03294-6. Epub 2024 Dec 5.
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 (R = 0.24, p < 0.001), left atrial volume index (R = 0.13, p = 0.01) and the mechanistic stiffness parameter (R = 0.21, p < 0.001). Adding MAR improved only the e' model (adjusted R increase: 0.08, p = 0.02). At 6 months follow-up, final IS was only associated with viscoelastic energy loss (R = 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.
研究急性心肌梗死（MI）急性期心肌梗死面积（IS）、心肌水肿与舒张功能障碍之间的关系，以及随访期间舒张功能障碍的发展情况。另一个目的是使用机械模型和传统参数研究舒张功能。患者在首次急性前壁心肌梗死后4 - 7天（急性期）和6个月接受了心血管磁共振（CMR）成像和超声心动图检查，包括使用参数化舒张期充盈方法进行机械分析（n = 74）。使用CMR IS对超声心动图舒张参数进行线性回归建模，包括纳入和不纳入危险心肌（MAR），并通过似然比检验进行模型比较。使用最终的IS对6个月随访时的舒张参数进行建模。对于大多数参数，与急性IS无关，除了减速时间（R = 0.24，p < 0.001）、左心房容积指数（R = 0.13，p = 0.01）和机械硬度参数（R = 0.21，p < 0.001）。添加MAR仅改善了e'模型（调整后R增加：0.08，p = 0.02）。在6个月随访时，最终IS仅与粘弹性能量损失相关（R = 0.22，p = 0.001）。在急性心肌梗死中，IS和MAR均与舒张功能相关，但程度有限。在梗死后6个月，IS增加与粘弹性能量损失减少相关，尽管程度也有限。IS与舒张功能障碍之间的关系似乎是由缺血或梗死空间范围之外的机制介导的。
