Longitudinal trends of remodeling mechanisms after acute myocardial infarction based on severity of ischemic insult: A quantitative MRI study
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KeywordsAcute Myocardial Infarction Acute Myocardial Infarction Ischemic Insult Microvascular Obstruction Infarct Zone
In acute myocardial infarction (AMI), the aim of any therapeutic intervention is to reduce the infarct size and attenuate adverse remodeling. The type and extent of infarction encountered clinically [transmural, hemorrhagic, heterogeneous, with microvascular obstruction (MVO)], is primarily determined by the severity of the initial ischemic insult. Understanding the in-vivo pathophysiological mechanisms after AMI as a function of severity will be key in predicting functional recovery, prognosis and assessing the efficacy of novel therapies.
To evaluate longitudinal fluctuations in edema, hemorrhage and vasodilatory function in infarcted and remote territories of porcine myocardium following different ischemic insult durations.
The study involved two groups of animals that were subjected to balloon occlusion of the LAD [90 min (N=4) and 45 min (N=3)], followed by reperfusion. Imaging was performed on a 3T MRI scanner (MR 750, GE Healthcare) pre-LAD occlusion, at day-2 as well as weeks- 1,2,4 and 6 post-LAD occlusion. Edema was evaluated by T2 quantification using a T2-prepared spiral sequence and hemorrhage was identified by T2* determined using a multi-echo gradient-echo acquisition. Vasodilatory function was assessed at rest and following Dipyridamole administration (stress), noting BOLD-induced T2 alterations. Non-infarcted basal myocardium was also analyzed to study remote zone remodeling. A contrast-enhanced IR-GRE sequence was used for infarct assessment.
Quantitative in-vivo MRI evaluation of disease evolution can distinguish longitudinal trends of the underlying remodeling processes based on severity of the ischemic insult. MRI parameters revealed faster resolution of edema and earlier restoration of vasodilatory function in less severe infarcts potentially indicating reduced adverse remodeling. This characterization may allow evaluation of novel therapies targeted to alleviate ischemic injury and prevent MVO/hemorrhage.
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