Area at Risk, Myocardial Infarction, and Myocardial Salvage

在过去的几年里，我们证明了T2加权MRI可以检测出与心肌梗死相关的缺血区。这意味着，单次MRI检查能够根据T2加权图像确定在冠状动脉闭塞期间有多少心肌受损，以及使用传统的延迟增强图像确定有多少心肌永久梗死。这种模式的优点在于，这两种检测方法都可以在心肌梗死后1-7天进行--这比基于急诊室的SPECT方法更可行，因为这种方法可能会干扰患者的急性稳定(Aletras等人)。发行量：2006年；113：1865)。 这一方法论为研究调整急性心肌梗死大小的治疗方法提供了可能性。在急性冠脉闭塞期间确定哪些心肌是缺血的具有潜在的临床价值和研究目的(Arai AE等人。J心脏ovasc Pharmacol Ther.2011；16(3-4)：313-20和施瓦茨·朗阿克雷等人。发行量。2011；124(10)：1172-9)。而锰造影剂可以确定危险区域(Natanzon A等人)。放射学。2005年9月；236(3)：859-66)，在人体中使用基于锰的造影剂的初步经验表明，该造影剂可能有太多副作用而不能用于临床。接下来，我们发现T2加权MRI可以确定急性心肌梗死的危险区域，因此是对急性再灌注心肌梗死延迟增强成像的补充(Aletras等人。循环2006年；113：1865)和非再灌流心肌梗死(Tilak等人。《调查放射学》2008；43：7-15)。我们开发了两种新的方法来成像与急性冠状动脉综合征相关的心肌水肿(Kellman等人Magn Resonance Med 2007；57：891)，第二种方法可能提供更好的信噪比，但更难实施(Aletras AH等人Magn ResonMed 2008；59：229)。T2-PREP SSFP方法显著提高了确定与急性心肌梗死相关的冠脉范围的诊断准确性(Kellman等人Magn Resonance Med 2007；57：891)。 T2-PREP SSFP方法在人类中也很有效，并与危险区域的冠状动脉造影测量相关(Berry C等人。中国心脏血管成像学会。2010年；3：527-)。最近，我们发现T2加权成像也能以出色的灵敏度和特异度检测心肌内出血(Payne AR等人)。中国心脏血管成像学会。2011年9月19日)。 我们最近扩大了对与高危区域相关的MRI异常的病理生理学理解。与心肌水肿一致，危险区域的T1也是异常的(Ugander M等人。JACC心脏血管成像。2012年；5(6)：596-603)。本研究使用T1和T2的定量图像，并与病理和微球进行比较，以作为梗塞和危险区域的参考标准测量。

Over the past few years, we demonstrated that T2-weighted MRI can detect the ischemic area at risk associated with a myocardial infarction. This means that a single MRI examination is capable of determining how much myocardium was jeopardized during the coronary occlusion based on T2-weighted images and how much was permanently infarcted using conventional delayed enhancement images. The beauty of this paradigm is that both determinations can be made 1-7 days after the myocardial infarction - something much more feasible than emergency room based SPECT methods that might interfere with acute stabilization of the patient (Aletras et al. Circulation 2006; 113: 1865). This methodology opens up the possibilities of studying treatments that might modulate the size of acute myocardial infarction. Determining what myocardium was ischemic during an acute coronary occlusion is potentially valuable clinically and for research purposes (Arai AE et al. J Cardiovasc Pharmacol Ther. 2011;16(3-4):313-20 and Schwartz Longacre Let al. Circulation. 2011;124(10):1172-9). While manganese contrast agents can determine area at risk (Natanzon A et al. Radiology. 2005 Sep;236(3):859-66), preliminary experience with a manganese based contrast agent in humans suggested this agent may have too many side effects to be clinically useful. Next, we found that T2-weighted MRI can determine the area at risk in acute MI and is thus complementary to delayed enhancement imaging in acute reperfused MI (Aletras et al. Circulation 2006; 113: 1865) and in non-reperfused myocardial infarction (Tilak et al. Investigative Radiology 2008; 43: 7-15). We developed 2 new methods for imaging myocardial edema associated with acute coronary syndrome (Kellman et al Magn Resonance Med 2007; 57: 891) and a second method that may offer better signal to noise ratio but is more difficult to implement (Aletras AH et al Magn Reson Med 2008; 59: 229). The T2-prep SSFP method markedly improved the diagnostic accuracy of determining the coronary territory associated with an acute myocardial infarction (Kellman et al Magn Resonance Med 2007; 57: 891). The T2-prep SSFP method also works well in humans and correlates with coronary angiographic measures of area at risk (Berry C et al. Circ Cardiovasc Imaging. 2010;3:527-535). More recently, we found that T2-weighted imaging can also detect intramyocardial hemorrhage with excellent sensitivity and specificity (Payne AR et al. Circ Cardiovasc Imaging. 2011 Sep 19). We recently extended the pathophysiological understanding of MRI abnormalities associated with the area at risk. Consistent with myocardial edema, the T1 of the area at risk is also abnormal (Ugander M et al. JACC Cardiovasc Imaging. 2012; 5(6): 596-603). This study used quantitative images of T1 and T2 and compared with pathology and microspheres for reference standard measurements of infarction and area at risk.