2011Lund University Publications (Lund University)Open access

Quantitative and Qualitative Assessment of the Myocardium at Risk

Joey F.A. Ubachs

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Abstract

One of the major determinants of the final infarct size during an acute coronary occlusion is the size of the myocardium subjected to ischemia. Identification and quantification of this so-called myocardium at risk in the acute phase of ischemia has been difficult in patients with conventional methods, such as myocardial perfusion single-photon emission computed tomography (SPECT) or electrocardiography. However, to assess cardioprotective strategies aimed at reducing infarct size, an accurate measure of both myocardium at risk and infarct size is needed. Both measurements are necessary in order to assess the amount of myocardium that has been salvaged by the provided treatment. Cardiac magnetic resonance imaging (CMR) has the opportunity to accurately assess both the myocardium at risk as well as the infarct size. This thesis has contributed to the knowledge on quantification of the myocardium at risk and subsequently myocardial salvage with the use of CMR imaging. Study I demonstrated, for the first time in humans, that there was a good correlation between the myocardium at risk assessed by T2-weighted CMR, which shows myocardial edema, and the myocardium at risk assessed by myocardial perfusion SPECT. Furthermore, the study also showed that T2-weighted CMR can be used up to 1 week after reperfusion therapy, allowing assessment of both myocardium at risk and infarct size to determine myocardial salvage in a single imaging session, without interfering with patient care. Study II showed a significant difference between the myocardium at risk assessed by T2-weighted CMR and the endocardial extent of infarction measured by late gadolinium enhancement. Thus, endocardial extent of infarction can not be used to determine myocardium at risk, especially in patients with early reperfusion therapy with little or no infarction. Study III demonstrated a good correlation between the myocardium at risk assessed by T2-weighted CMR and the myocardium at risk assessed by cine imaging early after injection of a gadolinium-based contrast agent, in patients 1 week after acute coronary occlusion. Thus, both methods can be used simultaneously or separately to determine MaR and subsequently myocardial salvage in a single imaging session. Finally, Study IV showed that T2-weighted CMR can be used to determine the myocardium at risk in an ex vivo experimental model, both with and without the presence of gadolinium.

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What this paper is about

One of the major determinants of the final infarct size during an acute coronary occlusion is the size of the myocardium subjected to ischemia. Identification and quantification of this so-called myocardium at risk in the acute phase of ischemia has been difficult in patients with conventional methods, such as myocardial perfusion single-photon emission computed tomography (SPECT) or electrocardiography. However, to assess cardioprotective strategies aimed at reducing infarct size, an accurate measure of both myocardium at risk and infarct size is needed. Both measurements are necessary in order to assess the amount of myocardium that has been salvaged by the provided treatment. Cardiac magnetic resonance imaging (CMR) has the opportunity to accurately assess both the myocardium at risk as well as the infarct size. This thesis has contributed to the knowledge on quantification of the myocardium at risk and subsequently myocardial salvage with the use of CMR imaging. Study I demonstrated, for the first time in humans, that there was a good correlation between the myocardium at risk assessed by T2-weighted CMR, which shows myocardial edema, and the myocardium at risk assessed by myocardial perfusion SPECT. Furthermore, the study also showed that T2-weighted CMR can be used up to 1 week after reperfusion therapy, allowing assessment of both myocardium at risk and infarct size to determine myocardial salvage in a single imaging session, without interfering with patient care. Study II showed a significant difference between the myocardium at risk assessed by T2-weighted CMR and the endocardial extent of infarction measured by late gadolinium enhancement. Thus, endocardial extent of infarction can not be used to determine myocardium at risk, especially in patients with early reperfusion therapy with little or no infarction. Study III demonstrated a good correlation between the myocardium at risk assessed by T2-weighted CMR and the myocardium at risk assessed by cine imaging early after injection of a gadolinium-based contrast agent, in patients 1 week after acute coronary occlusion. Thus, both methods can be used simultaneously or separately to determine MaR and subsequently myocardial salvage in a single imaging session. Finally, Study IV showed that T2-weighted CMR can be used to determine the myocardium at risk in an ex vivo experimental model, both with and without the presence of gadolinium.

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Available abstract

One of the major determinants of the final infarct size during an acute coronary occlusion is the size of the myocardium subjected to ischemia. Identification and quantification of this so-called myocardium at risk in the acute phase of ischemia has been difficult in patients with conventional methods, such as myocardial perfusion single-photon emission computed tomography (SPECT) or electrocardiography. However, to assess cardioprotective strategies aimed at reducing infarct size, an accurate measure of both myocardium at risk and infarct size is needed. Both measurements are necessary in order to assess the amount of myocardium that has been salvaged by the provided treatment. Cardiac magnetic resonance imaging (CMR) has the opportunity to accurately assess both the myocardium at risk as well as the infarct size. This thesis has contributed to the knowledge on quantification of the myocardium at risk and subsequently myocardial salvage with the use of CMR imaging. Study I demonstrated, for the first time in humans, that there was a good correlation between the myocardium at risk assessed by T2-weighted CMR, which shows myocardial edema, and the myocardium at risk assessed by myocardial perfusion SPECT. Furthermore, the study also showed that T2-weighted CMR can be used up to 1 week after reperfusion therapy, allowing assessment of both myocardium at risk and infarct size to determine myocardial salvage in a single imaging session, without interfering with patient care. Study II showed a significant difference between the myocardium at risk assessed by T2-weighted CMR and the endocardial extent of infarction measured by late gadolinium enhancement. Thus, endocardial extent of infarction can not be used to determine myocardium at risk, especially in patients with early reperfusion therapy with little or no infarction. Study III demonstrated a good correlation between the myocardium at risk assessed by T2-weighted CMR and the myocardium at risk assessed by cine imaging early after injection of a gadolinium-based contrast agent, in patients 1 week after acute coronary occlusion. Thus, both methods can be used simultaneously or separately to determine MaR and subsequently myocardial salvage in a single imaging session. Finally, Study IV showed that T2-weighted CMR can be used to determine the myocardium at risk in an ex vivo experimental model, both with and without the presence of gadolinium.

Key concepts: Medicine, Cardiology, Myocardial infarction, Internal medicine, Perfusion, Magnetic resonance imaging, Ischemia, Infarction

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