Effect of Ischemia Duration and Protective Interventions on the Temporal Dynamics of Tissue Composition After Myocardial Infarction

Abstract

Supplemental Digital Content is available in the text.

Effect of Early Metoprolol During ST-Segment Elevation Myocardial Infarction on Left Ventricular Strain

“…Edema is a very dynamic process during the first week after myocardial infarction (24), and strain closely associates with its intensity and volume (20). Moreover, cardioprotective therapies may affect the extent and intensity of post-myocardial infarction edema (25). We may reasonably assume that the differences in LV GCS and GLS between both treatment arms were more pronounced in the acute phase because of a blunted edematous reaction in metoprolol treated patients as compared to controls and have diluted at 6-month follow-up due an overall large resorption of edema and necrotic tissue (26,27).…”

Relationship between CMR-derived parameters of ischemia/reperfusion injury and the timing of CMR after reperfused ST-segment elevation myocardial infarction

“…Recent reports generated intense discussion on the dynamic changes of CMR-derived measures of ischemic damage in early post-STEMI phase with particular emphasis on myocardial edema. In elegant experimental studies [ 6 , 7 , 9 ], Fernàndez-Jiménez et al showed that edema features a bimodal pattern after reperfusion. An initial wave of edema appears abruptly and very early (≤3 h) to be attenuated at 24 h and followed by a second edema wave peaking at 4 to 7 days.…”

“…In particular, they underpinned that infarct-related myocardial edema features a highly dynamic course after reperfusion rising concerns about the optimal timing of CMR. However, these studies were limited by small and selective study populations, and the time course of edema was rather heterogeneous as compared to pivotal experimental studies conducted in well-controlled I/R animal models [ 6 – 9 ]. Indeed, in STEMI patients the pattern of infarct-related edema may be influenced by disparate poorly quantifiable factors, including the severity and duration of ischemia as well as spontaneous cardioprotection phenomena [ 9 , 13 ].…”

“…However, these studies were limited by small and selective study populations, and the time course of edema was rather heterogeneous as compared to pivotal experimental studies conducted in well-controlled I/R animal models [ 6 – 9 ]. Indeed, in STEMI patients the pattern of infarct-related edema may be influenced by disparate poorly quantifiable factors, including the severity and duration of ischemia as well as spontaneous cardioprotection phenomena [ 9 , 13 ]. Most important, the above studies relied largely on T2-weighted CMR for AAR quantification, which is less accurate, precise and robust than novel mapping techniques for edema quantification [ 14 , 15 ].…”

Myocardial Edema on T2-Weighted MRI

“…This study by Fernández-Jiménez et al 11 showed that the detection of myocardial edema with longer T2 relaxation times represents the complex pathophysiology post-I/R injury. The investigation systematically demonstrated that the myocardial edema does not correspond with the MaR detected by the initial perfusion defect.…”