Abstract

The extent of injured myocardium is directly related to infarct size after acute myocardial infarction (AMI). Myocardial hyperenhancement during ultrafast contrast enhanced magnetic resonance imaging (CEMRI) reflects ischemic injury and its mechanism; extracellular volume expansion with or without washout impairment may be related to the magnitude of ischemic injury; edema formation with or without cell death. To investigate the relationship between the extent of myocardial injury and the mechanism of myocardial hyperenhancement by CEMRI we studied 19 patients after AMI. Spoiled GRASS, TR = 6.5 ms, TE = 2.3 ms, 4 short-axis images were analyzed, and the ratio of signal intensity in myocardium to blood from injured (IN) and normal (NL) regions was obtained at 50 secs, 160 secs and 600 secs. after I.V contrast (gadoteridol 0.1 mmol/kg). Percent injured myocardial mass was calculated as the ratio of hyperenhanced myocardium to total LV mass by planimetry. Patients were divided into two groups according to the mechanism of signal hyperenhancement. Group 1 (N = 9) was defined by a parallel upwards displacement (ANOVA p < 0.002) of the injured myocardiumlblood ratio over time relative to normal myocardium consistent with pure extracellular expansion. Group 2 (N = 111 had upwards displacement (ANOVA p < 0,001) with significant slope (ANOVA p < 0.001) consistent with impaired washout (see Figure). Injured mass was greater in Group 2 (31.9 ± 6.4%) than in Group 1(15.9 ± 5.0%, P < 0.001). In conclusion, the mechanism of myocardial hyperenhancement is related to the extent of ischemic injury after AMI, with greater injury associated with the presence of washout impairment. suggesting cell death. These relationships may be explored to assess myocardial viability after AMI by CEMRI.

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