The prognostic significance of microvascular obstruction after myocardial infarction as defined by cardiovascular magnetic resonance.

Cardiac magnetic resonance imaging (CMR) has evolved into an important imaging tool in the assessment of patients with myocardial infarction (MI), with or without reperfusion. CMR is a gold standard technique for measuring left ventricular volumes and global function. The technique of delayed contrast enhancement has been carefully validated in animal markers as a measure of infarct size. The presence of hypo-enhanced regions at the core of hyper-enhanced infarctions is a marker of microvascular obstruction (MO) and a predictor of lack of functional recovery in the infarct zone and poor cardiovascular outcome in the patient post-MI. The paper by Hombach et al. is the largest report to date of these CMR techniques used in sequential fashion in patients with acute MI and thus is quite instructive regarding prognostic factors derived from CMR. These authors studied 110 patients at a mean of day 6 after acute MI, which is a relatively late initial time point as patients currently are typically discharged before day 6. Of the original 110 patients, 89 returned for followup imaging at an average of 9 months after MI. The remainder died (n 1⁄4 7), refused follow-up (n 1⁄4 11), or had inadequate imaging at follow-up (n 1⁄4 3). The authors should be commended for obtaining quality imaging follow-up data in 90% of eligible patients in this relatively large cohort. Hombach et al. defined MO as persistent MO (PMO) on delayed contrast enhanced imaging, rather than on imaging in the first few minutes after contrast infusion as defined in several previous papers. Interestingly, they found that 46% of their patients demonstrated MO as per their definition, a surprisingly high percentage. This may reflect the predominance of anterior MI in their population (53%) and the proportion of patients without TIMI 3 flow after reperfusion (12%). There are a number of findings in the present study that confirm and extend previous observations in CMR studies of acute MI and left ventricular (LV) remodelling. A principle finding was that predictors of LV remodelling, defined as an increase in end-diastolic volume of 20%, included total infarct size, PMO, and the transmural extent of infarction. These are interrelated risk factors as the amount of PMO correlates with infarct size. This finding makes pathophysiological sense because the size of no reflow is a predictor of ultimate infarct size. The second principle finding was that predictors of major adverse cardiac events (MACE) were end-diastolic volume, ejection fraction (EF), and PMO. PMO was a more powerful predictor of survival than was infarct size, as the latter showed only a trend. This finding is consistent with the results of the study of Wu et al., which showed that MO was a better discriminator of cardiovascular outcome than infarct size. Another important confirmatory finding in the study by Hombach et al. was the demonstration of the change in infarct size over time. The authors found that absolute infarct size as determined by the extent of delayed contrast enhancement decreased from 11.4+ 7.2 to 7.8+ 5.3% (a decline of 32%) from day 6 to month 9 post-MI. These findings are consistent with those of two recently published studies using contrast-enhanced CMR. Inkangisorn et al. found a 31% decrease in infarct