Intramyocardial hemorrhage contributes to microvascular obstruction in acute myocardial infarction
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POSTER PRESENTATION
Open Access
Intramyocardial hemorrhage contributes to microvascular obstruction in acute myocardial infarction Nilesh R Ghugre1*, Jennifer Barry1, Alan Moody2, Bradley H Strauss3, Graham Wright1,4 From 15th Annual SCMR Scientific Sessions Orlando, FL, USA. 2-5 February 2012 Summary The clinical implications of hemorrhagic versus nonhemorrhagic infarcts are currently unclear. Our study suggests that hemorrhage may not simply be a bystander but an active contributor to adverse left-ventricular remodeling following acute myocardial infarction. Background Patients with hemorrhagic infarcts appear to constitute a high-risk group in acute myocardial infarction (AMI). However, the clinical implications of hemorrhagic versus non-hemorrhagic infarcts are currently unclear, warranting a more systematic and mechanistic approach towards understanding the underlying consequences. The question of whether hemorrhage is simply a bystander or contributes to additional myocardial injury remains to be investigated. The purpose of the study was to artificially induce hemorrhage in normal and infarcted (but not hemorrhagic) porcine myocardium to determine whether hemorrhage, per se, worsens prior ischemic damage. Methods Firstly, hemorrhage was induced in normal porcine hearts (N=18) by direct intracoronary injection of collagenase using over-the-wire angioplasty balloon catheter advanced to mid LAD after 2nd diagonal branch; balloon inflation was maintained for 8 min (ischemia). Six doses of (250,600,800,1200,1600,3200) mcg were administered in equally divided groups. Animals were sacrificed at 24 hrs and hearts were explanted for histological analysis. Secondly, hemorrhage was artificially 1 Imaging Research, Sunnybrook Research Institute, Toronto, ON, Canada Full list of author information is available at the end of the article
induced in one animal subjected to a 45 min LAD occlusion. Collagenase was injected immediately after balloon deflation i.e. during reperfusion at an intermediate dose of 1000 mcg. For reference, another animal underwent a routine 45 min LAD occlusion. A comprehensive CMR examination was performed at day 2 postAMI. Edema and hemorrhage were evaluated using T2 and T2* quantification, respectively, and infarction was assessed by delayed hyperenhancement (DHE) imaging.
Results In the control animals, there was no mortality attributable to collagenase infusion. Epicardial and intramyocardial hemorrhage was observed in a dose-dependent manner with none or mild, focal hemorrhage up to 600 mcg, mild-moderate at 800-1600 mcg and severe at 3200 mcg (Fig. 1); no infarction was observed. In the collagenase treated infarction (Fig. 2), MRI examination at day 2 post-AMI revealed signal void on T2*-weighted images, indicative of hemorrhage. Alongside a surprising yet interesting finding was the presence of microvascular obstruction (MVO) on DHE images. This was unlike the reference 45 min infarction, which was non-hemorrhagic and with no MVO. Conclusions Hemorrhage has always been found to be associ
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