Intramyocardial hemorrhage contributes to microvascular obstruction in acute myocardial infarction
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KeywordsAcute Myocardial Infarction Collagenase Acute Myocardial Infarction Microvascular Obstruction Intracoronary Injection
The clinical implications of hemorrhagic versus non-hemorrhagic 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.
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.
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 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 post-AMI. Edema and hemorrhage were evaluated using T2 and T2* quantification, respectively, and infarction was assessed by delayed hyperenhancement (DHE) imaging.
Hemorrhage has always been found to be associated with MVO, however, the causal relationship between the two is currently unknown. We speculate that blood spilt in the interstitium might have compressed the microvasculature that was already vulnerable due to the initial ischemic insult; in other words, hemorrhage may have created the MVO. Our preliminary study suggests that hemorrhage may not simply be a bystander but an active contributor to adverse left-ventricular remodeling following AMI.
We would like to acknowledge funding support from the Ontario Research Fund, the Canadian Institutes of Health Research and GE Healthcare.
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