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Myocardial hemorrhage common after successful MI reperfusion with PCI
30 June 2009
MedWire News: Myocardial hemorrhage may occur in as many as a quarter of patients after successful mechanical reperfusion for acute myocardial infarction (MI), a study indicates.
The Belgian researchers say its presence was “easily detected” using T2-weighted magnetic resonance imaging (MRI), and was associated with larger infarct size, increased ventricular volumes, and a lack of functional recovery.
The team, from University Hospitals Leuven, adds that myocardial hemorrhage independently predicted adverse left ventricular (LV) remodeling regardless of the initial infarct size and say “depiction of myocardial hemorrhage using T2-weighted MRI is warranted.”
Jan Bogaert and colleagues studied 98 patients with MI reperfused with percutaneous coronary intervention at 1 week and 4 months after the event. T2-weighted MRI was used to identify myocardial hemorrhage, in which there was a hypointense core in the center of the area at risk, as distinct from nonhemorrhagic infarcts with a hyperintense core.
Overall, 25% of patients presented with a hemorrhagic MI. In the acute phase, myocardial hemorrhage was related to larger infarct size, infarct transmurality, lower LV ejection fraction, and lower systolic wall thickening in the infarcted myocardium (p<0.001).
LV ejection fraction improved significantly in patients with nonhemorrhagic MI, from a mean of 49.3% at baseline to 52.9% at 4 months (p<0.01), but not in those with hemorrhagic MI.
Multivariate analysis showed myocardial hemorrhage was an independent predictor of adverse LV remodeling, defined as an increase in LV-end systolic volume at 4 months, independently of initial infarct size.
“Because myocardial hemorrhage predicts adverse LV remodeling, treatment strategies aimed to reduce microvascular and endothelial damages and LV dilatation might be useful to improve these patients’ prognosis,” the researchers suggest in the European Heart Journal.
“Studies looking at the effect of agents that enhance mitochondrial or endothelial function such as nitric oxide donors, calcium channel blockers, or adenosine are warranted.”
