Impact of myocardial haemorrhage on left ventricular function and remodelling in patients with reperfused acute myocardial infarction

Top Cited Papers
Open Access
Publisher Website
Google Scholar
Abstract
Myocardial haemorrhage is a common complication following reperfusion of ST-segment-elevation acute myocardial infarction (MI). Although its presence is clearly related to infarct size, at present it is unknown whether post-reperfusion haemorrhage affects left ventricular (LV) remodelling. Magnetic resonance imaging (MRI) can be used to identify MI, myocardial haemorrhage, and microvascular obstruction (MVO), as well as measure LV volumes, function, and mass. Ninety-eight patients (14 females, 84 males, mean age: 57.7 years) with MI reperfused with percutaneous coronary intervention (PCI) were studied within the first week (1W) and at 4 months (4M) after the event. T2-weighted MRI was used to differentiate between haemorrhagic (i.e. hypointense core) and non-haemorrhagic infarcts (i.e. hyperintense core). Microvascular obstruction and infarct size were determined on contrast-enhanced MRI, whereas cine MRI was used to quantify LV volumes, mass, and function. Twenty-four patients (25%) presented with a haemorrhagic MI. In the acute phase, the presence of myocardial haemorrhage was related to larger infarct size and infarct transmurality, lower LV ejection fraction, and lower systolic wall thickening in the infarcted myocardium (all P-values P < 0.01). Left ventricular ejection fraction did, however, not improve in patients with haemorrhagic MI (baseline: 42.8 ± 6.5% vs. 4M: 41.9 ± 8.5%; P = 0.68). Multivariate analysis showed myocardial haemorrhage to be an independent predictor of adverse LV remodelling at 4M (defined as an increase in LV end-systolic volume). This pattern was independent of the initial infarct size. Myocardial haemorrhage, the presence of which can easily be detected with T2-weighted MRI, is a frequent complication after successful myocardial reperfusion and an independent predictor of adverse LV remodelling regardless of the initial infarct size.