Infarct haemorrhage detected by cardiac magnetic resonance imaging: are we seeing the latest culprit in adverse left ventricular remodelling?

Abstract

> The force of the heart decreases … as the greater number of its parts become tendinous instead of fleshy. De sedibus et causus morborum > > G. B. Morgagni, 1761 All myocardial infarctions are not equal, and those that produce more extensive left ventricular topographical alterations are much more likely to result in premature morbidity and mortality. The advent of non-invasive cardiac imaging, particularly echocardiography, provided a temporal window to evaluate the dynamics of the structural alterations produced by a myocardial infarction. In the late 1970s, infarct expansion was defined as an acute dilatation and thinning of the infarcted region leading to an elongation of that segment which was not accounted for by further necrosis.1 This early change in ventricular contour often leading to an aneurysm identified patients at higher risk for early mortality and other infarct complications. In animal models, it became apparent that the early distortion of ventricular architecture in response to an extensive loss of myocytes was part of a more insidious progressive process of ventricular enlargement which involved the viable segment as well as the infarcted region. This architectural-modifying process termed ‘ventricular remodelling after myocardial infarction’ results in a larger ventricular chamber.2 Although the early enlargement may provide some compensation by restoring stroke volume despite a reduced ejection fraction, the alterations in left ventricular architecture create a chronic imbalance in loading conditions that leads to further topographic changes which augment risks for adverse events. Larger infarct size is the major factor promoting adverse left ventricular remodelling, and myocardial reperfusion performed during the myocyte salvage period remains the most definitive therapeutic modality to reduce adverse ventricular remodelling. Early studies also indicated that re-establishing coronary perfusion just outside of the window of salvage could still favourably attenuate some of the adverse structural changes by promoting prompter healing in the infarcted region.3 The complementary … *Corresponding author. Tel: +1 617 732 5500, Fax: +1 617 732 5291, E-mail: mapfeffer{at}bics.bwh.harvard.edu or mpfeffer{at}rics.bwh.harvard.edu