Myocardial oedema: a forgotten entity essential to the understanding of regional function after ischaemia or reperfusion injury
- 1Department of Cardiology, University of Zagreb, Zagreb, Croatia
- 2University of Leuven, Leuven, Belgium
- 3Department of Cardiology, St George’s Hospital, London, UK
- Professor R Sutherland, Department of Cardiology, St George’s Hospital, Blackshaw Road, London SW17 0QT, UK;
It is well established that extracellular myocardial oedema is induced during reperfusion of an acute myocardial infarction and that the presence of oedema is related to cell death.1 With the current clinical developments in non-invasive imaging techniques it is now possible to image the presence of oedema and its effects on local contractile function.2 Yet, to date, the consequences of extracellular oedema related to reperfusion injury have been little studied in the clinical environment.3 Furthermore, although extracellular oedema is a clear marker of cell death, it is unclear whether ischaemia alone produces changes in either extracellular or intracellular water content.
To understand how different types and extents of oedema influence myocardial performance, it is essential to examine the relationship between regional deformation and force development by the contractile elements (true contractility). Bragadeesh et al4 started from the simple concept that strain is directly related to myocyte force development, but the relationship in a ventricle is more complicated (fig 1). Regional deformation is related to all forces (developed by and on the myocardium), through local elasticity (histology). Besides the contractile force, the external loading forces (intracavity pressure and the influence of neighbouring, contracting, segments) have to be taken into account. In the normal heart, segment interaction is non-existent and load is evenly distributed so that contractility and deformation are linearly related.5 When there is regional disease, there may no longer be a direct link between contractility and deformation.2 For example, the ischaemia-related passive phenomenon of post-systolic thickening (PST) is solely a result of segment interaction.6
In view of the above, we can look more closely at acute ischaemia and reperfusion (resulting in either stunning or acute infarction) and the influence of oedema.
In the experimental setting, reperfusion after a prolonged period of coronary occlusion …