Ischaemic cardiomyopathy is characterised by a total or partial asynergic involvement of the left ventricular (LV) wall, which can be dyskinetic (true aneurysm) or akinetic, or both. This still exists in spite of the recanalisation of culprit artery during the acute phase, which often only partially saves the infarcted myocardium. In 1967, Gorlin1 demonstrated that, when 20% to 25% of the ventricle area is scarred, there is a progressive evolution to global dilatation and congestive heart failure (CHF), which is now called LV remodelling. Nowadays, cardiac magnetic resonance (CMR) allows us to see, after myocardial infarct, the scarred area and to assess its consequences on LV performances and volumes. Since 1984,2 to repair such a scarred LV surgically, a patch is inserted inside the ventricle, on contractile muscle, in order to exclude all akinetic nonresectable areas and to rebuild the ventricular cavity as it was before the infarct. This left ventricular reconstruction (LVR) by endoventricular patch is now widely accepted as an efficient technique to treat LV aneurysms, as both systolic and diastolic function are improved. It is maybe time to revisit indications for more efficient therapy or prevention of post-ischaemic CHF.
The LV Wall After Infarct
The infarcted area is first necrotic, then fibrotic and finally calcified. However, since standardisation of the treatment of the myocardial infarct in the acute phase by thrombolysis, angioplasty and stenting, the necrosis is mostly not transmural. The sub-epicardial muscle is saved by recanalisation, but the subendocardial muscle is necrosed.3 Therefore, the LV wall can show two different aspects on the same area: living myocardium (seen at surgery or during a thallium test) surrounding an akinetic zone on echo or angiogram and found inside the LV after opening. With CMR using the gadolinium late enhancement (GLE), this necrotic area is perfectly delimited (see Figure 1).4,5
As a result of a partially diseased and scarred LV wall, and other reasons such as mural thrombi and calcifications, already identified by Gorlin in 1967, this asynergic LV wall can be dyskinetic more often than akinetic. Therefore, it is more important to determine in a patient the percentage of asynergic wall than the exact type of wall motion abnormality in the sense of dyskinetic (true aneurysm) or akinetic.
Even though disease in the right coronary artery is the leading cause of infarction, the antero-septoapical region is the most common location for LV scarring. This is probably due to the detrimental effect of occlusion of the left anterior descending (LAD) artery and its branches compared with the consequences of occlusion of the right or circumflex arteries with their balanced anatomy. The septum is not analysed correctly by right oblique projection of the angiogram. Echocardiography and, more precisely, CMR with four projections (two chambers, four chambers, left ventricular outflow tract (LVOT) and short axis) in the majority of cases illustrate the involvement of the septum (see Figures 1A, B and C).
The prognosis of the post-infarct evolution depends on the extent of the asynergic wall (Gorlin). This extension can be assessed by angiography with the centreline method in right oblique projection or echocardiogram or radionuclide ventriculogram and, more easily and precisely, by CMR if there is no contraindication (implantable pacer or defibrillator). By analysing the LV wall and the presence of a necrotic scar (white line traced by GLE) on four projections, the extension of the asynergic wall can be expressed as the ratio between the length of the necrotic scarred wall and the total length of the LV circumference (see Figure 2). When this ratio reaches 50%, the natural evolution can be considered as hopeless.
- M D Klein, M V Herman and R Gorlin, ├óÔé¼┼øA hemodynamic study of left ventricular aneurysm├óÔé¼┼Ñ, Circulation, 35 (1967), pp. 614├óÔé¼ÔÇ£630.
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