Left ventricular remodelling is a complex process by which mechanical, neurohormonal and genetic factors alter ventricular structure and function leading to reduced mechanical performance, electrical instability and sudden death [1]. It is an important aspect of heart failure progression, characterized by dilatation and change of shape of the left ventricle (LV) as well as alterations in the ventricular wall which include hypertrophy, loss of myocytes and increased interstitial fibrosis [2]. At the molecular level, it is characterized by a regression to the fetal pattern, i.e. increase of β-myosin heavy chain, α-actin, atrial natriuretic peptide overexpression, sarco/endoplasmic reticulum CaATPase activity decrease and a shift of myocardial metabolism towards glucose utilization [3, 4]. Acute myocardial infarction (MI) is a common cause of LV remodelling. It is estimated that despite primary percutaneous coronary intervention (PCI) and standard current therapy, around 30% of anterior MIs will develop remodelling. The three major biomechanical mechanisms contributing to the increase of LV volumes over time after MI are: (1) expansion of the infarct in the subacute phase [5], (2) subsequent non-ischaemic infarct extension into the adjacent non-infarcted region [6, 7] and (3) hypertrophy and dilatation of non-infarcted myocardium in the chronic phase [8–10]. The main factors associated with remodelling are size of infarction, anterior location and late or unsuccessful (or absence of) reperfusion therapy both at the epicardial vessel level and at the microvasculature level. LV remodelling, however, is a potentially reversible or even possibly preventable process. Regression is manifested as a return to a more normal ventricular size and shape and appears to be a good predictor of a reduction in morbidity and mortality [2, 11]. Several trials on post acute MI patients have demonstrated that this can be achieved by a combination of treatment regimes [12]. This is understandable considering that the three aforementioned mechanisms operate in different regions of the LV and during different time frames after MI, thus making it unlikely for any single drug to be completely effective in addressing all three mechanisms [12]. A major determinant to the selection of the appropriate treatment is the propensity of the underlying MI to result in LV remodelling. Therefore, accurate monitoring of post acute MI patients to identify those who are likely to develop LV remodelling is of great importance. Based on the mechanistic rationale described above, monitoring is performed with non-invasive imaging and usually includes assessment of heart size, shape and mass, ejection fraction (EF), end-diastolic and end-systolic volumes and regional contractility. Cardiac magnetic resonance (CMR) is the gold standard to assess these parameters as well microvascular obstruction and infarct size. A consistent finding from the CMR literature in the post acute MI setting is that scar size is a key determinant of long-term LV remodelling. Moreover, there are distinct time-dependent patterns of infarct healing and LV remodelling which suggest that the timing of CMR performance is important for assessment of infarct size and prediction of C. D. Anagnostopoulos (*) Nuclear Medicine Division, PET/CT Department, Clinical Research Center, Biomedical Research Foundation Academy of Athens, 4 Soranou Ephessiou St., 115 27 Athens, Greece e-mail: cdanagnostopoulos@bioacademy.gr
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Aug 1, 2018
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