Changes of the left ventricle after myocardial infarction—estimation with cine magnetic resonance imaging during the first six months
Authors: Konermann Martin , Sanner Bernd M. , Horstmann Eckard , Grötz Jürgen , Laschewski Frank , Josephs Wolfgang , Odenthal Hans J. , Sturm Alexander 
Published: February 2009

Background: In recent years, the interest of cardiologists has focused increasingly on the morphologic and functional changes of the left ventricle after myocardial infarction (MI), due to their great prognostic significance for the patient.

Hypothesis: The aim of this study was to evaluate changes in left ventricular morphology and function during the first 6 months following MI.

Methods: In all, 61 patients (17 women, 44 men, age 36–83 years) were examined with cine magnetic resonance imaging (CMRI) 1,4, and 26 weeks after myocardial infarction. Thirty‐two patients had anterior MI and 29 patients had posterior MI. According to enzyme‐derived infarct weight, 15 patients had small infarcts (<20 g), 19 had intermediate‐sized infarcts (20–40 g), and 27 patients had large infarcts (>40 g). CMRI was performed in the true short axis of the left ventricle. In each examination, left ventricular end‐diastolic and end‐systolic volume indices (LVEDVI, LVESVI), stroke volume index (LVSVI), ejection fraction (LVEF), and regional thickness, mass, and motility of the myocardial wall—diastolic thickness (IDdia), infarct mass (IM) and motility (MOT) of the infarct area and diastolic and systolic thickness (VDdia, VDsys), muscular mass (VM), and motility (VMOT)—were determined. In addition, patients were divided into subgroups according to New York Heart Association (NYHA) functional status at baseline.

Results: In the total group, LVEDVI increased from 73·9 ± 23·5 ml/m2 to 85·4 ± 28·1 ml/m2 (p <0·001) and LVESVI from 40·5 ± 19·4 ml/m2 to 51·2 ± 29·0 ml/m2 (p <0·001). In the subgroups the development depended on infarct size and location. LVSVI and LVEF remained more or less constant except for large anterior infarctions. All changes of the myocardial wall depended on infarct size and location: In all patients IDdia decreased from 10·4 ± 1·6 mm to 8·9 ± 1·7 mm (p <0·001), IMOT from 2·0± 1·6 mm to 0·5 ±2·9 mm (p<0·001). IM increased from 41 ± 21 g to 45 ± 25 g (p <0·001). In the total group, VDdia increased from 11·9 ± 1·6 mm to 12·4 ± 1·8 mm (p <0·05), VDsys from 16·6 ± 2·5 mm to 17·2 ± 3·1 mm (p <0·05). In the subgroups changes varied: VDdia and VDsys decreased markedly in large anterior wall infarctions. VM increased in the total cohort from a mean of 246 ± 66 g to 276 ± 80 g (p <0·001). VMOT decreased from 7·1 ±2·4 mm to 6·3 ± 2·7 mm (p <0·05). Loss of motility was most pronounced in anterior infarctions. The volume–mass ratio, a measure of the success of compensation of volume increase by myocardial hypertrophy, decreased in small infarcts, remained unchanged in intermediate infarcts, and increased in large infarcts. There was a trend toward improvement of the NYHA functional status during the observation period.

Conclusions: Changes of the left ventricular chamber during the first 6 months following MI are dependent on its size and location, with large anterior infarctions having the worst course. Myocardial wall remodeling is also dependent on infarct size and location, and the volume–mass ratio increases in the presence of large areas of necrosis, indicating the noncompensatory effect of myocardial hypertrophy. However, these changes have no clinical effect during the first half year after MI.