- Meeting abstract
- Open Access
1026 Infarct size determines infarct healing and ventricular remodeling in patients with successfully reperfused ST-elevation myocardial infarction
© Masci et al; licensee BioMed Central Ltd. 2008
- Published: 22 October 2008
- Infarct Size
- Large Infarct
- Small Infarct
- Global Leave Ventricular
- Remote Myocardium
We sought to evaluate the influence of infarct size on infarct healing and left ventricular (LV) remodeling in patients with a first, successfully reperfused ST-elevation myocardial infarction (STEMI) using MRI.
Fifty-eight patients were studied in the first week (1 W) and 4 months (4 M) after the acute event. At 1 W, infarct size was related to infarct transmurality (r = 0.62, p < 0.001), infarct surface (r = 0.78, p < 0.001), circumferential and longitudinal infarct length (r = 0.67, p < 0.001 and r = 0.69, p < 0.001, respectively), concomitant microvascular obstruction (r = 0.74, p < 0.001), area at risk (r = 0.78, p < 0.001) as well as the ratio of infarct size to area at risk (r = 0.68, p < 0.001), and inversely related to systolic wall thickening in the infarct (r = 0.45, p < 0.001) and peri-infarct area (r = 0.37, p = 0.004), and LV EF (r = 0.59, p < 0.001). The median of normalized infarct size at 1 W, ie, 17.1% of LV mass, was used to create a small and large size infarct group. Large infarcts presented with higher maximum serum troponin I levels than small infarcts (115 ± 68 μg/L versus 60 ± 28 μg/L, p = 0.003. While shrinkage in infarct size at 4 M was similar between groups (43 ± 18% in small versus 42 ± 16% in large infarcts, p = 0.99), the infarct surface did shrink significantly more in small (15.7 ± 15.9%) than large infarcts (4.0 ± 11.9%), p = 0.005 with most pronounced differences in longitudinal direction, i.e. 14.5 ± 12.5% in small versus 5.0 ± 8.6% in large infarcts, p = 0.003. On the other hand, thinning of the infarcted wall was more pronounced in large (29.8 ± 18.8%) than in small infarcts (13.5 ± 22%), p = 0.004. Functionally, small infarcts recovered systolic wall thickening in the infarct (p = 0.01) and peri-infarct area (p = 0.004), matching with improvement in LV EF (52.7 ± 7.0% at 1 W tot 55.7 ± 7.3% at 4 M, p = 0.003), while large infarcts showed a lack of recovery in regional or global LV function. At 1 W, large infarcts showed more pronounced flattening of the infarcted myocardium as expressed by a larger circumferential radius of curvature (p = 0.019). At 4 M infarct size was related to expansion of the remote myocardium (circumferential radius of curvature at end diastole: r = 0.45, p = 0.001, end systole: r = 0.54, p = 0.001), and global adverse remodeling (LV EDV r = 0.39, p = 0.003; LV ESV r = 0.58, p < 0.001, LV EF r = -0.61, p < 0.001).
The amount of necrotic myocardium strongly determines the pattern of infarct healing, and regional and global LV remodeling. Small infarcts show favorable infarct healing (less thinning, more surface shrinkage) and remodeling with a beneficial impact on regional and global function. Large infarcts, in contrast, show more extensive infarct thinning, lack of infarct surface shrinkage leading to adverse remodeling, and lack of functional recovery.
This article is published under license to BioMed Central Ltd.