1026 Infarct size determines infarct healing and ventricular remodeling in patients with successfully reperfused ST-elev
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BioMed Central
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Meeting abstract
1026 Infarct size determines infarct healing and ventricular remodeling in patients with successfully reperfused ST-elevation myocardial infarction Pier Giorgio Masci*, Steven Dymarkowski, Stefan Janssens, Frank E Rademakers and Jan Bogaert Address: Gasthuisberg University Hospital, Leuven, Belgium * Corresponding author
from 11th Annual SCMR Scientific Sessions Los Angeles, CA, USA. 1–3 February 2008 Published: 22 October 2008 Journal of Cardiovascular Magnetic Resonance 2008, 10(Suppl 1):A151
doi:10.1186/1532-429X-10-S1-A151
Abstracts of the 11th Annual SCMR Scientific Sessions - 2008
Meeting abstracts – A single PDF containing all abstracts in this Supplement is available here. http://www.biomedcentral.com/content/pdf/1532-429X-10-S1-info.pdfThis abstract is available from: http://jcmr-online.com/content/10/S1/A151 © 2008 Masci et al; licensee BioMed Central Ltd.
Background and purpose 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.
Methods and results 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 circumfere
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