Article Text


4 Extracellular volume in the infarct zone is associated with clinical and mri measures of infarct severity in survivors of acute stemi
  1. J Carberry1,
  2. D Carrick1,2,
  3. C Haig3,
  4. SM Rauhalammi1,
  5. N Ahmed1,
  6. I Mordi1,2,
  7. M McEntegart2,
  8. M Petrie1,
  9. H Eteiba1,
  10. S Hood1,
  11. S Watkins1,
  12. M Lindsay1,
  13. A Davie1,
  14. A Mahrous2,
  15. A Radjenovic1,
  16. I Ford3,
  17. KG Oldroyd1,
  18. C Berry1,2
  1. 1BHF Glasgow Cardiovascular Research Center, Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK
  2. 2West of Scotland Heart and Lung Center, Golden Jubilee National Hospital, Dumbartonshire, UK
  3. 3Robertson Center for Biostatistics, University of Glasgow, Glasgow, UK


Background The clinical significance of extracellular volume (ECV) expansion in infarcted myocardium post-STEMI is unknown. Myocardial ECV can be estimated by cardiac magnetic resonance imaging (CMR) using T1 MOLLI maps before and after contrast. We repeatedly measured infarct ECV in STEMI survivors, and assessed the relationships between ECV, peak troponin T and baseline infarct size.

Methods Acute STEMI survivors were enrolled in a single-centre cohort study (BHF MR-MI study – NCT02072850). Contrast-enhanced CMR was performed at 1.5 Tesla (Siemens MAGNETOM Avanto) 2 days and 6 months post-MI. T1 mapping with MOLLI was performed before and 15 min after contrast (0.15 mmol/kg gadoterate meglumine). ECV analysis was performed by outlining regions of interest (ROIs) in infarcted myocardium and left ventricular (LV) blood pool. ROIs were representative of the infarct including microvascular obstruction. ECV was calculated as the relaxation rate (R1=1/T1) for myocardium and LV blood pool before vs. after contrast, corrected for haematocrit. Infarct size was measured using late gadolinium images and expressed as a percentage of LV mass. Infarct ECV at baseline and follow up was compared with peak troponin T measured at presentation and infarct size at baseline. Peak troponin T was log-transformed to improve normality and linearity.

Results 201 STEMI patients (mean age 58 ± 11 years; 156 (77%) male) were enrolled. Infarct ECV was similar at baseline and follow-up (51.3 ± 9.5% vs. 50.3 ± 12.0%, p = 0.097). Peak troponin T was widely variable (4256.7 ug/L ± 4020.8 ug/L). Peak troponin T was positively associated with infarct ECV at baseline (p < 0.001) and follow-up (p < 0.001). Infarct size at baseline was 18 ± 13% of LV mass and was positively associated with infarct ECV at baseline (p < 0.001) and follow-up (p < 0.001) (Table 1).

Abstract 4 Table 1

Association of infarct ECV at baseline and follow-up with peak troponin T and infarct size in linear regression analysis (n = 201)

Conclusion High peak troponin T and a large infarct size are predictors of higher infarct ECV at baseline and follow-up. Infarct ECV is associated with clinical and MRI measures of MI severity in survivors of STEMI.

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.