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4 Four-dimensional left ventricular blood flow energetics independently predict adverse remodelling post st-elevation myocardial infarction
  1. Pankaj Garg1,
  2. Rob J van der Geest2,
  3. Peter P Swoboda1,
  4. Saul Crandon1,
  5. Graham J Fent1,
  6. James RJ Foley1,
  7. Laura E Dobson1,
  8. Tarique Al Musa1,
  9. Sebastian Onciul1,
  10. Sethumadhavan Vijayan1,
  11. Pei G Chew1,
  12. Louise AE Brown1,
  13. Malenka Bissell1,
  14. Mariëlla ECJ Hassell3,
  15. Robin Nijveldt3,
  16. Mohammed SM Elbaz2,
  17. Jos JM Westenberg2,
  18. Erica Dall’Armellina1,
  19. John P Greenwood1,
  20. Sven Plein1
  1. 1Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, UK
  2. 2Leiden University Medical Centre, Leiden, The Netherlands
  3. 3Department of Cardiology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands


Introduction Myocardial infraction (MI) leads to complex changes in left ventricular (LV) haemodynamics. It remains unknown how four-dimensional (4D) acute changes in LV-cavity blood flow kinetic energy (KE) affect LV remodelling. We hypothesised that LV blood flow energetics is independently associated with adverse LV-remodelling.

Methods We recruited 69 revascularised ST-elevation MI patients. All patients underwent cardiovascular magnetic resonance (CMR) at 1.5 T within 48 hours and at 3 months. CMR included cines, early/late gadolinium enhancement and whole-heart 4D flow. CMR analysis included: LV volumes, infarct size (IS,%), microvascular obstruction (MVO,%), two-dimensional, retrospective valve tracking derived mitral inflow metrics and 4D KE components. KE was derived using novel, semi-automated method by using endocardial contours on short-axis cines to extract intra-cavity velocity profile. Adverse LV-remodelling was defined as increase in LV end-diastolic volume by 15%.

Results Thirteen (19%) patients developed adverse LV-remodelling. Demographics were comparable between patients with/without remodelling. Baseline CMR in adverse LV-remodelling-group showed significantly lower EF, LV KE, Systolic, A-wave, in-plane KEs and increased MVO (p<0.05). In stepwise-regression analysis, only acute MVO (beta=0.17±0.06, p<0.05) and acute A-wave KE (beta=−0.17±0.08, p<0.05) independently predicted adverse remodelling at 3 months. A regression-model comprising of acute MVO and A-wave KE had high predictive value for adverse LV-remodelling (area under the curve=0.82, 95% confidence interval=0.7–0.9, p<0.001).

Conclusion LV haemodynamic assessment by novel, semi-automated, 4D KE mapping adds incremental value to predict adverse LV-remodelling. A-wave KE and MVO size early after acute MI are independently associated with adverse LV-remodelling.

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