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8 Myocardial haemorrhage after acute reperfused st-elevation myocardial infarction: temporal evolution, relation to microvascular obstruction and prognostic significance
  1. DJA Carrick1,
  2. C Haig2,
  3. N Ahmed1,
  4. H Eteiba3,
  5. M McEntegart3,
  6. S Watkins3,
  7. M Lindsay3,
  8. A Radjenovic1,
  9. KG Oldroyd1,
  10. C Berry1
  1. 1Cardiovascular Research Centre of Glasgow, Institute of Cardiovascular and Medical Sciences, Glasgow, UK
  2. 2University of Glasgow, Robertson Centre for Biostatistics, Glasgow, UK
  3. 3Golden Jubilee National Hospital, Cardiology, Glasgow, UK


Background The success of emergency coronary reperfusion therapy in ST-elevation myocardial infarction (STEMI) is commonly limited by failed tissue perfusion.

Purpose To assess the clinical significance of myocardial haemorrhage using cardiac magnetic resonance (CMR) in survivors of acute STEMI and assess the temporal evolution of intramyocardial haemorrhage (IMH) versus microvascular obstruction (MVO) in a serial imaging subset.

Methods 286 reperfused STEMI patients underwent CMR 2-days and 6-months post-MI. IMH was taken to represent a hypointense infarct core with a T2* value <20 ms. 30 STEMI patients underwent serial CMR at 4 time points: 4–12 h, 3-days, 10-days and 6–7 months post reperfusion. Cardiovascular death or heart failure hospitalisation (CVD/HF) was independently assessed during follow-up.

Results 245 STEMI patients had evaluable T2* data and 101 (41%) patients had IMH. 133 (51%) patients had MVO. All of the patients with IMH had MVO. IMH was multivariably associated with adverse remodelling, independent of baseline LVEDV (OR (95% CI): 2.64 (1.07, 6.49); p = 0.035). IMH was also multivariably associated with CVD/HF post-discharge (HR (95% CI): 12.9 (1.6, 100.8); p = 0.015).

In the serial imaging subgroup, IMH occurred in 7(23%), 13(43%), 11(33%), and 4(13%) patients at 4–12 h, 3-days, 10-days and 7-months, respectively. The amount of MVO was greatest 4–12 h post-reperfusion, then fell progressively over time. In contrast, the amount of IMH increased dynamically from 4–12 h with a peak at 3 days. MVO resolved by day 10 in 8 patients (44%), 2 (25%) of whom had IMH. Whereas MVO persisted in 10 patients (56%), all (100%) of whom had IMH.

Conclusion IMH is independently associated with adverse remodelling and ACD/HF post-discharge. T2* imaging differentiates persistent, structural microvascular destruction from functional, potentially reversible MVO. IMH is a biomarker with potential to reflect the efficacy of therapeutic interventions in STEMI patients.

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