Morphologic validation of reperfused hemorrhagic myocardial infarction by cardiovascular magnetic resonance

Cristina Basso1, Francesco Corbetti, Caterina Silva

  • 1Department of Medic-Diagnostic Sciences and Special Therapies, University of Padua Medical School, Padua, Italy.

Insights

Cardiovascular magnetic resonance (CMR) T2 hypointense signals and susceptibility artifacts in late gadolinium enhancement areas of reperfused myocardial infarction (MI) correlate with hemorrhage, indicating irreversible vascular injury.

Area of Science:

  • Cardiovascular Imaging
  • Pathology
  • Medical Diagnostics

Background:

  • Acute myocardial infarction (MI) requires assessment of tissue injury and microvascular obstruction.
  • Late gadolinium enhancement (LGE) on cardiovascular magnetic resonance (CMR) is used to identify infarcts, but its interpretation in reperfused MI can be complex.
  • Hemorrhage within the infarct zone is a potential factor influencing CMR signal characteristics.

Observation:

  • Ex vivo CMR T2 sequences showed low-signal intensity areas that strongly correlated with quantified hemorrhage on histology (R=0.93).
  • Ex vivo LGE sequences revealed bright areas with dark rims, consistent with magnetic susceptibility effects from hemorrhage.
  • In vivo CMR demonstrated corresponding hypointense T2 signals and hyperintense LGE areas with susceptibility artifacts within the MI core.

Findings:

  • Pathologic examination revealed significant myocardial infarction (MI) and hemorrhage, increasing from base to apex.
  • Ex vivo T2 CMR signal intensity directly correlated with the extent of hemorrhage.
  • Susceptibility effects on LGE imaging corresponded to areas of hemorrhage.

Implications:

  • CMR T2 hypointensity and LGE susceptibility artifacts in reperfused MI are indicative of interstitial hemorrhage.
  • These findings suggest irreversible vascular injury in the infarct core.
  • Pathologic correlation validates the use of specific CMR sequences for detecting hemorrhage in myocardial infarction.