Abstract
Background
Cardiovascular diseases are the leading cause of death worldwide due to population growth and aging. Myocardial infarction is one of the most crucial cardiovascular diseases. Acute myocardial infarction is conventionally imaged with T2 mapping due to its sensitivity related to the correlation times of edema and free-water molecules. Chronic myocardial infarction, which contains fibrosis and scar tissue, is conventionally imaged with MRI with T1 weighting using contrast agents involved in late gadolinium enhancement and extracellular volume since contrast agent wash out from fibrosis and scar tissue is delayed compared to myocardium. So far, imaging acute myocardial infarcts is related to T2 mapping, and imaging of scar tissue and fibrosis has been limited to techniques with contrast agent injection. Rotating frame relaxation times T1ρ and T2ρ mapping were developed to provide robust measurements with relatively wide B1 and B0 range for these quantities. Since rotating frame methods have different correlation times than T2 and T1, these methods can be used to sensitively and specifically characterize both acute and chronic myocardial infarctions. In this study, acute (2 hours) and chronic (7 days after occlusion) myocardial infarcts in and ex vivo mouse models were imaged with rotating frame relaxation time mapping without the use of contrast agents.
Methods
In vivo imaging protocol contained adiabatic T1ρ and adiabatic T2ρ, both with two different HSn pulses, continuous wave T1ρ and conventional T2, together with cine imaging. Mice were imaged 2 hours and 7 days after myocardial infarction. Mice were sacrificed at the 2-hour or at the 7-day time point. Ex vivo measurements contained adiabatic T1ρ and adiabatic T2ρ with two different HSn pulses, continuous wave T1ρ, T1 and T2. After MRI studies, mouse hearts were fixed, and myocardial infarcts were verified using dystrophin and hematoxylin and eosin histology stainings.
Results
A clear difference between infarcted and normal myocardium was visible at the 2-hour time point in rotating frame relaxation time mapping. Relative relaxation time difference in adiabatic T2ρ with HS4 pulse might be sensitive to both acute edema reaction and chronic infarction. Also, in vivo and ex vivo results of adiabatic T1ρ with both HSn pulses and continuous wave T1ρ measurements showed relative relaxation time, the difference between infarcted and normal myocardium at 2 hours after the occlusion, and the difference increased at the 7-day time point.
Conclusion
This study showed that rotating frame relaxation time methods have the potential to be a non-invasive MR diagnostic marker for acute and chronic myocardial infarcts.