Endogenous assessment of myocardial fibrosis with quantitative MRI

In this thesis, we have studied the use of quantitative MR contrast mechanisms, that could potentially be used for endogenous detection of myocardial fibrosis in the clinic. we have mainly focused on T2*, T1ρ MRI and Magnetization Transfer Imaging, and found that T1ρ -mapping, and Magnetization Transfer imaging are most promising. We found a significantly higher T1ρ-relaxation time in myocardial infarct tissue, compared to healthy remote tissue, both in a porcine animal model and chronic infarct patients. A comparison with LGE as gold standard for infarct detection, showed that native T1ρ –maps can be used to locate the myocardial scar area. For diffuse myocardial fibrosis, we have shown that T1ρ relaxation times correlate with the amount of fibrosis, determined by histology, and with extracellular volume fraction, measured in vivo. The results of native T1 –mapping in DCM patients did not indicate a significant relation with extracellular volume fraction in patients. Measurements of magnetization transfer in an animal model showed a decrease in magnetization transfer ratio in the infarct area, and the addition of an MT pulse in front of a T1ρ-mapping experiment resulted in a significantly higher T1ρ-relaxation time. For infarct detection with T1ρ –mapping the main advantage compared to gold standard LGE imaging is that a contrast agent is no longer required. As a first step towards clinical applications, this technique could be used as an alternative in patients that are unable to receive a gadolinium based contrast agent, such as patients with severe renal failure. Also for diffuse fibrosis, T1ρ –mapping can be used as an alternative to the gadolinium based ECV-mapping. When the sensitivity of the technique is significantly increased, it could be considered as an alternative for LGE and ECV-mapping in clinical practice for all patients.