Resting myocardial perfusion quantification with CMR arterial spin labeling at 1.5 T and 3.0 T

Eight subjects were imaged, with scans at 3.0 T showing significantly higher T1 values (P < 0.001) and signal-to-noise ratios (SNR) (P < 0.002) than scans at 1.5 T. The average MBF was found to be 0.990 ± 0.302 mL/g/min at 1.5 T and 1.058 ± 0.187 mL/g/min at 3.0 T. The repeatability at 3.0 T was improved 43% over that at 1.5 T, although no statistically significant difference was found between the two field strengths. In the simulation, the accuracy and the repeatability of the MBF calculations were 61% and 38% higher, respectively, at 3.0 T than at 1.5 T, but no statistically significant differences were observed. There were no significant differences between the myocardial perfusion data sets obtained from the two independent observers. Additionally, there was a trend toward less variation in the perfusion data from the two observers at 3.0 T as compared to 1.5 T.This suggests that this ASL technique can be used, preferably at 3.0 T, to quantify myocardial perfusion in humans and with further development could be useful in the clinical setting as an alternative method of perfusion analysis.Myocardial blood flow (MBF), defined as the rate at which blood enters the myocardial microvasculature through the coronary artery network, is an important indicator of myocardial perfusion changes, as seen in myocardial stress and ischemic heart disease [1-3]. The gold standard for human myocardial perfusion analysis is positron emission tomography (PET), but this technique is marred by limited spatial resolution, high cost, limited availability, and patient radiation exposure [4]. Additionally, first-pass perfusion cardiovascular magnetic resonance (CMR) would allow efficient measurement of myocardial perfusion, but the necessity of a gadolinium-based contrast agent would limit this technique in terms of repetition in a single CMR examination and use in the renal failure patient. However, arterial spin labeling (ASL), through measurement of myocardial and blood T1, is capable