Abstract
Cardiac magnetic resonance imaging (MRI) is a gold standard to assess functional and anatomical properties of the living heart. Inflammation changes the myocardial tissue and, furthermore, MR relaxation properties. Continuous-wave (CW) longitudinal rotating frame relaxation time (T(1ρ)) mapping has been used to assess myocardial fibrosis and inflammation. Conventional T(2) relaxation time is a known marker of edema in the myocardium. In this study, we assessed myocardial inflammation after viral infection in a mouse heart using CW-T(1ρ) and T(2) relaxation times. Adenoviral human vascular endothelial growth factor-A(165) (AdVEGF-A(165)) and empty control adenoviral vector with cytomegalovirus promoter (AdCMV) gene transfers were used to induce inflammation in the mouse myocardium. In vivo CW-T(1ρ) and T(2) relaxation time measurements were performed in both groups (AdVEGF-A(165) and AdCMV) after -1-, 1-, 3-, 7-, 14-, 21-, and 28-day post-injection. The inflammation associated with gene transfer was verified by hematoxylin and eosin staining after 14-day post-injection. One day after AdVEGF-A(165) and AdCMV injections and inflammatory reactions, CW-T(1ρ) showed a significant increase, which stayed increased as a function of time. T(2) also increased significantly after both injections and inflammatory reactions as compared to before injections. Contrast difference between inflammation and remote areas was visually observed in both groups in CW-T(1ρ) and T(2) maps. Hematoxylin and eosin staining revealed the area of inflammation after Ad injection in both groups after 14-day post-injection. This study showed that both acute and chronic phases of the inflammatory reaction in mouse myocardium caused by myocardial adenoviral injections were associated with increased CW-T(1ρ) and T(2) relaxation time constants. Furthermore, the inflammatory reaction can be followed up with rotating frame and conventional relaxation time mappings.