Oxygenation-sensitive cardiovascular magnetic resonance

Oxygenation-sensitive cardiovascular magnetic resonance (CMR) is a non-contrast technique that allows the non-invasive assessment of myocardial oxygenation. It capitalizes on the fact that deoxygenated hemoglobin in blood can act as an intrinsic contrast agent, changing proton signals in a fashion that can be imaged to reflect the level of blood oxygenation. Increases in O(2) saturation increase the BOLD imaging signal (T2 or T2*), whereas decreases diminish it. This review presents the basic concepts and limitations of the BOLD technique, and summarizes the preclinical and clinical studies in the assessment of myocardial oxygenation with a focus on recent advances. Finally, it provides future directions and a brief look at emerging techniques of this evolving CMR field

Cardiovascular magnetic resonance characterization of myocardial and vascular function in rheumatoid arthritis patients

BACKGROUND: Rheumatoid arthritis (RA) is a multisystem, autoimmune disorder and confers one of the strongest risks for cardiovascular disease (CVD) morbidity and mortality. OBJECTIVE: To assess myocardial function and vascular stiffness in RA patients with and without cardiovascular risk factors (CVRFs) using cardiovascular magnetic resonance (CMR). METHODS: Twenty-three RA patients with no CVRFs (17 female, mean age 52 ± 13 years), 46 RA patients with CVRFs (32 female, mean age 53 ± 12), 50 normal controls (32 female, mean age 50 ± 11 years), and 13 controls with CVRFs (7 female, mean age 55 ± 7 years), underwent CMR at 1.5 Tesla, including evaluation of left ventricular (LV) ejection fraction, strain, and vascular elasticity (aortic distensibility [AD] and pulse wave velocity [PWV]). Disease activity and duration were recorded for each patient. Subjects with known symptomatic CVD were excluded. RESULTS: LV volumes, mass, and ejection fraction were similar in the four groups. RA patients with CVRFs showed the greatest abnormality in mid short-axis circumferential systolic strain, peak diastolic strain rate, and vascular indices. RA patients without CVRFs showed a similar degree of vascular dysfunction and deformational abnormality as controls with CVRFs. AD and total PWV correlated with myocardial strain and RA disease activity. On multivariate regression analysis, strain was related to age, RA disease activity, AD, and PWV. CONCLUSION: CMR demonstrates impaired myocardial deformation and vascular function in asymptomatic RA patients, worse in those with CVRFs. Subclinical cardiovascular abnormalities are frequent and appear to be incremental to those due to traditional CVRFs and likely contribute to the excess CVD in RA