Purpose To determine the correlation in abdominal aortic stiffness obtained using magnetic resonance elastography (MRE) (μMRE) and MRI-based pulse wave velocity (PWV) shear stiffness (μPWV) estimates in normal volunteers of varying age; and also to determine the correlation between μMRE and μPWV. Methods In-vivo aortic MRE and MRI were performed on 21 healthy volunteers with ages ranging from 18 to 65 years to obtain wave and velocity data along the long-axis of the abdominal aorta. The MRE wave images were analyzed to obtain mean stiffness, and the phase contrast images were analyzed to obtain PWV measurements and indirectly estimate stiffness values from Moens-Korteweg equation. Results Both μMRE and μPWV measurements increased with age, demonstrating linear correlations with R2 values of 0.81 and 0.67, respectively. Significant difference (p≤0.001) in mean μMRE and μPWV between young and old healthy volunteers was also observed. Furthermore, a poor linear correlation of R2 value of 0.43 was determined between μMRE and μPWV in initial pool of volunteers. Conclusion The results of this study indicate linear correlations between μMRE and μPWV with normal aging of the abdominal aorta. Significant differences in mean μMRE and μPWV between young and old healthy volunteers were observed.

At this time, further evaluations must be done in the prehospital setting to determine the ease of use and true sensitivity and specificity of these scales in identifying LVOs.

Iron is an essential mineral in many proteins and enzymes in human physiology, with limited means of iron elimination to maintain iron balance. Iron accrual incurs various pathological mechanisms linked to cardiovascular disease. In atherosclerosis, iron catalyzes the creation of reactive oxygen free radicals that contribute to lipid modification, which is essential to atheroma formation. Inflammation further fuels iron-related pathologic processes associated with plaque progression. Given iron’s role in atherosclerosis development, in vivo detection techniques sensitive iron are needed for translational studies targeting iron for earlier diagnosis and treatment. Magnetic resonance imaging (MRI) is uniquely able to quantify iron in human tissues noninvasively and without ionizing radiation, offering appealing for longitudinal and interventional studies. Particularly intriguing is iron’s complementary biology vs. calcium, which is readily detectable by computed tomography (CT). This review summarizes the role of iron in atherosclerosis with considerable implications for novel diagnostic and therapeutic approaches.

Objective Iron has been implicated in atherogenesis and plaque destabilization, while less is known regarding iron-related proteins in this disease. We compared ex vivo quantities to in vivo vessel wall T2*, which is a noncontrast magnetic resonance relaxation time that quantitatively shortens with increased tissue iron content. We also tested the hypothesis that carotid atherosclerosis patients have abnormal T2* times vs. controls that would help support a role for iron in human atherosclerosis. Methods and Results 46 patients undergoing carotid endarterectomy and 14 subjects without carotid disease were prospectively enrolled to undergo carotid MRI. Ex vivo measurements were performed on explanted plaque and 17 mammary artery samples. Plaques vs. normal arteries had higher levels of ferritin (median = 7.3 [IQR=4 – 13.8] vs. 1.0 [0.6 – 1.3] ng/mg, P < .001) and oxidized low-density lipoprotein (0.17 [0.12 – 0.30] vs. 0.01 [0.003 – 0.03] ng/mg, P < .001) as well as hepcidin (8.7 [4.6 – 12.4] vs. 2.6 [1.3 – 7.0] ng/mL, P = .03); serum hepcidin levels did not distinguish atherosclerosis patients from controls (40.6 [18.8 – 88.6] vs. 33.9 [17.6 – 55.2], P = 0.42). Shorter in vivo T2* paralleled larger plaque volume (ρ = −.44, p = 0.01), and diseased arteries had shorter T2* values compared to controls (17.7 ± 4.3 vs. 23.0 ± 2.4 ms, P < .001). Conclusions Diseased arteries have greater levels of iron-related proteins ex vivo and shorter T2* times in vivo. Further studies should help define T2*'s role as a biomarker of iron and atherosclerosis.