A segmental, multislice, multi-echo T2* MRI approach could be useful in heart iron-overloaded patients to account for heterogeneous iron distribution, demonstrated by histological studies. However, segmental T2* assessment in heart can be affected by the presence of geometrical and susceptibility artefacts, which can act on different segments in different ways. The aim of this study was to assess T2* value distribution in the left ventricle and to develop a correction procedure to compensate for artefactual variations in segmental analysis. MRI was performed in four groups of 22 subjects each: healthy subjects (I), controls (II) (thalassemia intermedia patients without iron overload), thalassemia major patients with mild (III) and heavy (IV) iron overload. Three short-axis views (basal, median, and apical) of the left ventricle were obtained and analyzed using custom-written, previously validated software. The myocardium was automatically segmented into a 16-segment standardized heart model, and the mean T2* value for each segment was calculated. Punctual distribution of T2* over the myocardium was assessed, and T2* inhomogeneity maps for the three slices were obtained. In group I, no significant variation in the mean T2* among slices was found. T2* showed a characteristic circumferential variation in all three slices. The effect of susceptibility differences induced by cardiac veins was evident, together with low-scale variations induced by geometrical artefacts. Using the mean segmental deviations as correction factors, an artefact correction map was developed and used to normalize segmental data. The correction procedure was validated on group II. Group IV showed no significant presence of segmental artefacts, confirming the hypothesis that susceptibility artefacts are additive in nature and become negligible for high levels of iron overload. Group III showed a greater variability with respect to normal subjects. The correction map failed to compensate for these variations if both additive and percentage-based corrections were applied. This may reinforce the hypothesis that true inhomogeneity in iron deposition exists.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1002/nbm.1121 | DOI Listing |
Haematologica
January 2025
Department of Medicine, University of Verona and Azienda Ospedaliera Universitaria Integrata of Verona, Verona, Italy; Veneto Region Referral Center for Iron Disorders and European Reference Network Center for Rare Hematological Diseases "EuroBloodNet".
Not available.
View Article and Find Full Text PDFJ Med Chem
January 2025
Department of Pharmacy, University of Naples Federico II, Via D. Montesano 49, Naples 80131, Italy.
Iron homeostasis is strictly related to numerous physiological pathways including cell cycle progression and cell growth. The newest anticancer strategies focus on either depleting the cells with a suitable chelator or increasing their loading by administering iron complexes to induce ferroptosis. Iron depletion inhibits cell proliferation, while iron overload induces the damage of guanine nucleobases in G-quadruplex structures via ROS generation, leading to genome instability.
View Article and Find Full Text PDFRev Cardiovasc Med
December 2024
Department of Cardiology, Royal Gwent Hospital, NP20 2UB Newport, UK.
Atherosclerosis (AS) is a growing global health epidemic and is the leading cause of cardiovascular health problems, including ischemic stroke, coronary artery disease, and peripheral vascular disease. Despite extensive research on the underlying mechanisms of AS, iron remains an under-investigated mediator in the atherosclerotic process. Iron's involvement in AS is primarily linked to the iron-induced programmed cell death process known as ferroptosis.
View Article and Find Full Text PDFFront Pharmacol
December 2024
The Affiliated Traditional Chinese Medicine Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Backgrounds: Ferroptosis is a form of regulated cell death. The accumulation of iron in the brain is linked to trigger ferroptosis after an ischaemic stroke (IS). Naoqing formula (NQ) is a traditional Chinese medicine metabolites with the clinical function of activating blood circulation, which is applied to treat IS clinically in China.
View Article and Find Full Text PDFCureus
November 2024
Community Medicine, Baba Raghav Das Medical College, Gorakhpur, IND.
Background Thalassemia is the most common form of hereditary anemia caused by the impaired synthesis of one of the two globin chains in hemoglobin. A decrease in beta-globin chains occurs in beta-thalassemia, resulting in a relative excess of alpha-globin chains. Thalassemia major is the severe form of thalassemia, which requires frequent blood transfusions for survival.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!