Low T2 Research Articles

High levels of glycated haemoglobin (HbA1c) are associated with lower knee joint cartilage quality and higher knee joint symptoms in healthy individuals.

In an asymptomatic population, we investigated the relationships between glycated haemoglobin (HbA1c) and cartilage T2 relaxation time at the knee joint level. Fourteen and 17 participants with high and normal levels of HbA1c were recruited, respectively. A blood sample was used to determine the HbA1c level. T2 relaxation time (T2) of the superficial and deep parts of the femoral cartilage in the anterior, central, and posterior topographical sites was calculated using magnetic resonance (1.5T) images. Each participant completed a knee injury and osteoarthritis outcome score questionnaire (KOOS) and a series of biomechanical analyses while running at their self-selected speed. The group with a high level of HbA1c had a lower score of KOOS symptoms than the other group (P < 0.05). HbA1c was found to be negatively related to the KOOS symptoms score. The group with a high level of HbA1c had low T2 values in all of the investigated topographical sites of the knee femoral cartilage (P < 0.05 in all cases). T2 was negatively correlated with HbA1c levels in all investigated knee femoral cartilage regions. Our data suggest that the subjects with high levels of HbA1c were those with low knee joint symptoms and lower values of T2. These results indicate that HbA1c could be correlated with cartilage deterioration due to its ability to dehydrate collagen fibre, possibly acting as a risk factor for the development of osteoarthritis.

Characterizing T1 in the fetal brain and placenta over gestational age at 0.55T.

T1 mapping and T1-weighted contrasts have a complimentary but currently under utilized role in fetal MRI. Emerging clinical low field scanners are ideally suited for fetal T1 mapping. The advantages are lower T1 values which results in higher efficiency and reduced field inhomogeneities resulting in a decreased requirement for specialist tools. In addition the increased bore size associated with low field scanners provides improved patient comfort and accessibility. This study aims to demonstrate the feasibility of fetal brain T1 mapping at 0.55T. An efficient slice-shuffling inversion-recovery echo-planar imaging (EPI)-based T1-mapping and postprocessing was demonstrated for the fetal brain at 0.55T in a cohort of 38 fetal MRI scans. Robustness analysis was performed and placental measurements were taken for validation. High-quality T1 maps allowing the investigation of subregions in the brain were obtained and significant correlation with gestational age was demonstrated for fetal brain T1 maps ( ) as well as regions-of-interest in the deep gray matter and white matter. Efficient, quantitative T1 mapping in the fetal brain was demonstrated on a clinical 0.55T MRI scanner, providing foundations for both future research and clinical applications including low-field specific T1-weighted acquisitions.

Cardiac magnetic resonance characteristics of the athlete's heart: deeper insights into cardiac remodelling

Abstract Cardiac magnetic resonance (CMR) offers precise quantification for myocardial parameters. Understanding the effects of different training volumes on the athlete’s heart could be the key to distinguishing between cardiac conditions. This study aims to investigate CMR parameters including T1- and T2 mapping in healthy athletes and less active individuals and explore their relationship with training volumes in both sexes. We included healthy athletes (weekly training hours &amp;gt;7) and less active age- and sex-matched control individuals (weekly training hours ≤6), and performed CMR examinations. We assessed ventricular volumes, masses, and function, and conducted T1- and T2-mapping on non-contrast short-axis images. A total of 270 CMR examinations were conducted, comprising 185 athletes (119 males, mean age 22±6 years, weekly training hours: 19±7) and 85 controls (50 males, mean age 26±3 years, weekly training hours: 3±2). In male athletes compared to less active individuals, we observed pronounced signs of sports-related cardiac remodeling, including increased end-diastolic volume and mass index (Left ventricular end-diastolic volume index (LVEDVi): 120±16 vs 97±12 ml/m2, p&amp;lt;0.001; left ventricular mass index (LVMi): 70±14 vs 53±9 g/m2, p&amp;lt;0.001). Similarly, female athletes exhibited significant sports adaptations compared to controls (LVEDVi: 103±12 vs 86±11 ml/m2, p&amp;lt;0.001; LVMi: 54±9 vs 39±5 g/m2, p&amp;lt;0.001). T1-mapping values in athletes were lower than in the control group for both sexes (males: 939±25 vs 961±20 p&amp;lt;0.001, females: 966±21 vs 985±17, p&amp;lt;0.001). T1 values showed negative correlations with training hours (r=-0.362, p&amp;lt;0.001), LVEDVi (r=-0.411, p&amp;lt;0.001), and LVMi (r=-0.546, p&amp;lt;0.001). A significant association between T1 values and training hours persisted across various models. In the raw model, every additional training hour correlated with a T1 reduction of 0.946 ms (p&amp;lt;0.001). Adjusting for age, sex, and heart rate (HR) in model 2, the association remained significant, with each additional training hour corresponding to a T1 reduction of 0.825 ms (p&amp;lt;0.001). Further adjustments for LVMi in model 3 revealed a significant association, with a decrease of 0.565 ms in T1 values for each additional training hour (p=0.002). Among athletes, training years associated with decreased T1 and increased ventricular end-diastolic volumes and myocardial mass indices (LVEDVi: r=0,232, p=0,002; p&amp;lt;0,001; LVMi: r=0,279, p&amp;lt;0,001; T1-mapping: r=-0,169; p=0,026). Examining the differences between sexes we found that female athletes respond slightly less to a unit of exercise compared to males. Our findings underscore that different training hours and invested years have a meaningful impact on physiological adaptation. Female athletes’ heart responds slightly less to these effects. But in both sexes, higher training hours resulted in lower T1 and this relationship persisted independent of the influences of age, HR, and LVMi.

Efficacy of native T1 mapping for patients with non-ischemic cardiomyopathy and ventricular functional mitral regurgitation undergoing transcatheter edge-to-edge repair

Abstract Background The objectives of this study were to investigate the efficacy of LV myocardial damage assessment by native T1 mapping obtained with cardiac magnetic resonance (CMR) for symptomatic heart failure (HF) patients with non-ischemic cardiomyopathy (NICM) and ventricular functional mitral regurgitation (VFMR) undergoing transcatheter edge-to-edge repair (TEER). Methods We studied 40 symptomatic HF patients with NICM and VFMR undergoing TEER. LV myocardial damage was defined as the native T1 Z-score which was converted from native T1 value obtained with CMR before TEER. The primary endpoint was defined as first re-hospitalization for HF or cardiovascular death over a median follow-up period of 12 months after TEER. Results Multivariable Cox-proportional hazards analysis showed that a native T1 Z-score was the only independent parameter associated with cardiovascular events (hazard ratio: 3.40, 95% confidential interval: 1.51-7.67), and patients with native T1 Z-score &amp;lt; 2.41 experienced significantly fewer cardiovascular events than those with a native T1 Z-score ≥ 2.41 (log-rank P = 0.001). Moreover, such a low native T1 Z-score and more severe VFMR in an effective regurgitant orifice area (EROA) ≥ 0.30 cm2 was associated with fewer cardiovascular events than for a high native T1 Z-score of ≥ 2.41 and less severe VFMR of EROA &amp;lt; 0.30 cm2 (log-rank P = 0.002). Conclusion Assessment of baseline LV myocardial damage by means of native T1 Z-score obtained with CMR without the use of gadolinium-based contrast media is a valuable additional parameter for better management of symptomatic NICM patients with reduced LVEF and VFMR following TEER.

Quantitative molecular imaging of cardiac fibrosis and response to treatment using a novel collagen III-specific MR imaging probe

Abstract Background Heart failure (HF) remains a major cause of morbidity and death affecting 64 million people globally[1]. Myocardial fibrosis, characterised by changes in type I (COL1) and III (COL3) collagen levels, may lead to HF [2,3]. Cardiac magnetic resonance (CMR) is a preferred method to detect fibrosis non-invasively, however it provides only indirect measures of fibrosis. Molecular imaging can directly visualise fibrosis, but current imaging probes target COL1. Purpose Here, we developed a COL3-specific probe and used molecular CMR imaging to directly quantify, previously undetectable, COL3 remodelling following myocardial infarction and to monitor treatment response. Methods Myocardial infarction (MI) was induced in mice by permanent ligation of the left anterior descending artery (LAD). Functional and molecular CMR images were acquired at days 10 and 21 post-MI in untreated and mice treated with Enalapril (20mg/kg/day) (n=6/group) using a 3T clinical MRI scanner. A subgroup of untreated mice was also imaged using a negative control probe and Gadovist (n=3). Cardiac function was assessed using 2D short-axis cine images of the left ventricle, and late gadolinium enhancement (LGE) images were obtained using T1-weighted 3D inversion recovery (IR) imaging. T1 mapping was performed using a 2D Look-Locker sequence with thirty inversion recovery images. Results Molecular CMR enabled selective profiling of the natural turnover of COL3 after MI with strong signal enhancement at day 10, and decreased enhancement at day 21 when COL3 is replaced by COL1 (Fig. 1A). Quantitative T1 maps discriminated between infarcted and remote myocardium with lower T1 values in the infarct and higher in the remote myocardium. Importantly, there was no enhancement using the scrambled probe or the clinical agent Gadovist. The imaging data were validated by histology (Fig.1B). Mice treated with Enalapril showed similar enhancement at day 10 compared to untreated mice (Fig. 2A). However, at day 21 mice treated with Enalapril showed higher signal enhancement compared to untreated mice, suggesting that Enalapril may prolong the presence of COL3 in the infarcted myocardium. Quantification of signal enhancement showed the increase in LGE volume and R1 relaxation rates within the infarcted myocardium at day 10, the subsequent decrease at day 21 and the prolongation of the COL3 signal at day 21 in enalapril treated mice (Fig.2B-C) Despite changes in cardiac fibrosis detected with molecular imaging, cardiac function was similar between the groups (Fig. 2D), suggesting that molecular change may precede functional changes. Conclusion(s) Quantitative molecular CMR imaging of COL3 enabled visualisation of changes in COL3 after MI and in response to treatment for the first time. This approach may provide insights into the role of COL3 in cardiac fibrosis and provide an non-invasive method to detect fibrosis early, stage fibrosis and monitor therapeutic response.

Association between CMR derived hepatic T1 times, tricuspid regurgitation severity, and outcomes

Abstract Background Hepatic T1 times have been shown to predict adverse clinical outcomes. However, up to date, the various causes contributing to changes in hepatic T1 times are not fully understood. So far, strong correlations with liver congestion and hepatic fibrosis have been demonstrated. Valvular heart disease, especially tricuspid regurgitation (TR), can lead to congestive hepatopathy (CH) and might significantly increase liver T1 values. In contrast, hepatic steatosis – commonly present in patients with cardiovascular disease - would result in lower T1 values. Currently, no studies are investigating the relationship between hepatic T1 times and TR. Methods We retrospectively measured hepatic T1-times, displayed on standard cardiac T1-maps, in an all-comer CMR cohort. Only patients, who underwent a comprehensive transthoracic echocardiogram within three weeks of CMR were included. Results 1029 participants (67±17 y/o, 44% female) had mean hepatic T1-times of 605±79ms. Overall, 41% (417) presented with non/trace, 38% (391) mild, 13% (135) moderate, 8% (85) severe, massive, and torrential tricuspid regurgitation. Liver T1 times were significantly correlated with TR severity (no/trace: 586±72ms; mild: 601±74ms; moderate: 634±84ms; severe/massive/torrential: 665±83ms; r= 0.25, p&amp;lt;0.001). Additionally, when adjusted for higher NT-proBNP levels, and right ventricular function in a linear regression model, TR severity was associated with hepatic T1 times (p&amp;lt;0.001). During follow-up (mean 53±36months), a total of 326 (32%) events occurred. Patients with higher T1 times and more severe tricuspid regurgitation were more likely to suffer events (adj.HR 1.44 [95%CI:1.23-1.69] per 100ms increase, p&amp;lt;0.001). Conclusion Tricuspid regurgitation exerts a notable influence on hepatic T1 times which is likely attributable to hepatic congestion. Importantly, hepatic T1 times were associated with outcomes even after adjustment for NTproBNP, LVEF, and RVEF. This underscores the importance of hepatic T1 times as both a marker of tricuspid regurgitation and an independent predictor of clinical outcomes.

Hypoperfused myocardium and systolic function in patients with AMI undergoing complete revascularization

Abstract Background and Aim Coronary revascularization is the standard treatment for acute myocardial infarction (AMI), while the restoration of epicardial flow is non-parallel to myocardial reperfusion. This study sought to investigate the dynamic of myocardial perfusion and its association with left ventricular (LV) systolic function in AMI patients undergoing complete revascularization. Methods AMI patients who underwent complete revascularization were prospectively enrolled, and hybrid positron emission tomography/magnetic resonance (PET/MR) was performed at 2 months and 1 year. Hypoperfused myocardium was defined as myocardium with reduced perfusion and normal metabolism. Results Forty-five patients (59.80 ± 10.68 years, 80.0% male) were enrolled, and hypoperfused myocardium (median: 12% of LV) was detected in 21 (46.7%) patients 2 months post-AMI. Patients with hypoperfused myocardium (Group A) had significantly higher hypersensitive C-reactive protein (hs-CRP) (p = 0.016) and lower T2 value (p = 0.010) than those without (Group B). In the follow-up PET/MR at 1 year, significant LV ejection fraction improvement was observed in Group A (56.39 ± 9.76% vs. 54.58 ± 10.39%, p = 0.016) but not in Group B (51.63 ± 13.09% vs. 50.79 ± 16.95%, p = 0.615). Six (31.6%) patients in Group A showed recovery of perfusion, of which there were more females (p = 0.025), fewer diabetics (p = 0.044), or overweight (p = 0.035), with better global longitudinal strain (GLS) (p = 0.005). Conclusions Myocardial hypoperfusion is not rare and evolves over time in AMI patients undergoing complete revascularization, of which the reversal is probably associated with improved LV systolic function.Structured Graphical AbstractRepresentative PET/MR image of 2 separat

One-Pot Fabrication of Kinetically Inert Ultrasmall Manganese(II) Chelate-Backboned Polymer Contrast Agents for High-Performance Magnetic Resonance Imaging.

Traditional macromolecules or nanoscale Mn2+ chelate-based magnetic resonance imaging (MRI) contrast agents (CAs) suffer from complicated and laborious synthesis processes, relatively low kinetic stability and T1 relaxivity, limiting their clinical applications. Herein, we fabricated a series of kinetically inert Mn2+ chelate-backboned polymers, P(MnL-PEG), through a facile and one-pot polymerization process. Particularly, P(MnL-PEG)-3 demonstrates a significantly higher T1 relaxivity of 23.9 Mn mM-1 s-1 at 1.5 T than that of previously reported small molecules and macromolecules or nanoscale Mn2+ chelate-based CAs. Due to its high T1 relaxivity, extended blood circulation, hepatocyte-specific uptake, and kidneys metabolism, P(MnL-PEG)-3 presents significantly enhanced contrast in blood vessel, liver, and kidneys imaging compared to clinical Gd3+-based CAs (Gd-EOB-DTPA and Gd-DOTA) at a dosage of 0.05 mmol Mn/Gd kg-1 BW, and can accurately diagnose orthotopic H22 liver tumors in vivo in animal models. We anticipate that this work will promote the development of clinically relevant MRI CAs.

Prospects of vaccination against pneumococcal infection based on the asthma phenotype

According to recent studies, bronchial asthma is characterized by a wide variability of the mechanisms of occurrence and progression. This heterogeneity is caused by patterns of predominant cells and inflammatory mediators, which determine differences in immunological parameters observed in patients with certain endotypes depending on the dominant type of mediators (high and low T2 inflammation). In long-term observations, a substantial research base has been accumulated justifying the effectiveness of vaccination against pneumococcal infection in patients with asthma. The vaccination decreases the frequency of exacerbations of the disease and hospitalizations in the short and medium term. However, these studies evaluated the asthma patients as a wholesome population, and it remains unexplored whether the effect of pneumococcal vaccines on asthma differs depending on the endotype of the disease and what are the mechanisms of such a differentiated effect.The aim of this work is to present the results of recent quality studies on changes in the profile of inflammatory asthma mediators under the action of immunobiological substances based on Streptococcus pneumoniae antigens, primarily from the vaccines.Conclusion. The asthma heterogeneity can lead to different clinical outcomes in pneumococcal infection and, respectively, the clinical effects of immunization in patients differentiate according to the nature of inflammation. In other words, the uniformity of the clinical effect of vaccination against pneumococcal infection in all patients in ongoing studies may represent the combined effect of molecular mechanisms regulating the specific activity of Th1-, Th2-, Th17-, NKT-, and Treg-cells. The results of studies proving the ability of pneumococcal vaccines to modulate the Th1-, Th2-, Th17-, Treg immune response in patients with asthma contributed to increased interest in developing new immunoregulatory therapeutic agents based on S. pneumoniae antigens.

Organ-Specific Iron Overload in Non-Transfusion-Dependent Thalassemia Patients: Insights from Quantitative MRI Evaluation

ObjectiveTo elucidate the iron load in different organs of non-transfusion-dependent thalassemia (NTDT) patients using magnetic resonance imaging (MRI) T2* scan. MethodsThirty-four NTDT patients, including 28 NTDT iron chelation without and 6 NTDT with iron chelation, together with 15 normal controls, underwent MRI examination between December 2022 and July 2024 were enrolled in the study. Measured T2* of the pituitary gland, kidney cortex, heart, liver, pancreas, spleen. Liver and spleen volumes were evaluated. ResultsOf the 28 patients in NTDT without iron chelation group, 19 patients with iron overload in the liver, 9 patients with iron overload in the kidneys, and 4 patients with iron overload in the spleen. Most patients with abnormal kidney and spleen iron (76.9 %) had liver iron overload. Compared with the control group, NTDT without iron chelation patients had lower T2* in the liver, kidney, and spleen (p < 0.05). And heart T2* was correlated with kidney T2* (r = 0.480, p = 0.010) and pancreas (r = 0.411, p = 0.037). Liver T2* was correlated with spleen T2* (r = 0.479, p = 0.011). Pancreas T2* was correlated with pituitary T2* (r = -0.433, p = 0.031). ConclusionsNTDT patients exhibit significant organ-specific iron overload, particularly in the liver, kidneys, and spleen. The correlations between iron levels in different organs suggest interconnected mechanisms of iron accumulation. These findings highlight the importance of regular MRI screening to monitor and manage iron overload in NTDT patients.

12325 Adrenocortical Carcinoma Masquerading As Pheochromocytoma In A Patient With Congenital Adrenal Hyperplasia

Abstract Disclosure: E.M. Niedzialkowska: None. A.A. Banka: None. Introduction: The development of adrenocortical carcinoma (ACC) in patients with congenital adrenal hyperplasia (CAH) is rare. The patients with CAH are at increased risk of adrenal tumors which is attributed to ACTH stimulation of adrenal gland if the disease is not appropriately treated. ACC cases mistaken for pheochromocytomas have been reported in the literature and are attributed to the variety of immunohistochemical markers expressed by the tumors. Case description:59 y.o female with salt-wasting CAH diagnosed at the age of 2 (21-hydroxylase deficiency) on hydrocortisone supplementation reported to the hospital due to episodes of sweating, tachycardia and hypertension. Work up revealed mildly elevated plasma normetanephrine 1 nmol/l (N &amp;lt;0.9), urine normetanephrine 1762 mcg (N&amp;lt;899), VMA 11.2 mcg/24hr (N 3.3-7.2). MRI of the abdomen revealed 2 left adrenal masses of 3.7 and 2.4 cm, right adrenal gland hyperplasia and low T1 and T2 enhancement. I-123 MIBG revealed increased activity and thickness of the right adrenal gland and no significant uptake on the left with nodular masses. The patient underwent left adrenalectomy with pathological report consistent with pheochromocytoma due to positive chromogranin and synaptophysin staining and moderate Ki activity. A year later follow up imaging showed an enhancing mass up to 7 cm at the suprarenal fossa invading the left kidney that was positive for nodular adrenocortical hyperplasia per pathology report. The patient continued to have elevated 17-OH- progesterone (2740 ng/l, N &amp;lt;51) despite compliance with her steroid therapy and suppressed ACTH. She underwent mass resection along with nephrectomy, splenectomy, partial colectomy and partial pancreatectomy. Pathology report was positive for adrenocortical carcinoma (positive chromogranin, synaptophysin, CAM 5.2, polycystic cytokeratin, Ki positive in greater than 10% of the tumor cells) with renal and regional lymph node invasion and colonic metastases. The patient was started on mitotane therapy but a year later PET scan was positive for liver and omental metastases and was subsequently started on carboplatin/etoposide followed by streptozocin/adriamycin with initial good response, however repeat PET a year afterwards showed progression of the liver lesions, metastases to omentum and metastatic lesion to calvarium and the patient expired soon afterwards. Discussion: CAH predisposes patients to adrenal tumors which is attributed to increased ACTH stimulation of the adrenal gland but ACC in this population is extremely rare. In very rare cases ACC can present clinically as pheochromocytoma with elevated catecholamine levels and positive synaptophysin and chromogranin staining which poses a clinical challenge. Both CAH and ACC can lead to increased androgen levels and ACTH levels can help to differentiate the origin of the hyperandrogenemia. Presentation: 6/2/2024

Generation of a Human Induced Pluripotent Stem Cell Line Expressing a Magnetic Resonance Imaging Reporter Gene.

The objective of the current study is to develop a new method for tracking transplanted human induced pluripotent stem cells-derived cardiomyocytes (hiPSC-CMs) using magnetic resonance imaging (MRI). The CRISPR/dCas9 activation system is employed to overexpress ferritin heavy chain (FHC) in hiPSC-CMs. The mRNA and protein expression of FHC in hiPSC and hiPSC-CMs significantly increased after transfection. Iron chloride does not affect the cell viability in a concentration range from 0 to 2000 µm. hiPSCs overexpressing FHC (hiPSC- FHCOE) and hiPSC-CMs overexpressing FHC (hiPSC-CM-FHCOE) significantly enhanced cellular uptake of iron chloride but with no changes in electrophysiological properties compared to hiPSC-CM-Control. Furthermore, hiPSC-CM-FHCOE presented robust contrast and lower T2* values, signifying their potential as highly effective candidates for cardiac MRI. Next, hiPSC-CM-FHCOE is injected into mouse hearts and after 3 days of transplantation, MR images are obtained. hiPSC-CM-FHCOE cells exhibited clear signals in the hearts with lower T2* and rapid signal decay. Collectively, data from this proof-of-concept study demonstrated that endogenous labeling with FHC in hiPSC-CMs can be a potent strategy for enhancing the accuracy of cardiac MRI. This technology represents a significant step forward in tracking the transplanted hiPSC-CMs in the hearts of live animals.

Cardiovascular magnetic resonance insights into anomalies of the mitral valve apparatus in Fabry cardiomyopathy and hypertrophic cardiomyopathy.

Despite different etiopathogenesis, Fabry Disease cardiomyopathy (FDc) and sarcomeric hypertrophic cardiomyopathy (HCM) share a similar hypertrophic phenotype, including anomalies of the mitral valve apparatus (AMVA). Some of these anomalies have also been described in the pre-hypertrophic stage of both diseases. This cardiovascular magnetic resonance (CMR) study aimed to: (i) compare AMVA between FDc and HCM with a similar degree of left ventricular hypertrophy (LVH), to add new insights into differential diagnosis; (ii) assess whether AMVA represent an early and progressive alteration in FDc; (iii) propose simple and potentially reproducible measurements of AMVA. This observational, retrospective study enrolled: (i) 80 Fabry patients, divided into three groups with increasing severity of cardiac phenotype (20 patients LVH-/normal T1, 20 patients LVH-/low T1 and 40 patients LVH+), and (ii) 40 patients with HCM. All patients underwent CMR. The LVH + FDc and the HCM groups were matched for age, sex, body surface area and left ventricular (LV) mass. The following AMVA were measured on cine images: papillary muscles (PMs) hypertrophy (maximal diameter (Dmax) of anterolateral (Al) and posteromedial (Pm) PM), apical displacement, anteriorization of Al PM and anterior mitral valve leaflet (AMVL) elongation. Reference values for defining AMVA were derived from a matched healthy control group (n = 40). Both HCM and FDc LVH + patients showed PMs hypertrophy, with a greater degree in the FDc LVH + group [Dmax Al PM 16 ± 3.4 vs. 15 ± 3.1 mm, p 0.017; Dmax Pm PM 14 ± 4.0 vs.12 mm (10.0-14.0), p 0.039] As compared to controls, both HCM and FDc LVH + patients showed PMs apical displacement (HCM 83% vs. healthy volunteers 8%, p < 0.001; FDc LVH + 65% vs. healthy volunteers 8%, p < 0.001), with a greater prevalence in HCM. Anteriorization of Al PM was only evident in HCM (15 ± 6.2 vs. healthy controls 21 ± 5.3 mm, p < 0.001). Elongation of AMVL was detected both in HCM and FDc with LVH + (HCM 29 ± 4.0 vs. healthy volunteers 24 ± 2.9 mm, p < 0.001; FDc LVH + 27 ± 4.0 vs. healthy volunteers 24 ± 2.9 mm, p < 0.001) without significant differences between the two phenocopies. The prevalence of myocardial crypts was higher among HCM patients than in FDc LVH + patients (75% vs. 48%, p 0.012). we report greater PMs hypertrophy in FDc and a higher prevalence of PMs positional alterations (anterior and apical displacement) and myocardial crypts in HCM. All these AMVA became more pronounced with the progression of the FDc phenotype. We suggest the systematic inclusion of the analysis of AMVA by simple linear measurements on cine images in the CMR assessment of hypertrophic cardiomyopathies, to help in the differential diagnosis between HCM and FDc and to facilitate early detection of cardiac involvement in FDc.

An unusual cause of liver neoplasm in an older female.

We presented a 66-year-old woman with T2DM who had a liver mass discovered incidentally during hospitalization. She was asymptomatic with a right upper abdominal mass that was smooth, mobile, and non-tender. Hepatitis virus markers and tumor markers were normal. The computed tomography (CT) images showed a 4.7×4.0 cm lesion in the left liver lobe with indistinct borders. Further magnetic resonance imaging (MRI) revealed low T1 and high T2 signal intensity with ring-shaped enhancement following contrast administration. Surgical resection was performed, and histology confirmed hepatic angioleiomyoma with thick-walled vessels and spindle cell proliferation. Immunohistochemistry was positive for SMA, desmin, caldesmon, CD31, and CD34. The patient had no recurrence during 5 years follow-up.

Comparing the imaging characteristics of middle-aged patients with multiple sclerosis and CADASIL: A retrospective cross-sectional study

BackgroundFew studies have quantitatively analyzed the imaging disparities between multiple sclerosis (MS) and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). We aimed to compare the imaging characteristics of MS and CADASIL in middle-aged patients. Materials and MethodsThis retrospective study used a single-center database and included patients aged 40–60 years with MS and CADASIL who underwent the designated imaging protocol including 3D T1-weighted imaging and fluid attenuated inversion recovery (FLAIR), diffusion tensor imaging and susceptibility-weighted imaging between January 2018 and March 2023. Patients with MRI-detected macrobleeds were excluded. ResultsA total of 27 patients with MS (mean age, 46.7 years ± 4.4, 8 men) and 30 patients with CADASIL (mean age, 51.6 years ± 5.8, 14 men) were included. No significant differences were observed in the Fazekas grades of white matter lesions (WMLs). Patients with CADASIL exhibited greater external capsule involvement (56.7% vs.18.5 %; p = 0.006), whereas the MS group had more lesions in the corpus callosum (81.5% vs. 53.3 %, p = 0.02) and brainstem (74.1% vs. 46.7 %, p = 0.04). The CADASIL group exhibited a higher incidence of microbleeds (12.07 vs. 0.11, p = 0.001). The WMLs in the MS group exhibited a lower T1 lesion/cerebrospinal fluid signal index (2.206 vs. 2.882, p < 0.001). A value of ≤2.57 demonstrated a sensitivity of 92.6 % and a specificity of 90.0 % in differentiating MS. Patients with MS had a thinner corpus callosum (7.18 mm vs 7.86 mm, p = 0.04), while patients with CADASIL showed significantly higher mean diffusivity (0.8776 × 10–3 vs. 0.7637 × 10–3 mm2/s, p = 0.03) and lower fractional anisotropy (0.7581 vs. 0.8389, p = 0.04) in the splenium of the corpus callosum. ConclusionMiddle-aged patients with MS and CADASIL showed comparable Fazekas grades for WMLs. However, lesion distribution, T1 signal characteristics, and splenic diffusivity changes can help differentiate between MS and CADASIL.

T2 mapping post acute myocardial infarction: a novel technique in assessing myocardial edema

ObjectiveCardiovascular magnetic resonance (CMR) is considered the gold standard imaging modality for assessing myocardial infarction lesions, offering precise myocardial tissue characterization. Elevated transverse relaxation time (T2) serves as a specific indicator of increased myocardial water content, thus becoming a valuable index for myocardial edema. However, conventional T2-weighted CMR sequence exhibits several limitations, primarily providing qualitative information. In contrast, recently developed quantitative T2 mapping techniques overcome these limitations, enabling a more reliable assessment of myocardial edema. These techniques offer the advantage of diagnosing and monitoring myocardial injury without the necessity of contrast agents. Our study aims to add to a growing literature demonstrating the efficacy of quantitative T2 mapping technique to detect and quantify regions of myocardial edema post-myocardial infarction.ResultNative T1 and T2 mapping accurately identified myocardial edema in all patients enrolled in the study. Notably, native T1 and T2 values exhibited a significant elevation in the infarcted myocardium compared to the remote myocardium (for T1: 1295.50 ± 87.65 vs. 1074.95 ± 92.86 ms, respectively; and for T2: 74.63 ± 6.51 vs. 52.53 ± 6.26 ms, respectively; p < 0.0001 for both). Microvascular obstruction was observed in 12 out of 20 patients, affecting one or more myocardial segments within the infarct areas. Among this subgroup, regions with a microvascular obstruction within the infarct zone displayed lower T1 and T2 values compared to areas of infarction without microvascular obstruction (for T1: 1115.05 ± 64.70 vs. 1295.50 ± 87.65 ms, respectively; and for T2: 53.65 ± 3.56 vs. 74.63 ± 6.51 ms, respectively; p < 0.0001 for both). Additionally, we provided reference values for myocardial T1 and T2 specific to our facility’s 1.5 Tesla CMR system, applicable to both infarct and remote myocardium.ConclusionParametric T1 and T2 mapping techniques can detect and quantify myocardial edema resulting from myocardial infarction. The presence of microvascular obstruction that results from revascularization injury affects both T1 and T2 values. This information can be used and has broad clinical implications for diagnosis and guiding or monitoring the treatment of myocardial infarction.

Quantitative assessment of gadolinium deposition in dentate nuclei with MR fingerprinting

Gadolinium deposition in the dentate nucleus (DN) has been evaluated by T1-weighted imaging (T1WI) and T1 (R1) mapping, but not MR fingerprinting (MRF). This study investigated associations between T1 and T2 values of DN and gadolinium-based contrast agents (GBCAs) using 2-dimensional MRF. This study included 101 patients. Region of interest analysis was performed for T1 and T2 values of DN on MRF (T1-MRF, T2-MRF) and T1-weighted images (T1WI ratio). T1 and T2 ratios compared to normal cerebellar white matter (T1-MRF ratio, T2-MRF ratio) were calculated. The type of previous GBCA was confirmed in 79 patients, and linear regressions were performed between T1, T2 values and number of GBCAs. Good correlations were observed between T1-MRF and T1WI ratio (ρ=-0.69, P<0.001) and between T1-MRF ratio and T1WI ratio (ρ=-0.76, P<0.001). Mild correlations were observed between T2-MRF and T1WI ratio (ρ=-0.32, P<0.001) and between T2-MRF ratio and T1WI ratio (ρ=-0.44, P<0.001). The number of linear-type GBCAs was associated with T1-MRF (β=-0.62, P<0.001) and T1-MRF ratio (β=-0.54, P<0.001) in univariate linear regression analyses, and with T1-MRF (β=-0.61, P<0.001) and T1-MRF ratio (β=-0.53, P<0.001) in multivariate analysis. The number of linear-type GBCAs was associated with T2-MRF (β=-0.30, P<0.001) and T2-MRF ratio (β=-0.29, P<0.001) in univariate analyses, and with T2-MRF (β=-0.31, P<0.001) and T2-MRF ratio (β=-0.32, P<0.001) in multivariate analyses. No associations were observed between number of macrocyclic GBCAs and T1-MRF (ratio) or T2-MRF (ratio). The number of linear-type GBCA administrations was associated with lower T1 and T2 values (ratios) in DN.

The Association Between Periodontal Disease and Cardiovascular Disease: Insights From Imaging, Observational, and Genetic Data

BackgroundPeriodontal disease is the sixth most common disease worldwide and may be a contributory risk factor for cardiovascular disease (CVD). ObjectivesThis study utilizes noninvasive cardiac imaging and longitudinal and genetic data to characterize the association between periodontal disease and both cardiovascular magnetic resonance (CMR) imaging biomarkers of remodeling and incident coronary artery disease (CAD). MethodsFrom the UK Biobank, 481,915 individuals were included, 91,022 (18.9%) of whom had self-reported periodontal disease. For imaging analysis, 59,019 had paired CMR data. Multivariable linear regression models were constructed to examine the association of periodontal disease on CMR outcomes. The endpoints for the CMR analyses were left ventricle (LV) end-diastolic volume, LV ejection fraction, LV mass, LV mass:volume ratio, LV global longitudinal strain, and native T1 values. The relationship between periodontal disease and CVD was assessed using Cox proportional hazards regression models, with incident CAD as the endpoint. To examine the relationship of genetically determined periodontal disease on CAD, a genome-wide polygenic risk score was constructed. ResultsPeriodontal disease was associated with a significantly higher LV mass:volume ratio (effect size: 0.00233; 95% CI: 0.0006-0.004) and significantly lower T1 values (effect size: −0.86 ms; 95% CI: −1.63 to −0.09). Periodontal disease was independently associated with an increased hazard of incident CAD (HR: 1.09; 95% CI: 1.07-1.13) at a median follow-up time of 13.8 years. Each SD increase in the periodontal disease polygenic risk score was associated with increased odds of CAD (OR: 1.03; 95% CI: 1.02-1.05). ConclusionsUsing an integrated approach across imaging, observational, and genomic data, periodontal disease is associated with biomarkers of subclinical remodeling as well as incident CAD. These findings highlight the potential importance of periodontal disease in the broader context of CVD prevention.

Quantitative ultrashort echo time MR imaging of knee osteochondral junction: An ex vivo feasibility study.

Compositional changes can occur in the osteochondral junction (OCJ) during the early stages and progressive disease evolution of knee osteoarthritis (OA). However, conventional magnetic resonance imaging (MRI) sequences are not able to image these regions efficiently because of the OCJ region's rapid signal decay. The development of new sequences able to image and quantify OCJ region is therefore highly desirable. We developed a comprehensive ultrashort echo time (UTE) MRI protocol for quantitative assessment of OCJ region in the knee joint, including UTE variable flip angle technique for T1 mapping, UTE magnetization transfer (UTE-MT) modeling for macromolecular proton fraction (MMF) mapping, UTE adiabatic T1ρ (UTE-AdiabT1ρ) sequence for T1ρ mapping, and multi-echo UTE sequence for T2* mapping. B1 mapping based on the UTE actual flip angle technique was utilized for B1 correction in T1, MMF, and T1ρ measurements. Ten normal and one abnormal cadaveric human knee joints were scanned on a 3T clinical MRI scanner to investigate the feasibility of OCJ imaging using the proposed protocol. Volumetric T1, MMF, T1ρ, and T2* maps of the OCJ, as well as the superficial and full-thickness cartilage regions, were successfully produced using the quantitative UTE imaging protocol. Significantly lower T1, T1ρ, and T2* relaxation times were observed in the OCJ region compared with those observed in both the superficial and full-thickness cartilage regions, whereas MMF showed significantly higher values in the OCJ region. In addition, all four UTE biomarkers showed substantial differences in the OCJ region between normal and abnormal knees. These results indicate that the newly developed 3D quantitative UTE imaging techniques are feasible for T1, MMF, T1ρ, and T2* mapping of knee OCJ, representative of a promising approach for the evaluation of compositional changes in early knee OA.

Feasibility of using synthetic MRI to predict lymphatic vascular space invasion status in early-stage cervical cancer: added value to morphological MRI

To investigate the feasibility of synthetic magnetic resonance imaging (syMRI) in predicting the lymphatic vascular space invasion (LVSI) status of early-stage cervical cancer, and its added value to morphological MRI. A total of 72 patients with pathology-confirmed early-stage cervical cancer were enrolled, and classified into LVSI- positive (n=41) and LVSI- negative (n=31) groups. Together with morphological parameters including gross tumor volume (GTV) and maximum tumor diameter (MTD), the T1, T2, and proton density (PD) values of the tumors were also measured and compared between two groups. Binary logistic regression analysis was used to identify the independent variable associated with LVSI. Receiver operating characteristic curve analyses and DeLong tests were used to evaluate and compare the performances of significant parameters or their combination in predicting LVSI. LVSI- positive group showed significantly higher GTV (P=0.008) and MTD (P=0.019), and lower T1 (P<0.001) and PD values (P=0.041) than LVSI- negative group. However, no statistical significance was observed regarding the T2 values (P=0.331). Binary logistic regression indicated that T1 value (odds ratio [OR]=0.993; P=0.001) and MTD (OR=1.903, P=0.027) were independent variables associated with LVSI in early cervical cancer. Optimal performance could be achieved [area under ROC curve (AUC)=0.784; cut-off value=0.56; sensitivity=80.5%; specificity=71.0%] when combining T1 and MTD for predicting LVSI. Its performance was significantly better than that of MTD alone (AUC, 0.784 vs 0.662, P=0.035). syMRI might be a feasible approach, and it can provide added value to morphological MRI in predicting the LVSI status of early-stage cervical cancer.