Ultra-high resolution for accurate analysis in cardiac mapping: a path towards fulfillment of assumptions in omnipolar technology.

Effect of age and sex on cardiac magnetic resonance native T1 mapping and synthetic extracellular volume.

Cardiac T1 and T2 Mapping: The Importance of Rest Periods in Quantitative Tissue Property Mapping

Free-breathing three-dimensionalwhole-heart adiabatic T1ρ mapping for non-contrast tissue characterization at 0.55T.

Myocardial tissue characterization by cardiac MRI for the evaluation of heart failure with preserved ejection fraction in hypertrophic cardiomyopathy.

Heart transplantation significantly enhances survival and quality of life for patients with end-stage heart failure. Despite advances in surgical and postoperative care, immune-mediated complications, acute graft rejection and cardiac allograft vasculopathy (CAV), remain major barriers to long-term success. Acute rejection predominantly affects early posttransplant survival, whereas CAV becomes a leading cause of mortality in later years. The gold standards for diagnosis, endomyocardial biopsy for rejection and coronary angiography for CAV, are invasive and imperfect. Noninvasive multimodality imaging is increasingly used to complement or, in selected scenarios, defer invasive testing. Echocardiography with strain detects early myocardial dysfunction when ejection fraction is preserved; stress echocardiography provides prognostic information for CAV. Quantitative techniques, positron emission tomography myocardial blood flow/myocardial flow reserve and quantitative cardiac magnetic resonance perfusion, improve detection of diffuse, stage-dependent CAV compared with qualitative assessments. Cardiac magnetic resonance tissue mapping characterizes edema and fibrosis relevant to rejection surveillance; fluorodeoxyglucose-positron emission tomography for inflammation is emerging but remains investigational in most centers. Cardiac computed tomography angiography defines coronary anatomy and plaque with excellent negative predictive value and offers physiologic assessment with computed tomography-myocardial perfusion imaging/computed tomography-derived fractional flow reserve; it is best used strategically rather than as an annually repeated test. This contemporary review synthesizes the strengths, limitations, and practical roles of echocardiography, nuclear imaging, cardiac magnetic resonance, and cardiac computed tomography angiography across adult and pediatric populations; highlights areas where quantitative methods add incremental value; and provides pragmatic, stage-aware surveillance frameworks. Integrating modalities can reduce reliance on invasive procedures, lower procedural risk, and refine therapeutic decision-making benefits that are particularly relevant for children and other patients for whom repeated invasive testing is undesirable.

To develop a free-breathing method for multi-slice co-registered cardiac T1, T2, and ADC maps using single-shot spin-echo echo planar imaging (SE-EPI). T1, T2, and diffusion weighted images in five slices were acquired with SE-EPI readouts during free breathing using interleaved acquisition of slices, non-selective inversion recovery, varying echo times (TE), and second-order motion-compensated diffusion gradients in three orthogonal directions with different b values. All images were registered to a single target image followed by parameter fitting to generate co-registered T1/T2/ADC maps. This approach was evaluated in phantom measurements, 13 healthy volunteers, two myocardial infarction (MI) swine, and two cardiac amyloidosis (CA) patients by comparison to reference mapping techniques. Qualitative assessments were performed by two expert readers. Phantom experiments showed strong agreement with reference measurements (R2 > 0.96). In volunteers, myocardial T1 values were higher than MOLLI (1341 ± 59 vs. 1252 ± 36 ms, p = 0.003); the proposed T2 values were shorter than T2prep-FLASH (38.7 ± 2.2 vs. 41.0 ± 2.2 ms; p = 0.009), and mean ADC values were comparable to the reference cDTI-derived mean diffusivity (MD) values (1.57 ± 0.05 vs. 1.56 ± 0.05 μm2/ms; p = 0.404). Proposed relaxation maps received significantly lower quality scores than references, and diffusivity maps were comparable. Myocardial abnormalities in CA patients and MI swine were consistent with conventional methods. The proposed method enables five-slice, co-registered, and free-breathing myocardial T1, T2, and ADC maps in less than 5 min, facilitating integrated multi-contrast tissue characterization in cardiac MRI. Future work will aim to optimize map quality and expand clinical applications.

Accurate quantification of extracellular volume (ECV) and fractional myocardial blood volume (fMBV) in cardiac magnetic resonance (CMR) relies on precise alignment between precontrast and postcontrast images. Variable image contrast often undermines conventional motion correction, causing misalignment due to respiration or cardiac motion. Herein, we present a registration approach that accounts for varying image contrast levels and cardiac motion to achieve more precise and high-quality quantitative cardiac mapping. Patients with suspected myocardial diseases underwent cardiac MRI with Gadavist (0.1 mmol/kg, n = 11) and ferumoxytol (4.0 mg/kg cumulative, n = 9) enhancement for ECV and fMBV measurements, respectively. T1 maps were generated using the MOLLI sequence. To remove contrast variations across different inversion times and contrast doses, precontrast and postcontrast MOLLI images were grouped and processed using correlation-weighted representations based on the myocardium and blood pool signals. Groupwise registration is performed based on the maximization of mutual information. The image registration accuracy and mapping precision of the proposed method were assessed relative to those of conventional methods. ResultsCompared with the conventional groupwise registration approach, the proposed decontrasted approach showed superior alignment between images of different contrasts, as evidenced by the higher Dice scores (mean 0.77 vs. 0.69, p < 0.001). It also eliminated artifacts commonly observed owing to image misalignment (all 11 cases showed improvement). Improved myocardial mapping precision was observed for both ECV (median coefficient of variation, 0.14 vs. 0.27; p < 0.001) and fMBV (median coefficient of variation, 0.59 vs. 0.71; p < 0.001). It also reduced individual myocardial segmental variations in the ECV (5.8 to 3.58, p < 0.001) and fMBV maps (9.86 to 7.93, p < 0.001). Overall, decontrasted image registration improves the precision of contrast-enhanced myocardial parametric mapping by reducing the misalignment between multicontrast images. This framework may be extended to other postprocessing tasks in cardiac MRI that involve variable image contrasts.

Mitral annular disjunction is an increasingly recognized structural abnormality associated with myocardial remodeling. While related functional and structural alterations have been well documented in adults, data on pediatric mitral annular disjunction remain scarce. To assess early myocardial structural and functional changes in pediatric patients with mitral annular disjunction using cardiac magnetic resonance (CMR) feature-tracking strain and parametric mapping. In this retrospective study, 32 pediatric patients with mitral annular disjunction confirmed by CMR and 16 age- and sex-matched controls with normal CMR findings were included. Cine imaging, late gadolinium enhancement, native T1 mapping, extracellular volume, and CMR strain analysis were performed. Holter monitoring data were evaluated for ventricular ectopy. Patients with mitral annular disjunction demonstrated significantly reduced global, mean basal, and segmental basal radial, circumferential, longitudinal strain values compared to controls. Also, native T1 and extracellular volume were significantly higher in the mitral annular disjunction group. Late gadolinium enhancement was present in 21.9% of patients with mitral annular disjunction. Ventricular ectopy was observed in 48.3%, with no significant association with late gadolinium enhancement. Subgroup analysis showed longer mitral annular disjunction distances, more frequent systolic curling, late gadolinium enhancement, and ventricular ectopy in patients with mitral annular disjunction and mitral valve prolapse, compared to those with isolated mitral annular disjunction. Pediatric mitral annular disjunction is associated with early myocardial alterations, including impaired deformation, elevated native T1, and extracellular volume. These findings suggest that subclinical myocardial remodeling may begin in childhood, and CMR is valuable in detecting these subtle changes.

Regular vigorous exercise brings about cardiovascular adaptations, but the relationship between cardiac magnetic resonance-derived T1 and T2 mapping and physical fitness is not fully understood, with conflicting literature results. This study aims to define the associations between cardiorespiratory fitness evaluated using cardiopulmonary exercise testing (CPET) and cardiac remodelling using cardiac magnetic resonance (CMR), including T1 and T2 mapping. We enrolled elite, healthy athletes undergoing pre-participation screening (including personal and family history, physical examination, and 12-lead ECG) who volunteered for maximal CPET and non-contrast CMR with a 1.5T scanner, performed no more than 31 days apart. Our study population comprised 125 athletes: median age 19 [16-24.5] years; 65% males; median hours of training 20 [15-24.5]; 9% power, 36% endurance, 55% mixed. Overall, female athletes showed less pronounced cardiorespiratory and cardiac morphological remodelling compared to their male counterparts, and endurance athletes exhibited the highest levels of cardiorespiratory fitness and the most pronounced cardiac remodelling of the sport types considered. Greater overall fitness was associated with larger cardiac volumes and mass, and lower T1 and T2 values. In multivariate analysis, sex, sport type, LVMi, EDWT, VO2 max, and peak lactate collectively explained ∼27% of the variation in T1 values. Cardiac remodelling in athletes appears to be influenced by training load, sex, and sport type. In this study, we demonstrate for the first time an association between myocardial tissue characteristics, assessed by mapping, and cardiopulmonary fitness, evaluated through CPET. This finding suggests a potential link between aerobic adaptation and tissue-level myocardial properties. Further studies are warranted to validate these associations and to clarify their role in distinguishing physiological athletic remodelling from early pathological changes.

Background: Genetic testing is now recommended for select patients with early-onset atrial fibrillation (AF). Hemochromatosis is an autosomal recessive syndrome that occurs in patients who carry two pathogenic or likely-pathogenic (P/LP) variants in HFE. HFE is included on some genetic testing panels used for patients with AF. Hemochromatosis causes cardiomyopathy due to iron overload in the ventricle; however, it is unknown whether AF can be an early manifestation that is identified by genetic testing. Methods: A total of 347 patients were referred to a dedicated AF precision medicine clinic. The clinical diagnostic evaluation included an H&amp;P, 12-lead ECG, ambulatory ECG monitoring, and cardiac imaging (cardiac MRI and/or TTE). Genetic testing was performed using CLIA-approved laboratories: Labcorp/Invitae, GeneDx, or Vanderbilt University Medical Center. HFE was included on the cardiomyopathy panel used by 2 of the 3 laboratories. Results: HFE was tested in 165 participants (median age 46 years [IQR 35-55], 115 [70%] male, 149 [90%] White). Six participants (4%) had two pathogenic variants in HFE. All of them were C282Y/H63D compound heterozygotes. Forty-one participants (25%) were heterozygous carriers of one pathogenic HFE variant. Among the 6 participants with 2 pathogenic HFE variants, the median ferritin level was 346 mcg/L [IQR 262, 496] (normal &lt;300 mcg/L males, &lt;200 mcg/L females). Three participants (50%) met laboratory criteria for iron overload. One individual had isolated ferritin elevation with normal transferrin saturation. All 6 underwent cardiac MRI as part of the genetic evaluation for early onset AF, and there was no evidence of cardiac siderosis based on cardiac T1 mapping, median 990 ms [IQR 968-1024] (normal 960-1030 ms). Dedicated sequences to evaluate for iron overload demonstrated short hepatic T2* in one individual, indicating presence of hepatic iron overload (9 ms, normal &gt;11.4 ms; liver iron concentration 3.4 mg/g, normal &lt;2 mg/g). Three out of 6 participants were referred for a hematology evaluation and 2 out of 6 were started on therapeutic phlebotomy. Conclusion: Genetic testing can identify patients with early-onset AF who are genetically susceptible to hemochromatosis, have evidence of iron overload, and receive early intervention with therapeutic phlebotomy. These results suggest HFE should be sequenced as part of genetic testing for early-onset AF, but larger sample sizes are needed to confirm these results.

Introduction: Non-invasive estimation of blood oxygen saturation (O2sat) by cardiac magnetic resonance (CMR) has clinical application in single ventricle heart disease. A T2-mapping based CMR method has been described to estimate O2sat in the heart and great vessels in specific regions of interest. This study builds on our prior validation of CMR oximetry maps to visualize O2sat data and determine optimal regions for evaluation in single ventricle hearts. Methods: 14 single ventricle (age 17.1±6.8 years, 4 female) and 15 transplant control (age 16.6±4.6 years, 6 female) patients undergoing clinically indicated cardiac catheterization and CMR were recruited in a tertiary care children’s hospital. A series of T2-prepared single-shot steady-state free-precession images were acquired of intracardiac chambers and great vessels in free-breathing across T2-preparation times of 0 to 200 ms (Fig 1). Inter-echo spacing (τ) ranged from 0 to 25 ms. Color-coded maps were calculated representing estimated O2sat based on voxel-wise fitting of T2 data to the Luz-Meiboom model (S,T,τ,α). Regional O2sat from oximetry maps were compared to corresponding invasive catheterization data. Results: Oximetry maps allowed visualization of O2sat to identify regions with uniform blood pools and with heterogenous O2sat (Fig 2). Correlation between O2sat via oximetry maps and catheterization were favorable overall (r=0.69, p&lt;0.001), in single ventricle patients (r=0.70, p&lt;0.001) and in transplant patients (r=0.69, p&lt;0.001). Bland Altman plots (Fig 3) comparing O2sat via oximetry maps and catheterization demonstrated reasonable agreement overall (mean difference=-5.2, limits of agreement=-21.4,8.3), in single ventricle patients (mean difference=-4.3, limits of agreement=-22.5,14.0) and in transplant patients (mean difference=-5.6, limits of agreement=-21.0, 9.8). Pulmonary veins, atria, and regions with foreign material were difficult to visualize due to data heterogeneity and noise. Conclusion: CMR can be utilized for non-invasive estimation of O2sat in complex heart disease with good correlation to current gold standard catheter-derived measurements. Oximetry maps can enhance visualization of regional O2sat and may guide further optimization of image acquisition and analysis. Streaming effects in human hearts altered by palliation surgeries may explain why oximetry maps visually depicted heterogenous O2sat. Ongoing patient recruitment is warranted.

Background: Renal denervation ( RDN ) has been widely studied to treat ventricular arrhythmias. Besides the neuronal and structural remodeling, electrical remodeling of the infarcted heart plays a crucial role in ventricular arrhythmogenesis after acute myocardial infarction ( AMI ). Given that connexin 43 ( Cx43 ) serves as one of the most important ventricular gap junction proteins for maintaining normal cardiac electrical conduction, our study aims to test whether RDN achieves its antiarrhythmic effect through modulating Cx43-regulated electrical activity of the AMI heart. Methods and Results: Rat AMI was induced by surgical ligation of the left anterior descending coronary artery. Completed bilateral RDN was performed immediately after AMI. Terminal experiments were performed at 2 weeks post-AMI. Data from ELISA demonstrated that early RDN reduced AMI-elevated Angiotensin II ( Ang II ) levels in the serum and border zone ( BZ ) of the infarcted heart. IF staining showed that Cx43 demonstrated a linear staining pattern with a homogeneous distribution in the sham heart, whereas its expression was lateralized and illustrated a cluster staining pattern with a heterogeneous distribution in the BZ of the AMI heart. Data from cardiac optical mapping demonstrated that AMI markedly reduced conduction velocity and elongated action potential durations in the left ventricle. More importantly, alongside restoring AMI-decreased protein expression of Cx43, early RDN also improved AMI-induced lateralization and heterogeneous distribution of Cx43 in the BZ of the infarcted heart. 24-hour ECG telemetry recording in conscious rats found that early RDN not only improved AMI-increased heterogeneity of ventricular electrical activity but also reduced the incidence and cumulative duration of ventricular arrhythmias in AMI rats. To validate the contribution of Ang II on cardiac electrical remodeling, Ang II (1.44mg/kg/day) was subcutaneously infused into sham rats for 2 weeks. Our data showed that Ang II infusion induced the lateralization of Cx43 in the sham heart, which was accompanied by an increased heterogeneity of ventricular electrical activity with elevated susceptibility to ventricular arrhythmias in sham rats. Conclusions: These data suggest that early RDN reduces ventricular arrhythmogenesis by damping Ang II-promoted electrical remodeling of the AMI heart. Targeting the Ang II/Cx43 signaling could be a novel therapeutic strategy to treat ventricular arrhythmias after AMI.

We examined whether trajectories of urine albumin-creatinine ratio (UACR) over 5- and 10-year periods were associated with subclinical and clinical heart failure (HF), heart failure subtypes, atrial fibrillation (AF), and coronary heart disease (CHD). We modelled 5-year UACR trajectories in 5,581 participants (mean age 61.7 years) from the Multi-Ethnic Study of Atherosclerosis using latent class mixed modelling across baseline, Exam 2, and Exam 3 (2000-2005). A separate sample of 4,343 participants with UACR measured at baseline, Exam 5, and at least one intermediate exam (2000-2012) was used for 10-year trajectory modelling. Cox proportional hazards models were used to assess associations between UACR trajectories and clinical endpoints. Linear regression analyses examined associations between UACR trajectories and N-terminal pro-brain natriuretic peptide (NT-proBNP) and high-sensitivity troponin T (hs-TnT), as well as myocardial fibrosis assessed by cardiac MRI T1 mapping. Three distinct trajectory groups were identified for each time window. In the 5-year model, the "sustained medium to high" group, and in the 10-year model, the "rapid rise" group (each ∼8%) had 1.5- to 3.7-fold higher risks of HF, HF subtypes, composite of HF/death, AF, and CHD. Most of these associations were independent of baseline UACR levels and remained significant even among individuals with normoalbuminuria at baseline. After censoring for interim AF or CHD, associations persisted for HF and HFpEF, but not HFrEF. These groups also exhibited elevated NT-proBNP, hs-TnT, native T1, and extracellular volume fraction. Progressive UACR increases identify individuals at elevated cardiovascular risk, particularly for HF.

Prognostic Value of Myocardial T1 Mapping and Extracellular Volume Fraction in Heart Failure: A Meta-Analysis.

Cardiac quantitative MRI (qMRI) is a powerful imaging technique for diagnosing pathologies such as diffuse myocardial fibrosis. One main challenge is cardiac motion, which requires synchronization of data acquisition with the heartbeat, leading to long scan times. We present a novel deep learning-based image registration method for cardiac qMRI that enables non-rigid motion correction of data acquired continuously over multiple cardiac cycles, thereby reducing scan times. Our method is a zero-shot approach that utilizes the physical qMRI signal model for accurate motion estimation. Non-rigid motion of dynamic images is estimated with a U-Net-based architecture. This exploits the intrinsic smoothness of cardiac motion, allowing sharing information between neighboring images. The approach is robust to undersampling artifacts, enabling motion estimation from dynamic images reconstructed from very few k-space data even without advanced image reconstruction methods. We evaluated the method for fast cardiac T1 mapping using a Golden radial sampling scheme on numerical simulations and in-vivo acquisitions. On numerical simulations, our method achieved a 61.64% improvement in T1 accuracy. On in-vivo data, our approach yielded a 45.13% improvement in sharpness of T1 maps, and temporal image alignment of motion-corrected dynamics improved on average by 11.78%. Our method enables accurate non-rigid motion correction of highly undersampled cardiac qMRI data obtained from continuously acquired data. As our method is individually optimized for each scan without the need for training on large datasets, it can easily be adapted to other cardiac qMRI approaches.

Electrocardiography and echocardiography are essential tools for the diagnosis, prognosis, and therapeutic management of canine heart diseases, with echocardiography considered the gold standard for several conditions. In some cases, however, chemical restraint is required to perform these examinations due to aggression, stress, or respiratory difficulty. The aim of this study was to assess the cardiovascular effects of sedation with acepromazine alone or combined with morphine in healthy dogs undergoing electrocardiographic and echocardiographic evaluation. Sixteen dogs were randomly allocated into 2 groups: the acepromazine group (AG, n=8), which received 0.2% acepromazine at 0.05 mg/kg intramuscularly, and the acepromazine and morphine group (AMG, n= 8), which received 0.2% acepromazine at 0.05 mg/kg combined with 1% morphine at 0.5 mg/kg, both administered intramuscularly. Before sedation, animals were placed in lateral recumbency for baseline assessment (M0) of electrocardiographic and echocardiographic parameters, as well as systolic, diastolic, and mean blood pressure (SBP, DBP and MAP). The same assessment was repeated 20 minutes after treatment (M1). Both groups showed reductions in cardiac output, SBP and MAP. Additional effects were observed in the AMG, including reductions in aortic valve pressure gradient, E-wave peak velocity, heart rate and DBP, together with a prolonged QT interval on the electrocardiogram. In conclusion, both protocols proved effective for chemical restraint. However, acepromazine alone produced only a decrease in cardiac output on echocardiography, while other variables remained relatively stable. Thus, acepromazine alone has a less pronounced effect on electrocardiographic and conventional echocardiographic findings in healthy dogs.

A 69-year-old woman presented with heart failure and progressive muscle weakness and was diagnosed as anti-mitochondrial antibody (AMA) myositis with cardiac involvement. Immunosuppressive therapy with prednisolone and intravenous cyclophosphamide significantly improved the symptoms, hemodynamics, and cardiac function. Cardiac magnetic resonance (CMR) T1 and T2 mapping showed elevated native T1, T2, and extracellular volume fractions during heart failure exacerbation (day 37) compared to pre-hospitalization values (10 months before admission) and follow-up conducted 6 and 12 months after admission. This case underscores the importance of comprehensive evaluation, such as serial CMR imaging and immunosuppressive therapy, in managing myocardial involvement in AMA-positive myositis.

Sevoflurane preconditioning improves Cx43 localization and electrical conduction by stabilizing myocardial microtubule structure during ischemia-reperfusion.

Background/Objectives: Myocarditis is a recognized complication of COVID-19 infection, with potential long-term cardiac sequelae. While acute cardiac involvement has been frequently reported, late-stage myocardial effects remain less well characterized. Cardiac magnetic resonance (CMR) imaging, particularly T1 and T2 mapping, offers non-invasive tissue characterization for myocardial inflammation and fibrosis. This study aimed to evaluate segmental myocardial tissue changes in patients with late-stage COVID-19-related myocarditis using CMR and compare findings with patients with non-COVID-19 myocarditis and healthy controls. Methods: This retrospective, single-center study included 25 patients with clinically suspected COVID-19 myocarditis who underwent CMR between 36 and 565 days post-infection. T1 and T2 mapping values and late gadolinium enhancement (LGE) patterns were assessed and compared with 14 non-COVID-19 myocarditis patients and 19 healthy controls. Subgroup analyses were performed according to vaccination status and left ventricular ejection fraction (LVEF). Results: Patients with reduced LVEF had significantly higher T1 and T2 values in several myocardial segments. Compared to controls, the COVID-19 myocarditis group showed significantly elevated T1 values in all segments except 2 and 3. No significant difference in T2 values was observed. LGE was present in 61% of COVID-19 myocarditis patients, predominantly with a subepicardial pattern. No significant differences were observed between vaccinated and unvaccinated patients. Conclusions: Late-stage COVID-19 myocarditis is associated with persistent segmental myocardial tissue abnormalities, particularly elevated T1 values and subepicardial LGE. Segmental CMR mapping may provide additional diagnostic value in identifying residual myocardial injury in patients with ongoing cardiac symptoms after COVID-19 infection.