The ebb and flow of cardiac lymphatics: a tidal wave of new discoveries.

The heart is imbued with a vast lymphatic network that is responsible for fluid homeostasis and immune cell trafficking. Disturbances in the forces that regulate microvascular fluid movement can result in myocardial edema, which has profibrotic and proinflammatory consequences and contributes to cardiovascular dysfunction. This review explores the complex relationship between cardiac lymphatics, myocardial edema, and cardiac disease. It covers the revised paradigm of microvascular forces and fluid movement around the capillary as well as the arsenal of preclinical tools and animal models used to model myocardial edema and cardiac disease. Clinical studies of myocardial edema and their prognostic significance are examined in parallel to the recent elegant animal studies discerning the pathophysiological role and therapeutic potential of cardiac lymphatics in different cardiovascular disease models. This review highlights the outstanding questions of interest to both basic scientists and clinicians regarding the roles of cardiac lymphatics in health and disease.

Quantitative Assessment of Myocardial Edema by MR T2 Mapping in Children With Kawasaki Disease.

BACKGROUND: Few studies assessed myocardial inflammation using Cardiovascular Magnetic Resonance Imaging in Kawasaki disease (KD) patients. PURPOSE: To quantify myocardial edema in KD patients using T2 mapping and explore the independent predictors of T2 values. STUDY TYPE: Prospective. SUBJECTS: Ninety KD patients including 40 in acute phase (26 males, 65.0%) and 50 in chronic phase (34 males, 68.0%). Thirty-one healthy volunteers (21 males, 70.0%). FIELD STRENGTH/SEQUENCE: 3.0 T T2-weighted Turbo Spin Echo-Short Time of Inversion Recovery sequence, True fast imaging with steady precession flash sequence and fast low-angle shot 3D spoiled gradient echo sequence. ASSESSMENT: T2 values were compared among KD groups and controls. STATISTICAL TEST: Student's t test and Fisher's exact test; One-way analysis of variance; Pearson correlation analysis; Receiver operating curve analysis; Multivariable linear regression. RESULTS: Global T2 value of KD patients in acute phase was the highest, followed by those of chronic-phase patients and controls (38.83 ± 2.41 msec vs. 37.55 ± 2.28 msec vs. 36.05 ± 1.64 msec). Regional T2 values showed a same trend. There were no significant differences in global and regional T2 values between KD patients with and without coronary artery (CA) dilation, no matter in acute or chronic phase (all KD patients: P = 0.51, 0.51, 0.53, 0.72; acute KD: P = 0.61, 0.37, 0.33, 0.83; chronic KD: P = 0.65, 0.79, 0.62, 0.79). No significant difference was observed in global T2 values between KD patients with Z score > 5.0 and 2.0 < Z score ≤ 5.0 (P = 0.65). Multivariate analysis demonstrated that stage of disease (ß = -0.123) and heart rate (ß = 0.280) were independently associated with global T2 values. DATA CONCLUSION: The degree of myocardial edema was more severe in acute-phase than in chronic-phase KD patients. Myocardial edema persists in patients regardless of the existence or degree of CA dilation. EVIDENCE LEVEL: 2 TECHNICAL EFFICACY: Stage 2.

Serial electrocardiograms at follow-up for early detection of transplanted heart rejection: A viewpoint.

This viewpoint proposed that serial electrocardiograms (ECG) could be used to monitor for heart transplantation (HT) rejection, based on the expected attenuation of the amplitude of ECG QRS complexes (attQRS) engendered by the rejection-induced decrease in electrical resistance due to the underlying myocardial edema (ME). Previous work in humans has shown attQRS in the setting of a diverse array of edematous states, affecting the myocardium (i.e, ME) and the body volume conductor "enveloping" the heart. Also, animal and human experience has revealed low electrical resistance during mild/moderate HT rejection. Studies with serial correlations of endomyocardial biopsy (EMB), echocardiography, cardiac magnetic resonance imaging, and ECG are recommended, which will merely require recording of an ECG, when EMB and imaging studies are carried out for monitoring of post-HT rejection.

Exercise-induced myocardial T1 increase and right ventricular dysfunction in recreational cyclists: a CMR study.

PURPOSE: Although cardiac troponin I (cTnI) increase following strenuous exercise has been observed, the development of exercise-induced myocardial edema remains unclear. Cardiac magnetic resonance (CMR) native T1/T2 mapping is sensitive to the pathological increase of myocardial water content. Therefore, we evaluated exercise-induced acute myocardial changes in recreational cyclists by incorporating biomarkers, echocardiography and CMR. METHODS: Nineteen male recreational participants (age: 48 ± 5 years) cycled the 'L'étape du tour de France" (EDT) 2021' (175 km, 3600 altimeters). One week before the race, a maximal graded cycling test was conducted to determine individual heart rate (HR) training zones. One day before and 3-6 h post-exercise 3 T CMR and echocardiography were performed to assess myocardial native T1/T2 relaxation times and cardiac function, and blood samples were collected. All participants were asked to cycle 2 h around their anaerobic gas exchange threshold (HR zone 4). RESULTS: Eighteen participants completed the EDT stage in 537 ± 58 min, including 154 ± 61 min of cycling time in HR zone 4. Post-race right ventricular (RV) dysfunction with reduced strain and increased volumes (p < 0.05) and borderline significant left ventricular global longitudinal strain reduction (p = 0.05) were observed. Post-exercise cTnI (0.75 ± 5.1 ng/l to 69.9 ± 41.6 ng/l; p < 0.001) and T1 relaxation times (1133 ± 48 ms to 1182 ± 46 ms, p < 0.001) increased significantly with no significant change in T2 (p = 0.474). cTnI release correlated with increase in T1 relaxation time (p = 0.002; r = 0.703), post-race RV dysfunction (p < 0.05; r = 0.562) and longer cycling in HR zone 4 (p < 0.05; r = 0.607). CONCLUSION: Strenuous exercise causes early post-race cTnI increase, increased T1 relaxation time and RV dysfunction in recreational cyclists, which showed interdependent correlation. The long-term clinical significance of these changes needs further investigation. TRIAL REGISTRATION NUMBERS AND DATE: NCT04940650 06/18/2021. NCT05138003 06/18/2021.

Healing process of myocardial edema in acute perimyocarditis: Observation by speckle-tracking echocardiography and cardiac magnetic resonance parametric mapping.

This report describes the case of a 42-year-old male patient with acute viral perimyocarditis. The case study serves as a demonstration of the use of speckle-tracking echocardiography and cardiac magnetic resonance (CMR) imaging in monitoring myocardial changes associated with perimyocarditis. It explores the possibility that regional longitudinal strain (LS) may predict prognosis in the affected areas of the myocardium, and could reflect more advanced areas of myocyte damage within myocardial edema.

Increasing myocardial edema is associated with greater microvascular obstruction in ST-segment elevation myocardial infarction.

Microvascular obstruction (MVO) frequently develops after ST-elevation myocardial infarction (STEMI) and is associated with increased mortality and adverse left ventricular remodeling. We hypothesized that increased extravascular compressive forces in the myocardium that arise from the development of myocardial edema because of ischemia-reperfusion injury would contribute to the development of MVO. We measured MVO, infarct size, and left ventricular mass in patients with STEMI (n = 385) using cardiac MRI 2 to 3 days following successful percutaneous coronary intervention and stenting. MVO was found in 57% of patients with STEMI. The average infarct size was 45 ± 29 g. Patients with MVO had significantly greater infarct size and reduced left ventricular (LV) function (P < 0.01) compared with patients without MVO. Patients with MVO had significantly greater LV mass than patients without MVO and there was a linear increase in MVO with increasing LV mass (P < 0.001). Myocardial edema by T2-weighted imaging increased with increasing LV mass and patients with MVO had significantly greater myocardial edema than patients without MVO (P < 0.01). Patients with MVO had significantly greater left ventricular end-diastolic pressure (LVEDP) than patients without MVO (P < 0.05). In a cohort of patients with STEMI who underwent primary percutaneous intervention, we observed that MVO increased linearly with increasing LV mass and was associated with increased myocardial edema and higher LVEDP. These observations support the concept that extravascular compressive forces in the left ventricle may increase with increasing ischemic injury and contribute to the development of MVO.NEW & NOTEWORTHY Patients with STEMI (n = 385) had cardiac MRIs 2 to 3 days following reperfusion with primary PCI to determine the relationship between myocardial edema, LV mass, and MVO. We observed that MVO increased linearly with LV mass and that myocardial edema measured by T2-imaging also increased linearly with LV mass. Patients with MVO had greater edema and LVEDP than subjects without MVO. These findings suggest that myocardial edema which arises from ischemia-reperfusion injury may result in extravascular compression of the microcirculation manifested as MVO on cardiac MRI.

T2 mapping in myocardial disease: a comprehensive review.

Cardiovascular magnetic resonance (CMR) is considered the gold standard imaging modality for myocardial tissue characterization. Elevated transverse relaxation time (T2) is specific for increased myocardial water content, increased free water, and is used as an index of myocardial edema. The strengths of quantitative T2 mapping lie in the accurate characterization of myocardial edema, and the early detection of reversible myocardial disease without the use of contrast agents or ionizing radiation. Quantitative T2 mapping overcomes the limitations of T2-weighted imaging for reliable assessment of diffuse myocardial edema and can be used to diagnose, stage, and monitor myocardial injury. Strong evidence supports the clinical use of T2 mapping in acute myocardial infarction, myocarditis, heart transplant rejection, and dilated cardiomyopathy. Accumulating data support the utility of T2 mapping for the assessment of other cardiomyopathies, rheumatologic conditions with cardiac involvement, and monitoring for cancer therapy-related cardiac injury. Importantly, elevated T2 relaxation time may be the first sign of myocardial injury in many diseases and oftentimes precedes symptoms, changes in ejection fraction, and irreversible myocardial remodeling. This comprehensive review discusses the technical considerations and clinical roles of myocardial T2 mapping with an emphasis on expanding the impact of this unique, noninvasive tissue parameter.

[The role of cardiac magnetic resonance imaging in defining the prognosis of patients with acute ST-segment elevation myocardial infarction. Part 2. Assessment of the disease prognosis].

Currently the incidence of congestive heart failure after ST-segment elevation myocardial infarction (STEMI) tends to increase. Reperfusion therapy is still the only effective method to reduce an infarct size. Therefore, there is a high unmet need of novel cardioprotective treatments that would improve outcomes in such patients. Recent advances in cardiovascular magnetic resonance (CMR) methods enabled the identification of certain new infarct characteristics associated with the development of heart failure and sudden cardiac death. These characteristics can help identify new groups of high risk patients and used as a targets for novel cardioprotective treatments. This part of the review summarizes novel CMR-based characteristics of myocardial infarction and their role in the prognostic stratification of STEMI patients.

The role of AQP3 and AQP4 channels in cisplatin-induced cardiovascular edema and the protective effect of melatonin.

BACKGROUND: The present study evaluates the development of edema, the change in the AQP3, AQP4, p53 and Bax gene expressions, and the protective effects of melatonin in rat hearts administered with cisplatin. METHODS AND RESULTS: A total of 28 Wistar albino rats were divided into four groups. The vehicle was administered intraperitoneally (i.p.) to the rats in the control group. The melatonin group (Mel) received melatonin at a dose of 10 mg/kg for 13 days. The cisplatin group (Cis) received cisplatin on days 1, 5, 9 and 13 at a dose of 4 mg/kg. The rats in the cisplatin + melatonin (Cis+Mel) group underwent the procedures both in the Mel and Cis groups. Blood and left ventricular samples were taken and analyzed on day 14 of the study. AQP3, p53 and Bax gene expressions were found to be significantly increased following cisplatin administration compared to the control, while melatonin administration significantly decreased the expression of these genes (p < 0.05). Melatonin administration also significantly decreased the level of AQP4 gene expression compared to the cis. On histological examination, congestion, hemorrhage, extracellular and intracellular edema, and degenerative changes were significantly more common in the Cis than in the control. Melatonin administration significantly decreased intracellular edema (p = 0.010) and degenerative changes (p = 0.010), and the improvement in extracellular edema was close to statistical significance (p = 0.051) in melatonin. CONCLUSIONS: These results indicate that melatonin had an ameliorative effect on myocardial edema and AQP channels, and that it may be used as a protective molecule against myocardial edema secondary to cisplatin administration.

"Apical sparing" T-wave inversion in a case of mid-ventricular takotsubo syndrome.

Previous studies showed that myocardial edema correlates with dynamic T-wave inversion and QTc prolongation in a variety of acute cardiovascular diseases including takotsubo syndrome (TTS). We reported the case of a patient with "atypical" (mid-ventricular) TTS showing a unique pattern of diffuse T-wave inversion that spared only the apical precordial leads V3-V4. Cardiac magnetic resonance (CMR) showed myocardial edema involving all mid-ventricular segments but not the apex. Both ECG and CMR normalized at follow-up evaluation. This case further reinforces the theory of an association between presence and regional distribution of acute myocardial inflammation and dynamic repolarization changes.

Cardiovascular Magnetic Resonance of Myocardial Fibrosis, Edema, and Infiltrates in Heart Failure.

Cardiac magnetic resonance (CMR) imaging is a unique imaging modality, which provides accurate noninvasive tissue characterization. Various CMR sequences can be utilized to identify and quantify patterns of myocardial edema, fibrosis, and infiltrates, which are important determinants for diagnosis and prognostication of heart failure. This article describes available methods of tissue characterization imaging applied in CMR. The presence and patterns of abnormal tissue characterization are related to common etiologies of heart failure and the techniques employed to demonstrate this. CMR provides the opportunity to identify the etiology of heart failure based on the recognition of different patterns of myocardial abnormalities.

A murine model of increased coronary sinus pressure induces myocardial edema with cardiac lymphatic dilation and fibrosis.

Myocardial edema is a consequence of many cardiovascular stressors, including myocardial infarction, cardiac bypass surgery, and hypertension. The aim of this study was to establish a murine model of myocardial edema and elucidate the response of cardiac lymphatics and the myocardium. Myocardial edema without infarction was induced in mice by cauterizing the coronary sinus, increasing pressure in the coronary venous system, and inducing myocardial edema. In male mice, there was rapid development of edema 3 h following coronary sinus cauterization (CSC), with associated dilation of cardiac lymphatics. By 24 h, males displayed significant cardiovascular contractile dysfunction. In contrast, female mice exhibited a temporal delay in the formation of myocardial edema, with onset of cardiovascular dysfunction by 24 h. Furthermore, myocardial edema induced a ring of fibrosis around the epicardial surface of the left ventricle in both sexes that included fibroblasts, immune cells, and increased lymphatics. Interestingly, the pattern of fibrosis and the cells that make up the fibrotic epicardial ring differ between sexes. We conclude that a novel surgical model of myocardial edema without infarct was established in mice. Cardiac lymphatics compensated by exhibiting both an acute dilatory and chronic growth response. Transient myocardial edema was sufficient to induce a robust epicardial fibrotic and inflammatory response, with distinct sex differences, which underscores the sex-dependent differences that exist in cardiac vascular physiology.NEW & NOTEWORTHY Myocardial edema is a consequence of many cardiovascular stressors, including myocardial infarction, cardiac bypass surgery, and high blood pressure. Cardiac lymphatics regulate interstitial fluid balance and, in a myocardial infarction model, have been shown to be therapeutically targetable by increasing heart function. Cardiac lymphatics have only rarely been studied in a noninfarct setting in the heart, and so we characterized the first murine model of increased coronary sinus pressure to induce myocardial edema, demonstrating distinct sex differences in the response to myocardial edema. The temporal pattern of myocardial edema induction and resolution is different between males and females, underscoring sex-dependent differences in the response to myocardial edema. This model provides an important platform for future research in cardiovascular and lymphatic fields with the potential to develop therapeutic interventions for many common cardiovascular diseases.

IL-1 receptor antagonist, anakinra, prevents myocardial dysfunction in a mouse model of Kawasaki disease vasculitis and myocarditis.

Kawasaki disease (KD) vasculitis is an acute febrile illness of childhood characterized by systemic vasculitis of unknown origin, and is the most common cause of acquired heart disease among children in the United States. While  histological evidence of myocarditis can be found in all patients with acute KD, only a minority of patients are clinically symptomatic and a subset demonstrate echocardiographic evidence of impaired myocardial function, as well as increased left ventricular mass, presumed to be due to myocardial edema and inflammation. Up to a third of KD patients fail to respond to first-line therapy with intravenous immunoglobulin (IVIG), and the use of interleukin (IL)-1 receptor antagonist (IL-1Ra, anakinra) is currently being investigated as an alternative therapeutic approach to treat IVIG-resistant patients. In this study, we sought to investigate the effect of IL-1Ra on myocardial dysfunction and its relation to myocarditis development during KD vasculitis. We used the Lactobacillus casei cell-wall extract (LCWE)-induced murine model of KD vasculitis and investigated the effect of IL-1Ra pretreatment on myocardial dysfunction during KD vasculitis by performing histological, magnetic resonance imaging (MRI) and echocardiographic evaluations. IL-1Ra pretreatment significantly reduced KD-induced myocardial inflammation and N-terminal pro B-type natriuretic peptide (NT-proBNP) release. Both MRI and echocardiographic studies on LCWE-injected KD mice demonstrated that IL-1Ra pretreatment results in an improved ejection fraction and a normalized left ventricular function. These findings further support the potential beneficial effects of IL-1Ra therapy in preventing the cardiovascular complications in acute KD patients, including the myocarditis and myocardial dysfunction associated with acute KD.

Black blood myocardial T2 mapping.

PURPOSE: To develop a black blood heart-rate adaptive T2 -prepared balanced steady-state free-precession (BEATS) sequence for myocardial T2 mapping. METHODS: In BEATS, blood suppression is achieved by using a combination of preexcitation and double inversion recovery pulses. The timing and flip angles of the preexcitation pulse are auto-calculated in each patient based on heart rate. Numerical simulations, phantom studies, and in vivo studies were conducted to evaluate the performance of BEATS. BEATS T2 maps were acquired in 36 patients referred for clinical cardiac MRI and in 1 swine with recent myocardial infarction. Two readers assessed all images acquired in patients to identify the presence of artifacts associated with slow blood flow. RESULTS: Phantom experiments showed that the BEATS sequence provided accurate T2 values over a wide range of simulated heart rates. Black blood myocardial T2 maps were successfully obtained in all subjects. No significant difference was found between the average T2 measurements obtained from the BEATS and conventional bright-blood T2 ; however, there was a decrease in precision using the BEATS sequence. A suppression of the blood pool resulted in sharper definition of the blood-myocardium border and reduced partial voluming effect. The subjective assessment showed that 16% (18 out of 108) of short-axis slices have residual blood artifacts (12 in the apical slice, 4 in the midventricular slice, and 2 in the basal slice). CONCLUSION: The BEATS sequence yields dark blood myocardial T2 maps with better definition of the blood-myocardium border. Further studies are warranted to evaluate diagnostic accuracy of black blood T2 mapping.

Stress Cardiomyopathy in a Patient with Hypertrophic Cardiomyopathy: Case Presentation and Review of the Literature.

Stress cardiomyopathy and hypertrophic cardiomyopathy are two distinct entities with different pathophysiologic causes. In the recent medical literature their concurrency has been described. During the acute phase of a stress cardiomyopathy making the diagnosis of a concomitant hypertrophic cardiomyopathy may be challenging, and has important implications in both the acute and longterm clinical management. Herein, we present a case of a stress cardiomyopathy occurring in a patient with hypertrophic cardiomyopathy, along with a review of the literature.

Relationship between CMR-derived parameters of ischemia/reperfusion injury and the timing of CMR after reperfused ST-segment elevation myocardial infarction.

BACKGROUND: To investigate the influence of cardiovascular magnetic resonance (CMR) timing after reperfusion on CMR-derived parameters of ischemia/reperfusion (I/R) injury in patients with ST-segment elevation myocardial infarction (STEMI). METHODS: The study included 163 reperfused STEMI patients undergoing CMR during the index hospitalization. Patients were divided according to the time between revascularization and CMR (Trevasc-CMR: Tertile-1 ≤ 43; 43 < Tertile-2 ≤ 93; Tertile-3 > 93 h). T2-mapping derived area-at-risk (AAR) and intramyocardial-hemorrhage (IMH), and late gadolinium enhancement (LGE)-derived infarct size (IS) and microvascular obstruction (MVO) were quantified. T1-mapping was performed before and > 15 min after Gd-based contrast-agent administration yielding extracellular volume (ECV) of infarct. RESULTS: Main factors influencing I/R injury were homogenously balanced across Trevasc-CMR tertiles. T2 values of infarct and remote regions increased with increasing Trevasc-CMR tertiles (infarct: 60.0 ± 4.9 vs 63.5 ± 5.6 vs 64.8 ± 7.5 ms; P < 0.001; remote: 44.3 ± 2.8 vs 46.1 ± 2.8 vs ± 46.1 ± 3.0; P = 0.001). However, T2 value of infarct largely and significantly exceeded that of remote myocardium in each tertile yielding comparable T2-mapping-derived AAR extent throughout Trevasc-CMR tertiles (17 ± 9% vs 19 ± 9% vs 18 ± 8% of LV, respectively, P = 0.385). Similarly, T2-mapping-based IMH detection and quantification were independent of Trevasc-CMR. LGE-derived IS and MVO were not influenced by Trevasc-CMR (IS: 12 ± 9% vs 12 ± 9% vs 14 ± 9% of LV, respectively, P = 0.646). In 68 patients without MVO, T1-mapping based ECV of infarct region was comparable across Trevasc-CMR tertiles (P = 0.470). CONCLUSION: In STEMI patients, T2 values of infarct and remote myocardium increase with increasing CMR time after revascularization. However, these changes do not give rise to substantial variation of T2-mapping-derived AAR size nor of other CMR-based parameters of I/R. TRIAL REGISTRATION: ISRCTN03522116 . Registered 30.4.2018 (retrospectively registered).

In vivo MRI and ex vivo histological assessment of the cardioprotection induced by ischemic preconditioning, postconditioning and remote conditioning in a closed-chest porcine model of reperfused acute myocardial infarction: importance of microvasculature.

BACKGROUND: Cardioprotective value of ischemic post- (IPostC), remote (RIC) conditioning in acute myocardial infarction (AMI) is unclear in clinical trials. To evaluate cardioprotection, most translational animal studies and clinical trials utilize necrotic tissue referred to the area at risk (AAR) by magnetic resonance imaging (MRI). However, determination of AAR by MRI' may not be accurate, since MRI-indices of microvascular damage, i.e., myocardial edema and microvascular obstruction (MVO), may be affected by cardioprotection independently from myocardial necrosis. Therefore, we assessed the effect of IPostC, RIC conditioning and ischemic preconditioning (IPreC; positive control) on myocardial necrosis, edema and MVO in a clinically relevant, closed-chest pig model of AMI. METHODS AND RESULTS: Acute myocardial infarction was induced by a 90-min balloon occlusion of the left anterior descending coronary artery (LAD) in domestic juvenile female pigs. IPostC (6 × 30 s ischemia/reperfusion after 90-min occlusion) and RIC (4 × 5 min hind limb ischemia/reperfusion during 90-min LAD occlusion) did not reduce myocardial necrosis as assessed by late gadolinium enhancement 3 days after reperfusion and by ex vivo triphenyltetrazolium chloride staining 3 h after reperfusion, however, the positive control, IPreC (3 × 5 min ischemia/reperfusion before 90-min LAD occlusion) did. IPostC and RIC attenuated myocardial edema as measured by cardiac T2-weighted MRI 3 days after reperfusion, however, AAR measured by Evans blue staining was not different among groups, which confirms that myocardial edema is not a measure of AAR, IPostC and IPreC but not RIC decreased MVO. CONCLUSION: We conclude that IPostC and RIC interventions may protect the coronary microvasculature even without reducing myocardial necrosis.

Free-breathing, motion-corrected, highly efficient whole heart T2 mapping at 3T with hybrid radial-cartesian trajectory.

PURPOSE: To develop and test a time-efficient, free-breathing, whole heart T2 mapping technique at 3.0T. METHODS: ECG-triggered three-dimensional (3D) images were acquired with different T2 preparations at 3.0T during free breathing. Respiratory motion was corrected with a navigator-guided motion correction framework at near perfect efficiency. Image intensities were fit to a monoexponential function to derive myocardial T2 maps. The proposed 3D, free breathing, motion-corrected (3D-FB-MoCo) approach was studied in ex vivo canine hearts and kidneys, healthy volunteers, and canine subjects with acute myocardial infarction (AMI). RESULTS: Ex vivo T2 values from proposed 3D T2 -prep gradient echo were not different from two-dimensional (2D) spin echo (P = 0.7) and T2 -prep balanced steady-state free precession (bSSFP) (P = 0.7). In healthy volunteers, compared with 3D-FB-MoCo and breath-held 2D T2 -prep bSSFP (2D-BH), non-motion-corrected (3D-FB-Non-MoCo) myocardial T2 was longer, had a larger coefficient of variation (COV), and had a lower image quality (IQ) score (T2 = 40.3 ms, COV = 38%, and IQ = 2.3; all P < 0.05). Conversely, the mean and COV and IQ of 3D-FB-MoCo (T2 = 37.7 ms, COV = 17%, and IQ = 3.5) and 2D-BH (T2 = 38.0 ms, COV = 15%, and IQ = 3.8) were not different (P = 0.99, P = 0.74, and P = 0.14, respectively). In AMI, T2 values and edema volumes from 3D-FB-MoCo and 2D-BH were closely correlated (R(2) = 0.88 and 0.96, respectively). CONCLUSION: The proposed whole heart T2 mapping approach can be performed within 5 min with similar accuracy to that of the 2D-BH T2 mapping approach.

T2 mapping at 7T MRI can quantitatively assess intramyocardial hemorrhage in rats with acute reperfused myocardial infarction in vivo.

PURPOSE: To investigate T2 mapping at 7T magnetic resonance imaging (MRI) for the detection and quantification of reperfused intramyocardial hemorrhage (IMH) in a rat model. MATERIALS AND METHODS: Myocardial infarction (MI) was induced in 25 female rats. Rats were scanned at a 7T MRI 48 hours after reperfusion, using T2 mapping and late gadolinium enhancement imaging. Gross sections of the left ventricular myocardium and corresponding hematoxylin and eosin staining were assessed for IMH. T2 mapping images were matched with the gross sections. The IMH volume, expressed as a percentage of the left ventricular myocardial volume, of each heart determined by T2 mapping was compared with that calculated by pathological gross examination. RESULTS: Six rats died. In all, 97 gross sections of the left ventricular myocardium from the 19 rats were matched with T2 mapping images. IMH occurred pathologically in 68 gross sections, which was detected as hypointense cores by T2 mapping in 63 images (93% sensitivity). Three T2 mapping images with hypointense cores showed no hemorrhage on pathological sections (90% specificity). The positive and negative predictive values of hemorrhage on T2 mapping were 95% and 84%, respectively. In terms of the IMH volume, there was no significant difference between T2 mapping and pathological gross measurements (4.8 ± 2.4% vs. 5.3 ± 3.2%; P = 0.11). CONCLUSION: T2 mapping at 7T MRI can reliably detect and quantify IMH in rats in vivo. This may be useful as a noninvasive quantitative approach to investigating the mechanisms and evolution of MI and reperfusion injury. J. Magn. Reson. Imaging 2016;44:194-203.

Relationship between T-wave inversion and transmural myocardial edema as evidenced by cardiac magnetic resonance in patients with clinically suspected acute myocarditis: clinical and prognostic implications.

BACKGROUND: The pathophysiologic mechanisms and the prognostic meaning of electrocardiographic (ECG) T-wave inversion (TWI) occurring in a subgroup of patients with clinically suspected acute myocarditis remain to be elucidated. Contrast-enhanced cardiac magnetic resonance (CMR) offers the potential to identify myocardial tissue changes such as edema and/or fibrosis which may underlie TWI. METHODS AND RESULTS: We studied 76 consecutive patients (median age 34years) with clinically suspected acute myocarditis, using a comprehensive CMR protocol which included T2 weighted sequences for myocardial edema. At the time of CMR, TWI was observed in 21 (27%) patients. There was a statistically significant association of TWI with the median number of left ventricular (LV) segments showing both any pattern of myocardial edema (transmural and non-transmural) [5 (3-7) vs. 3 (2-4); p=0.015] and myocardial late-gadolinium-enhancement [4 (3-7) vs. 3 (2-4); p=0.002]. Transmural myocardial edema involving ≥2 LV segments was found in 17/21 (81%) patients with TWI versus 13/55 (24%) patients without TWI (p<0.001) and remained the only independent predictor of TWI at multivariable analysis (OR=9.96; 95%CI=2.71-36.6; p=0.001). Overall, topographic concordance between the location of TWI across the ECG leads and the regional distribution of transmural myocardial edema was 88%. There was no association between acute TWI and reduced LV ejection fraction (<55%) at 6-months of follow-up. CONCLUSIONS: This is the first study to demonstrate an association between LV transmural myocardial edema as evidenced by CMR sequences and TWI in clinically suspected acute myocarditis. As an expression of reversible myocardial edema, development of TWI during the acute disease phase was not a predictor of LV systolic dysfunction at follow-up.