Localization of Late Gadolinium Enhancement and Its Association with Ventricular Tachycardia in Patients with Cardiac Sarcoidosis.

Sustained ventricular tachycardia (sVT), leading to sudden cardiac death, is one of the common manifestations in cardiac sarcoidosis (CS). Although late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) has been reported to be associated with sVT, the relationships of its localization to sVT have not been fully evaluated.To evaluate the localization of LGE and its relationships to sVT in patients with CS, we reviewed medical record of consecutive 31 patients with CS who underwent CMR. The localization of LGE was divided into four categories: Left ventricular (LV) septum, LV free wall, right ventricular (RV) septum, and RV free wall. We investigated the association of sVT with localization of LGE and other parameters including serum biomarkers LV ejection fraction on echocardiography and Fluorine-18-fluorodeoxyglucose (FDG) accumulation on positron emission tomography (PET) -CT.Of the studied population, 8 patients (25.8%) were known to present with sVT among 31 CS patients. LGE was observed in the RV free wall in 6 patients with sVT, whereas it was in 5 patients without sVT (75.0% versus 21.7%, P = 0.022). Univariate analysis showed that only LGE in the RV free wall was associated with sVT (odds ratio [OR]: 10.80; 95% confidence interval [CI]: 1.64-70.93, P = 0.013).LGE in the RV free wall was associated with sVT in patients with CS.

Extracellular volume fraction assessed using cardiovascular magnetic resonance can predict improvement in left ventricular ejection fraction in patients with dilated cardiomyopathy.

T1 mapping using cardiac magnetic resonance (CMR) is useful for myocardial assessment. However, its prognostic value is not well defined. The aim of this study was to determine whether T1 mapping with CMR can predict reverse cardiac remodeling in patients with non-ischemic dilated cardiomyopathy (NIDCM). We also investigated the predictive prognostic value of T1 mapping with CMR in these patients. We included 33 patients with NIDCM admitted to Nippon Medical School Hospital between February 2012 and October 2015. All patients underwent CMR and echocardiography for clinical assessment within 1 month of admission (13 ± 16 days). Follow-up echocardiography was performed no sooner than 6 months after the initial echocardiogram (536 ± 304 days). We evaluated the correlations between native and post-contrast T1 values/extracellular volume fraction (ECV) and the difference in left ventricular ejection fraction (ΔLVEF) determined at baseline and follow-up echocardiography. No correlation was noted between ΔLVEF and native (p = 0.150, r = - 0.256) or post-contrast T1 values (p = 0.956, r = - 0.010). However, a significant and substantial correlation was found between ΔLVEF and ECV (p = 0.043, r = - 0.355). Four patients were hospitalized for heart failure (HF), but no cardiovascular-related deaths occurred over a median follow-up period of 34 months (interquartile range 25-49 months). Kaplan-Meier curves stratified by the median value of ECV were created. The higher ECV groups experienced a significantly higher incidence of HF-related hospitalization (p = 0.0159). ECV measured by CMR can predict improvements in LVEF in patients with NIDCM. In addition, ECV may be a predictive factor for HF-related hospitalization.

Relationship of Nonseptal Late Gadolinium Enhancement to Ventricular Tachyarrhythmia in Hypertrophic Cardiomyopathy.

OBJECTIVE: This study aimed to determine the relationship between the extent and the location of late gadolinium enhancement (LGE) and ventricular tachyarrhythmia or implantable cardioverter defibrillator (ICD) in hypertrophic cardiomyopathy (HCM). METHODS: We enrolled 115 patients with HCM and LGE. The location of LGE was divided into septal and nonseptal segments. Clinical backgrounds and LGE were compared in patients between with and without the arrhythmia or consequent ICD installation. RESULTS: There were significant differences in the number of risk markers, left ventricular ejection fraction, extent of global LGE, and extent of nonseptal LGE between the groups (P < 0.01). Multivariate analysis revealed that the number of risk markers and extent of nonseptal LGE contributed to ventricular tachyarrhythmia or ICD installation (P < 0.01). CONCLUSIONS: The nonseptal LGE is related to ventricular tachyarrhythmia or ICD installation. We should be vigilant for nonseptal LGE when applying LGE to risk stratification for HCM.

Myocardial T2 Mapping in Patients With Hypertrophic Cardiomyopathy.

OBJECTIVE: The aim of this study was to evaluate the usefulness of T2 mapping for detecting myocardial injuries in patients with hypertrophic cardiomyopathy (HCM). METHODS: Twenty-one HCM patients and 7 healthy volunteers were examined. The T2 values were measured at hyperintense areas (high-T2 areas) identified with T2 mapping, at late gadolinium enhancement (LGE) areas, and in nullified myocardium of the HCM patients. The associations between T2 values and laboratory data or LGE areas were assessed. RESULTS: High-T2 areas had significantly greater T2 values than LGE areas (P < 0.05) and nullified areas (P < 0.01) of HCM and normal myocardium (P < 0.01). The presence of high-T2 areas was associated with an increase in troponin T levels (P = 0.02), and T2 values correlated with the levels of brain natriuretic peptide (P = 0.036, r = 0.86). CONCLUSIONS: T2 mapping identified myocardial injuries suggested by the laboratory data in HCM.

Relationship of postcontrast myocardial T1 value and delayed enhancement to reduced cardiac function and serious arrhythmia in dilated cardiomyopathy with left ventricular ejection fraction less than 35.

BACKGROUND: Dilated cardiomyopathy (DCM) is often associated with progressive heart failure or ventricular arrhythmia. Look-Locker magnetic resonance imaging (MRI) allows quantitative evaluation of interstitial fibrosis by measuring the myocardial T1 value, and delayed enhancement (DE) MRI visualizes myocardial scar. PURPOSE: To determine the relationship of postcontrast myocardial T1 value or DE to reduced cardiac function or sustained ventricular tachycardia (SVT) in DCM patients with a left ventricular ejection fraction (LVEF) <35%. MATERIAL AND METHODS: We enrolled 41 patients with DCM. Correlations between the cardiac function parameters and postcontrast myocardial T1 value or extent of DE were evaluated. The relationship between SVT and the T1 values or extent of DE was assessed. The correlation between the extent of DE and the T1 value was also examined. RESULTS: The postcontrast myocardial T1 value was significantly correlated with the LVEF (P < 0.05; r = 0.31) and end-diastolic volume (P < 0.01; r = -0.40) in 40 patients with LVEF <35%. DE was not correlated with the cardiac function, but provided a high negative predictive value of 94.7% for SVT. No correlation was found between the myocardial T1 value and extent of DE. CONCLUSION: In DCM patients with LVEF <35%, the postcontrast myocardial T1 value correlated with the severity of cardiac dysfunction, and the absence of DE indicated the low risk of SVT. Both MRI parameters should be estimated because they may reflect discrete forms of myocardial damages in patients with DCM.

Magnetic resonance imaging of microvascular obstruction in hypertrophic obstructive cardiomyopathy after percutaneous transluminal septal myocardial ablation.

BACKGROUND: The clinical significance of microvascular obstruction (MO) in hypertrophic cardiomyopathy (HOCM) after percutaneous transluminal septal myocardial ablation (PTSMA) remains unknown. PURPOSE: To assess the relationship between the location of MO and the improvement in symptoms and pressure gradient after PTSMA in patients with HOCM. MATERIAL AND METHODS: Twenty-three patients with HOCM underwent MRI within 24 weeks after PTSMA. The MO was defined visually as the hypointense region adjacent to the left or right ventricular cavity, which was surrounded by myocardial infarction. The location of MO and improvement in clinical symptoms and pressure gradient at 3-6 months follow-up were assessed. RESULTS: MO was observed in 16 patients who underwent MRI within 7 weeks after PTSMA. Left-sided MO was observed in 12 patients, and right-sided MO was observed in four patients. Improvement in clinical symptoms and reduction in the pressure gradient were not sufficient in the patients with right-sided MO, while PTSMA was effective in the patients with the left-sided MO. CONCLUSION: The location of MO identified by MRI may be related to the effectiveness of PTSMA at the short-term follow-up. The left-sided MO is related to complete improvement in clinical symptoms and pressure gradients.

Myocardial fibrosis evaluated by Look-Locker and late gadolinium enhancement magnetic resonance imaging in apical hypertrophic cardiomyopathy: association with ventricular tachyarrhythmia and risk factors.

PURPOSE: To evaluate the distribution and extent of myocardial fibrosis identified by either contrast-enhanced Look-Locker or late gadolinium enhancement magnetic resonance imaging (LGE MRI) and their relationships between ventricular tachyarrhythmia or risk factors in apical hypertrophic cardiomyopathy (APH). MATERIALS AND METHODS: Twenty-five APH patients were examined using a 3.0 T or 1.5 T instrument. We used MRI to evaluate myocardial T1 values and scar. We compared the myocardial fibrosis assessed by contrast-enhanced Look-Locker or LGE MRI with ventricular tachyarrhythmia or risk factors for hypertrophic cardiomyopathy. RESULTS: Myocardial scar was present in 17 of the 25 patients with APH. Myocardial scar was distributed predominantly in the apical myocardium (P < 0.01), whereas myocardial T1 values did not differ between the apical, midventricular, and basal septum. The extent of myocardial scar according to 16-segment model and ejection fraction were related to ventricular tachyarrhythmia or risk factors in APH (P < 0.05 for both). The myocardial T1 value was not associated with the tachyarrhythmia or risk factors. CONCLUSION: In APH, the extent of myocardial scar on LGE MRI is associated with ventricular tachyarrhythmia and risk factors. Quantification of the myocardial T1 value is not necessary for its risk stratification.

Delayed enhancement magnetic resonance imaging in hypertrophic cardiomyopathy with Basal septal hypertrophy and preserved ejection fraction: relationship with ventricular tachyarrhythmia.

OBJECTIVE: This study aimed to determine the relationship between delayed enhancement magnetic resonance imaging (DE MRI) and ventricular tachyarrhythmia in patients with hypertrophic cardiomyopathy (HCM) with basal septal hypertrophy and preserved ejection fraction (EF). METHODS: One hundred seven patients with HCM with basal septal hypertrophy and EF greater than 50% underwent cine and DE MRI. Myocardial scar was identified with DE MRI. We assessed whether patient,s background, cine MRI findings, presence of myocardial scar, or number of scarred myocardial segments was related to the occurrence of ventricular tachyarrhythmia. RESULTS: Patient,s age, family history of HCM, and number of scarred segments differed between the patients with and without the arrhythmia. A family history of HCM and number of scarred segments were significantly related to ventricular tachyarrhythmia (P < 0.01). CONCLUSIONS: The number of scarred segments is the significant DE MRI parameter related to ventricular tachyarrhythmia in HCM with basal septal hypertrophy and preserved EF.

Evaluation of nonscarred myocardial T1 value using contrast-enhanced look-locker cardiac MRI and its relationship to cardiac function in dilated cardiomyopathy: Comparison of 1.5 and 3.0 Tesla MRI.

PURPOSE: To assess relationship between nonscarred myocardial T1 value measured using contrast-enhanced Look-Locker MRI and cardiac function in dilated cardiomyopathy (DCM) at 1.5 Tesla (T) and 3.0T MRI. MATERIALS AND METHODS: Contrast-enhanced Look-Locker MRI was performed in 35 DCM patients. Nonscarred myocardial and blood T1 values were calculated from the signal intensity values and the delay time obtained on Look-Locker MRI. We assessed the correlation between the myocardial T1 value or myocardial T1 minus blood T1 value and cardiac function estimated using cine MRI (e.g., end-diastolic volume: EDV, left ventricular ejection fraction: LVEF) or brain natriuretic peptide (BNP). RESULTS: With 1.5T MRI (n = 16), the myocardial T1 value correlated negatively with the EDV(r = -0.66) and end-systolic volume (ESV; r = -0.68), and positively with the LVEF (r = 0.51); the myocardial T1 minus blood T1 value correlated inversely with EDV (r = -0.70), ESV (r = -0.62), and brain natriuretic peptide (BNP; r = -0.56). With 3.0T MRI (n = 17), the myocardial T1 value correlated negatively with ESV (r = -0.44), septal thickness (r = -0.60), and BNP (r = -0.51), and positively with LVEF (r = 0.61); the myocardial T1 minus blood T1 value negatively correlated with BNP (r = -0.50) and positively with LVEF (r = 0.54). CONCLUSION: The nonscarred myocardial T1 value measured with either 1.5T or 3.0T contrast-enhanced Look-Locker MRI is significantly related to cardiac dysfunction in DCM.

Three-dimensional Look-Locker MRI for evaluation of postcontrast myocardial and blood T1 values: comparison with two-dimensional Look-Locker and late gadolinium enhancement MRI.

BACKGROUND: Two-dimensional (2D) Look-Locker MRI technique can identify myocardial fibrosis, but cannot cover the whole left ventricle during a single scan. PURPOSE: To develop breath-hold three-dimensional (3D) Look-Locker MRI for the evaluation of postcontrast myocardial and blood T1 values and myocardial scarring in the left ventricle. MATERIAL AND METHODS: A phantom and 24 patients with myocardial diseases underwent gadolinium-enhanced 2D and 3D Look-Locker MRI using a 1.5-T unit. We compared the T1 value of the phantom and the values of the myocardium and blood in the patients between the two Look-Locker MRI sequences. In the patient study, the scan ordering of the two Look-Locker MRI was selected randomly. We also assessed the ability of the 3D imaging to detect myocardial scarring that was confirmed by late gadolinium enhancement MRI. RESULTS: The phantom study showed a good agreement for the T1 value between 2D and 3D Look-Locker MRI. There were no significant differences in the myocardial T1 values after contrast between 2D and 3D Look-Locker MRI or in the T1 values between the two imaging slices on the 3D Look-Locker MRI (P > 0.10). A better agreement for the myocardial T1 values was found when the 3D Look-Locker imaging was performed first. The T1 values for blood were affected by the scan order (P < 0.05). The 3D Look-Locker MRI showed myocardial scarring with a shorter T1 value (290.4 ± 62.7 ms) than those for unscarred myocardium (360.8 ± 30.3 ms). CONCLUSION: Three-dimensional Look-Locker MRI may precisely estimate the postcontrast myocardial and blood T1 values for the entire left ventricle during a single scan.

Simultaneous assessment of myocardial scar and coronary arteries using navigator-gated 3-dimensional fat-suppressed delayed-enhancement MRI at 3.0 T: a technical feasibility study.

OBJECTIVE: To assess technical feasibility of navigator-gated 3-dimensional (3D) fat-suppressed delayed-enhancement magnetic resonance imaging (DE-MRI) at 3.0 T for simultaneous visualization of myocardial scars and coronary arteries. METHODS: Thirty patients with various myocardial diseases underwent navigator-gated 3D fat-suppressed DE-MRI using a 3.0-T scanner. The ability of this imaging technique to detect myocardial scars was compared with that of 2D DE-MRI. Visualization of the coronary arteries by this MRI technique was scored, and the relationship between myocardial scars and coronary arteries was assessed. RESULTS: Navigator-gated 3D fat-suppressed DE-MRI detected 71 of 75 segments with a myocardial scar. This imaging visualized proximal coronary arteries with an acceptable image quality and demonstrated a relationship between the myocardial scars and coronary arteries in 11 of the patients with scars. CONCLUSION: Navigator-gated 3D fat-suppressed DE-MRI at 3.0 T was feasible for simultaneous visualization of myocardial scars and proximal coronary arteries.

T2-weighted cardiac magnetic resonance imaging of edema in myocardial diseases.

The purpose of this paper is to describe imaging techniques and findings of T2-weighted magnetic resonance imaging (MRI) of edema in myocardial diseases. T2-weighted cardiac MRI is acquired by combining acceleration techniques with motion and signal suppression techniques. The MRI findings should be interpreted based on coronary artery supply, intramural distribution, and comparison with delayed-enhancement MRI. In acute myocardial diseases, such as acute myocardial infarction and myocarditis, the edema is larger than myocardial scarring, whereas the edema can be smaller than the scarring in some types of nonischemic cardiomyopathy, including hypertrophic cardiomyopathy. T2-weighted MRI of edema identifies myocardial edema associated with ischemia, inflammation, vasculitis, or intervention in the myocardium and provides information complementary to delayed-enhancement MRI.

Measurement of Turbulent Kinetic Energy in Hypertrophic Cardiomyopathy Using Triple-velocity Encoding 4D Flow MR Imaging.

PURPOSE: The turbulent kinetic energy (TKE) estimation based on 4D flow MRI has been currently developed and can be used to estimate the pressure gradient. The objective of this study was to validate the clinical value of 4D flow-based TKE measurement in patients with hypertrophic cardiomyopathy (HCM). METHODS: From April 2018 to March 2019, we recruited 28 patients with HCM. Based on echocardiography, they were divided into obstructed HCM (HOCM) and non-obstructed HCM (HNCM). Triple-velocity encoding 4D flow MRI was performed. The volume-of-interest from the left ventricle to the aortic arch was drawn semi-automatically. We defined peak turbulent kinetic energy (TKEpeak) as the highest TKE phase in all cardiac phases. RESULTS: TKEpeak was significantly higher in HOCM than in HNCM (14.83 ± 3.91 vs. 7.11 ± 3.60 mJ, P < 0.001). TKEpeak was significantly higher in patients with systolic anterior movement (SAM) than in those without SAM (15.60 ± 3.96 vs. 7.44 ± 3.29 mJ, P < 0.001). Left ventricular (LV) mass increased proportionally with TKEpeak (P = 0.012, r = 0.466). When only the asymptomatic patients were extracted, a stronger correlation was observed (P = 0.001, r = 0.842). CONCLUSION: TKE measurement based on 4D flow MRI can detect the flow alteration induced by systolic flow jet and LV outflow tract geometry, such as SAM in patients with HOCM. The elevated TKE is correlated with increasing LV mass. This indicates that increasing cardiac load, by pressure loss due to turbulence, induces progression of LV hypertrophy, which leads to a worse prognosis.

Long-term prognostic value of ultrastructural features in dilated cardiomyopathy: comparison with cardiac magnetic resonance.

AIMS: This study aims to determine the implications associated with long-term prognosis of heart failure (HF) in patients with dilated cardiomyopathy (DCM) presenting initially as decompensated HF. We stratified the phase of DCM patients without late gadolinium enhancement (LGE) based on ultrastructural changes in cardiomyocytes. METHODS AND RESULTS: Left ventricular (LV) endomyocardial biopsy was performed in 55 consecutive DCM patients with initial decompensated HF. Ultrastructural changes in cardiomyocytes detected by electron microscopy were compared with data including LGE with cardiac magnetic resonance and HF recurrence. Of the 55 DCM patients, 24 (44%) showed LGE, and 26 (47%) showed recurrence decompensated HF, while 23 patients (42%) showed autophagic vacuoles in cardiomyocytes by electron microscopy. Multivariate analysis identified atrial fibrillation [hazard ratio (HR), 3.40; 95% confidence interval (CI), 1.45-7.98], haemoglobin level (HR, 0.82; 95% CI, 0.68-0.99), beta-blocker use (HR, 0.18; 95% CI, 0.05-0.74), and autophagic vacuoles (HR, 0.25; 95% CI, 0.09-0.65) as predictors of HF recurrence in the total patient population. In patients without LGE, only autophagic vacuoles were independent predictors of readmission because of HF (HR, 0.29; 95% CI, 0.09-0.90). In patients with LGE, atrial fibrillation (HR, 19.10; 95% CI, 2.97-123.09), and mid-linear LGE (HR, 12.96; 95% CI, 2.02-82.94) were independent predictors of readmission because of HF. CONCLUSIONS: In DCM patients with LGE, characterised by progression of LV remodelling, the LGE pattern was a predictor of HF recurrence, whereas in patients without LGE, absence of autophagic vacuoles was a predictor of HF recurrence.

Non-contrast-enhanced T1 Mapping of Dilated Cardiomyopathy: Comparison between Native T1 Values and Late Gadolinium Enhancement.

PURPOSE: We sought to use non-contrast-enhanced T1 mapping to determine the native T1 values required to identify myocardial fibrosis in patients with dilated cardiomyopathy (DCM). METHODS: A total of 25 patients with DCM and 15 healthy controls were enrolled. All subjects underwent T1 mapping using modified look-locker inversion recovery, and the patients underwent late gadolinium-enhancement (LGE) imaging. Basal and mid-ventricular levels were divided into eight segments and the T1 value was measured in each segment. The T1 values of septal segments with LGE were compared with those of the septal segments without LGE, the minimum T1 value of each patient, and the T1 values of the normal septal myocardium. RESULTS: Late gadolinium-enhancement was present in 12 septal segments (24.0%) from 10 patients (40.0%). T1 values were significantly higher in septal segments with LGE than in those without (1373.7 vs. 1288.0 ms; P = 0.035) or in normal septal myocardium (1209.1 ms; P < 0.01). A receiver operating characteristic analysis revealed the appropriate cutoff value of 1349.4 ms for identifying LGE with a sensitivity of 75% and specificity of 92.1%. When the minimum T1 value + 1.2 standard deviation (SD) was used as the threshold, the sensitivity was 75% and specificity was 89.5%. CONCLUSION: Non-contrast-enhanced T1 mapping can be used for assessment of myocardial fibrosis associated with DCM by using the appropriate threshold.

Cardiac MR Imaging of Hypertrophic Cardiomyopathy: Techniques, Findings, and Clinical Relevance.

Hypertrophic cardiomyopathy (HCM) is a relatively common myocardial genetic disease having a wide variety of symptoms and prognoses. The most serious complications of HCM are sudden cardiac death induced by ventricular arrhythmia or inappropriate changes in blood pressure, and heart failure. Cardiac MR imaging is a valuable imaging method for detecting HCM because of its accurate measurement of wall thickness and myocardial mass without limited view and the unique ability of late gadolinium enhancement (LGE) to identify myocardial fibrosis related to the prognosis of HCM. Tagging and T1 or T2 mapping MR imaging techniques have emerged as quantitative methods for the evaluation of disease severity. In this review, we introduce the MR imaging techniques applied to HCM and demonstrate the typical phenotypes and some morphological characteristics of HCM. In addition, we discuss the clinical relevance of MR imaging for risk stratification and management of HCM.

Three-dimensional Cardiac MR Imaging: Related Techniques and Clinical Applications.

Three-dimensional (3D) cardiac magnetic resonance (MR) imaging has several advantages, including the easy coverage of the entire heart without misregistration, reduction of breath-holding times, and availability for postprocessing reconstruction. These advantages are associated with some techniques such as breath-hold or navigator gating and parallel imaging. However, the image quality of 3D cardiac MR images is compromised by the use of a shorter repetition time and parallel imaging. Thus, a steady-state free precession sequence, contrast agent administration, and presaturation pulses are used to maintain the image quality. In this review, we introduce the MR imaging techniques used in 3D cardiac MR imaging and demonstrate the typical 3D cardiac MR images, followed by discussion about their advantages and disadvantages.

Contrast-enhanced Steady-state Free Precession in the Assessment of Hypertrophic Obstructive Cardiomyopathy after Alcohol Septal Ablation.

PURPOSE: We evaluated the feasibility of contrast-enhanced steady-state free precession (ceSSFP) in the assessment of myocardial injury and obstruction of the left ventricular outflow tract (LVOT) in patients with hypertrophic obstructive cardiomyopathy (HOCM) after alcohol septal ablation (ASA). METHODS: Twelve patients with HOCM underwent 16 magnetic resonance (MR) examinations following ASA. Precontrast SSFP, ceSSFP and late gadolinium enhancement (LGE) imaging were performed with a 1.5-tesla imager. ceSSFP was performed 3 to 7 min after gadolinium injection. We visually and quantitatively evaluated the signal patterns of the myocardium after ASA on SSFP and LGE MR imaging. We observed the LVOT using ceSSFP in the 3-chamber view. RESULTS: We could visualize ASA-induced myocardial infarction (MI) in all 16 studies by LGE and ceSSFP but in only 6 studies (37.5%) by precontrast SSFP. Contrast was higher between MI and remote myocardium with LGE than ceSSFP (P < 0.01). ASA-induced hypointense regions were well visualized by the 2 sequences after contrast in the 7 patients who underwent MR imaging within 7 weeks of ASA and in a few patients after 80 weeks from ASA. The ceSSFP allowed comparable visualization of the jet flow crossing the LVOT to that derived from echocardiographic data. CONCLUSION: Contrast-enhanced steady-state free precession allows assessment of myocardial injury as well as of the left ventricular outflow tract after alcohol septal ablation in a single scan without penalty in scan time and cine imaging contrast.

Superiority of the extracellular volume fraction over the myocardial T1 value for the assessment of myocardial fibrosis in patients with non-ischemic cardiomyopathy.

PURPOSE: This study aimed to assess the efficacies of the myocardial T1 value and the extracellular volume fraction (ECV) for determining the severity of myocardial fibrosis in patients with non-ischemic cardiomyopathy. MATERIALS AND METHODS: Myocardial fibrosis is considered the most important indicator of cardiac damage associated with non-ischemic cardiomyopathy. Recently, modified Look-Locker inversion recovery imaging (MOLLI) has been used for T1 mapping and measurement of the ECV for the assessment of myocardial fibrosis. The present study included 22 patients (mean age, 61.5±12.7; 21 male) with non-ischemic heart failure. Motion corrected myocardial T1 mapping was automatically performed using a MOLLI sequence, and the ECV was estimated from the pre- and post-contrast blood and myocardial T1 values corrected for the hematocrit level. All endomyocardial biopsy specimens were obtained from the inferoposterior left ventricular wall. The percentage of myocardial fibrosis (%F) was determined after Elastica Masson-Goldner staining as follows: (fibrosis area/[fibrosis area+myocardial area])×100. RESULTS: No correlation was noted between the %F and the pre- (r=0.290, p=0.191) or post-contrast T1 values (r=-0.190, p=0.398); however, a significant correlation was noted between the %F and ECV (r=0.750, p<0.001). CONCLUSIONS: In this study, the ECV reflected the extent of myocardial fibrosis, but the pre- and post-contrast T1 values did not. The ECV may be used to estimate the severity of myocardial fibrosis in patients with non-ischemic cardiomyopathy.

Continuous exposure to nitric oxide enhances diazepam binding inhibitor mRNA expression in mouse cerebral cortical neurons.

Effects of sustained exposure to nitric oxide (NO) formed by long-term activation of N-methyl-D-aspartate (NMDA) receptors and liberated from a long-lasting NO generator, DETA NONOate, on diazepam binding inhibitor (DBI) and its mRNA expressions were examined using mouse cerebral cortical neurons. Long-term exposure to NMDA increased DBI mRNA expression, and NO synthase inhibitors dose-dependently inhibited this increase. DETA NONOate dose-dependently increased DBI mRNA expression when exposing the neurons to this agent for 3 days and a maximal enhancement of the expression was found at 100 microM of the NO generator. In addition, a significant increase in DBI mRNA expression was observed 1 day after the exposure to 100 microM DETA NONOate, and the maximal expression was observed 2 days after the exposure, whereas transient exposure for less than 3 h to 100 microM DETA NONOate produced no changes in the expression. DETA NONOate (100 microM)-induced increase in DBI mRNA expression was completely abolished by concomitant exposure to hemoglobin. DBI content was also dose-dependently increased by DETA NONOate after the exposure for 3 days. The inhibition of cGMP formation by 1H-[1,2,4] oxadiazolo [4,3-alpha]quinoxalin-1-one (ODQ) showed no affects on the DETA NONOate-induced expression, suggesting that the increased expression of DBI mRNA is mediated via processes independent of cGMP. These results indicate that continuous exposure of the neurons to NO is an essential factor for increasing DBI mRNA expression in the neurons.