Left Ventricular Lumen Research Articles

Left Ventricular Non-Compaction in Children: Aetiology and Diagnostic Criteria.

Left ventricular non-compaction (LVNC) is a heterogeneous myocardial disorder characterized by prominent trabeculae protruding into the left ventricular lumen and deep intertrabecular recesses. LVNC can manifest in isolation or alongside other heart muscle diseases. Its occurrence among children is rising due to advancements in imaging techniques. The origins of LVNC are diverse, involving both genetic and acquired forms. The clinical manifestation varies greatly, with some cases presenting no symptoms, while others typically manifesting with heart failure, systemic embolism, and arrhythmias. Diagnosis mainly relies on assessing heart structure using imaging tools like echocardiography and cardiac magnetic resonance. However, the absence of a universally agreed-upon standard and limitations in diagnostic criteria have led to ongoing debates in the scientific community regarding the most reliable methods. Further research is crucial to enhance the diagnosis of LVNC, particularly in early life stages.

Evaluation of intrapulmonary arteriovenous anastomoses before and after oxygen supplementation, using transthoracic agitated saline contrast echocardiography in rescued Korean raccoon dogs.

Intrapulmonary arteriovenous anastomoses (IPAVAs) are defined as relatively large, dynamic shunt vessels that connect the pulmonary arterial and venous systems, thereby bypassing the pulmonary capillary system. IPAVAs lower elevated pulmonary arterial pressure; however, the presence of the shunt can result in impaired pulmonary gas exchange and paradoxical embolism. Furthermore, the prevalence and effects of IPAVAs in raccoon dogs remain unknown. This study aimed to determine the prevalence of IPAVA among rescued Korean raccoon dogs and evaluate the changes in IPAVA following oxygen supplementation. Nineteen raccoon dogs rescued by the Jeonbuk Wildlife Centre between August 2022 and December 2023 were subjected to echocardiography. Sixteen healthy and three abnormal raccoon dogs were subjected to transthoracic agitated saline contrast echocardiography (bubble study) based on the echocardiography results. IPAVA was considered to be present if the left heart contrast was visualised after four cardiac cycles following the visualisation of the first right heart contrast. Bubble scores (BS0-5) were assigned based on the maximum number of microbubbles observed in the left ventricular lumen per frame of the ultrasound image. BS was assigned before and after supplementation with 100% oxygen for 5 min. IPAVA was detected in 12 of the 16 healthy raccoon dogs at rest (75%). The BS of the 15 IPAVA-positive raccoon dogs ranged from 1 to 4 points (BS1, 1; BS2, 4; BS3, 8; and BS4, 2). Blood flow through the IPAVA (QIPAVA) was reduced or absent in the 15 IPAVA-positive raccoon dogs after supplementation with 100% oxygen (BS0, 11; BS2, 4). Moreover, BS of the IPAVA showed a significant correlation with the cardiac output per body weight (BW). The prevalence of IPAVA in healthy raccoon dogs at rest was 75%. Adequate oxygen supplementation was found to be effective in reducing QIPAVA, which may help prevent potential negative factors such as pulmonary gas exchange impairments and paradoxical embolism that can occur with IPAVA.

Abstract 13419: Transient Coronary Artery to Left Ventricular Fistula With Diastolic Mitral Regurgitation

Introduction: A fistula from a coronary artery to the cardiac chamber is incidentally found in 0.08% to 0.3% of patients undergoing coronary angiography. Case Presentation: A 73-year-old woman with hypertension, diabetes mellitus, chronic renal failure, and nephrosis visited our department due to dyspnea. The patient’s physical examination revealed a blood pressure of 191/109 mmHg and a pulse rate of 77 beats per min. The blood sampling results revealed a plasma brain natriuretic peptide level of 2,001 pg/mL. A 12-lead electrocardiogram showed poor R wave progression in leads V1 to V4. Chest radiography revealed left pleural effusion. Parasternal transthoracic echocardiography showed left ventricular hypertrophy. Left ventricular (LV) ejection fraction was 41%. A pulsed-wave Doppler echocardiography at the mitral inflow showed diastolic mitral regurgitation and a fusion of E and A waves. An unusual myocardial flow was noted in the apical myocardium. It was directed toward the apical surface during systole (Fig. 1a), and directed toward the LV lumen during diastole (Fig. 1b), suggesting coronary artery to LV fistula through sinusoid. Global strain obtained from apical long axis imaging showed myocardial shortening continued to diastole, suggesting post-systolic shortening (PSS). After treatment for hypertension, both of myocardial flow and diastolic MR disappeared. A longitudinal global strain imaging revealed disappearance of PSS. Conclusion: This is a rare case of diastolic MR due to PSS at the fistula from the coronary artery to the left ventricle.

Structural and Functional Cardiac Parameters in Patients with AL Amyloidosis Correlate with Uptake of the Amyloidophilic Radiotracer Iodine ( 124I) Evuzamitide

Background: The deposition of fibrillar aggregates of monoclonal free light chains in the heart is a characteristic feature of light chain associated (AL) amyloidosis. Cardiac amyloid is the major cause of morbidity and mortality in these patients. Structural and functional sequelae of cardiac amyloidosis can be appreciated clinically using echocardiography, cardiac magnetic resonance imaging, and measurement of serum NT-proBNP and troponins. These measures are not particularly amyloid-specific, and the correlation between parameters derived from these evaluations and amyloid burden remain enigmatic. The iodine-124 labeled peptide (p5+14), iodine ( 124I) evuzamitide, is a novel radiotracer that is being evaluated for the detection of systemic amyloidosis, of any type, by PET/CT imaging. As an amyloid binding peptide, this radiotracer has the potential to serve as a first line diagnostic agent capable of providing whole body semi-quantitative estimation of organ-specific amyloid load. Nascent studies of the relationship between 124I-evuzamitide uptake and established clinical parameters in patients with amyloidosis are underway. Here we report a single site, open label pilot study of 18 ( n=18) patients with AL ( n=8) and ATTR amyloidosis ( n=10) that evaluates the cardiac uptake of 124I-evuzamitide with contemporaneous echocardiographic and serum biomarkers (NCT05968846). Methods: The data described herein was collected as part of an open label single site repeat imaging study that plans to enroll up to 20 ( n=20) patients with AL ( n=10) and ATTR ( n=10) amyloidosis. To date, eight ( n=8) patients with AL and ten ( n=10) with ATTR amyloidosis have undergone 124I-evuzamitide PET/CT imaging with contemporaneous transthoracic echocardiography and assessment of serum NTproBNP within ~30 h of imaging. Patients received 37 or 74 MBq 124I-evuzamitide, and PET/CT imaging was performed at ~5 h post injection. Images were interpreted by a single reviewer, experienced in evaluating this tracer, for positive cardiac uptake. A fully manual 2D region of interest (ROI) analysis was performed encompassing the free left ventricular (LV) wall, LV lumen and interventricular septum (IVS). Blood pool was used as a reference tissue to determine standard uptake value ratios (SUVR mean) and to control for the rate of tracer clearance from the central compartment. Cardiac uptake of radiotracer was compared with free LV wall thickness (cm), IVS thickness (cm), global longitudinal strain (GLS, %), and serum NT-proBNP (pg/mL) measurements. Pearson and Spearman correlations were used to test for associations between variables. Results: Patients with AL amyloidosis were 2012 Mayo Stage I ( n=2/8) or Stage II ( n=6/8). The mean serum NTproBNP was 672.9±762.4 pg/mL (min=98, max=2327). With singular exception, all patients with AL amyloidosis had visually evident cardiac uptake of 124I-evuzamitide in the PET/CT images. In patients with AL amyloidosis ( n=8), the SUVR mean (encompassing the LV, lumen and IVS) correlated strongly with LV thickness (cm) (Pearson r=0.83, p=0.011) and GLS (%) (Pearson r=0.74, p=0.037), but not the IVS thickness (cm) (Pearson r=0.57, p=0.142). In contrast, in patients with ATTR ( n=10), there was no significant correlation of SUVR mean with GLS ( p=0.395), but a moderate significant correlation of SUVR mean with the LV ( p=0.037) and IVS ( p=0.017) thickness was observed. Similarly, in this pilot cohort, we observed a strong positive correlation between serum NTproBNP and cardiac SUVR mean (Pearson r=0.81, p=0.015), but not for patients with ATTR amyloidosis (Pearson r=0.58, p=0.079). Conclusion: Serum NTproBNP is a validated and qualified measure of overall survival for patients with AL amyloidosis (PMID: 27416985). Global longitudinal strain, with or without inclusion of other structural parameters such as left atrial volume, is a strong predictor of survival in patients with AL amyloidosis (PMID: 29111123, PMID: 37143609). PET/CT imaging using 124I-evuzamitide is a promising technique for diagnosing and monitoring AL and other types of amyloidosis. In light of these early results that demonstrate a strong relationship between validated metrics of all cause mortality in patients with AL, larger studies should seek to evaluate similar relationships with some metric of 124I-evuzamitide uptake in the heart, and indeed other organs.

Knockout of M-LP/Mpv17L, a newly identified atypical PDE, induces physiological afferent cardiac hypertrophy in mice

M-LP/Mpv17L (Mpv17-like protein) is an atypical cyclic nucleotide phosphodiesterase (PDE) without the molecular structure characteristic of the PDE family. Deficiency of M-LP/Mpv17L in mice has been found to result in development of β-cell hyperplasia and improved glucose tolerance. Here, we report another phenotype observed in M-LP/Mpv17L-knockout (KO) mice: afferent cardiac hypertrophy. Although the hearts of M-LP/Mpv17L-KO mice did not differ in size from those of wild-type mice, there was marked narrowing of the left ventricular lumen and thickening of the ventricular wall. The diameter and cross-sectional area of cardiomyocytes in 8-month-old M-LP/Mpv17L-KO mice were increased 1.16-fold and 1.35-fold, respectively, relative to control mice, but showed no obvious abnormalities of cell structure, fibrosis or impaired cardiac function. In 80-day-old KO mice, the expression of hypertrophic marker genes, brain natriuretic peptide (BNF), actin alpha cardiac muscle 1 (ACTC1) and actin alpha 1 skeletal muscle (ACTA1), as well as the Wnt/β-catenin pathway target genes, lymphoid enhancer-binding factor-1 (LEF1), axis inhibition protein 2 (AXIN2) and transcription factor 7 (TCF7), was significantly up-regulated relative to control mice, whereas fibrosis-related genes such as fibronectin 1 (FN1) and connective tissue growth factor (CTGF) were down-regulated. Western blot analysis revealed increased phosphorylation of molecules downstream of the cAMP/PKA signaling pathway, such as β-catenin, ryanodine receptor 2 (RyR2), phospholamban (PLN) and troponin I (cTnI), as well as members of the MEK1-ERK1/2 signaling pathway, which is strongly involved in afferent cardiac hypertrophy. Taken together, these findings indicate that M-LP/Mpv17L is one of the PDEs actively functioning in the heart and that deficiency of M-LP/Mpv17L in mice promotes physiological cardiac hypertrophy.

Attenuation of stretch-induced arrhythmias following chemical ablation of Purkinje fibres, in isolated rabbit hearts.

Purkinje fibres (PFs) play an important role in some ventricular arrhythmias and acute ventricular stretch can evoke mechanically-induced arrhythmias. We tested whether Purkinje fibres, play a role in these arrhythmias. Pseudo-ECGs were recorded in isolated, Langendorff-perfused, rabbit hearts in which the left ventricular endocardial surface was also irrigated with Tyrode, via an indwelling catheter placed in the left ventricular lumen. The number and period of ectopic activations was measured during left ventricular lumen inflation via an indwelling fluid-filled balloon (500μL added over 2s and maintained for 15s in total). Mechanically-induced arrhythmias occurred in 70% of balloon inflations: they were maximal in the first 5s and ceased within 15s. Brief, (10s) irrigation of the left ventricular lumen with Lugol solution (IK/I2), via the indwelling catheter, reduced inflation-induced ectopics by 98% (p < 0.05). Ablation of endocardial PFs by Lugol was confirmed by Triphenyltetrazolium Chloride staining. Optical mapping revealed the left ventricular epicardial activation patterns of ectopics could have PF-mediated and focal sources. In silico modelling predicted ectopic sources originating in the endocardial region propagate to and through the Purkinje fibres network. Acute distention-induced ectopics are multi-focal, their attenuation by Lugol, their activation patterns and in silico modelling indicate a participation of Purkinje fibres in these arrhythmias.

Endocardial role in arrhythmias induced by acute ventricular stretch and the involvement of Purkinje fibres, in isolated rat hearts

Purkinje fibres (PFs) play an important role in some ventricular arrhythmias and acute ventricular stretch can evoke mechanically-induced arrhythmias. We tested whether PFs and specifically TRPM4 channels, play a role in these mechanically-induced arrhythmias. Pseudo-ECGs and left ventricular (LV) activation, measured by optical mapping, were recorded in isolated, Langendorff-perfused, rat hearts. The LV endocardial surface was irrigated with experimental agents, via an indwelling catheter. The number and period of ectopic activations was measured during LV lumen inflation via an indwelling fluid-filled balloon (100 μL added over 2 s, maintained for 38 s). Mechanically-induced arrhythmias occurred during balloon inflation: they were multifocal, maximal in the first 5 s and ceased within 20 s. Optical mapping revealed activation patterns indicating PF-mediated and ectopic focal sources. Irrigation of the LV lumen with Lugol solution (IK/I2) for 10s reduced ectopics by 93% (n = 16, P < 0.001); with ablation of endocardial PFs confirmed by histology. Five min irrigation of the LV lumen with 50 μM 9-Phenanthrol, a blocker of TRPM4 channels, reduced ectopics by 39% (n = 15, P < 0.01). Immunohistochemistry confirmed that TRPM4 was more abundant in PFs than myocardium. Our results show that the endocardial surface plays an important role in these mechanically-induced ectopic activations. Ectopic activation patterns indicate a participation of PFs in these arrhythmias, with a potential involvement of TRPM4 channels, shown by the reduction of arrhythmias by 9-Phenanthrol.

Detection of left ventricular dysfunction on axial non-contrast chest CT

PurposeTo evaluate the performance of axial non-contrast CT images in detecting systolic and diastolic left ventricular (LV) dysfunction. MethodThis single-center retrospective study assessed 178 participants who underwent transthoracic ultrasonography and had non-contrast chest CT data within three months of ultrasonography. The patients were divided into LV systolic dysfunction (<52% ejection fraction in men and <54% in women), LV diastolic dysfunction (at least three of the following four criteria were met: average E/e' ratio >14; septal e' <7 cm/s or lateral e' <10 cm/s; peak tricuspid regurgitation velocity >2.8 m/s; or left atrial maximum volume index >34 ml/m2), and normal LV function groups. CT parameters were evaluated as predictive factors for LV dysfunction. These parameters were: I, maximum minor axis diameter of the LV lumen; II, I plus myocardial wall thickness; III, maximum left atrium anteroposterior diameter; IV, maximum transverse cardiac diameter; V, myocardial wall thickness; I-IV divided by maximum medial thoracic diameter; and I-IV divided by anteroposterior thoracic diameter. All parameters were measured on axial images: diameters were maximized. ResultsLV systolic dysfunction was indicated when parameter IV exceeded 131.2 mm with sensitivity and specificity of 71.8% and 77.0%, respectively. Moreover, LV diastolic dysfunction was indicated when parameter III divided by anteroposterior thoracic diameter exceeded 0.165 with sensitivity and specificity of 77.8% and 83.0%, respectively. ConclusionsAxial non-contrast chest CT is useful for detecting LV dysfunction. Even CT scans for other purposes provide LV function information that may lead to appropriate examination.

Sudden cardiac death as a naturally-occurring ventricular hypertrophy in Macaca fascicularis

Naturally occurring left ventricular hyperplasia is a rare but lethal disease. There are very few reports of this cardiac disease in captive nonhuman primates. In a colony of Macaca mulatta (Rhesus monkey) at California National Primate Research Center, a large number of rhesus macaques were diagnosed by autopsy with naturally occurring left ventricular hypertrophy without obvious underlying diseases over a 22-year period. The confirmatory diagnosis of ventricular hypertrophy was based on findings of notable left ventricular concentric hypertrophy with reduced left ventricular lumen, which is very similar to human ventricular hypertrophy cases. This report discusses an 11-year-old Macaca fascicularis monkey (Cynomolgus monkey, crab-eating macaque), weighing 2.95 kg, that was presented for enrollment in a pharmacokinetic (PK) study. During the PK experiment, the monkey died following a sudden decrease in percutaneous oxygen saturation and heart rate. Gross and histological examinations of the heart were performed. On gross pathology, the left ventricular wall was thickened, and the chamber lumen was reduced. In histopathological examination using hematoxylin-eosin and Masson-trichrome stains, fibrosis and myocyte disarray were not observed, but an increased cell density, compared to the normal heart, was confirmed. The autopsy results confirmed left ventricular hyperplasia as the major cause of death.

Characterization of Cardiac Diseases in Dogs Prevalent in Indian Conditions

Background: Cardiac diseases defined as structural, functional, mechanical and electrical abnormality of heart. Characterization of different cardiac diseases in dogs prevalent in North Indian conditions is least studied. Methods: Out of total 2582 registered dogs, 41 were suspected for cardiac diseases based on clinical signs. Further confirmation and characterization was done by electrocardiography, radiography, echocardiography and cardiac biomarkers. Statistical analysis was done through SPSS 23. Result: Present study inferred, Dilated cardiomyopathy (DCM) as the most prevalent cardiac affection. Left ventricular dilation, interventricular septum thinning, increased E point septal separation and left atrial enlargement were characteristic echocardiographic indices in DCM. Echocardiographic indices in hypertrophic cardiomyopathy were increased interventricular septum, left ventricular posterior wall and reduced left ventricular lumen. Labrador retriever found to be most predisposed breed for DCM while Rottweiler reported to be most affected with pericardial effusion. Cardiac Troponin-I (cTnI) was statistically (p less than 0.05) increased in all cardiac categories with cut off value above 92 ng/l indicating cardiac affection, while Lactate dehydrogenase serve as screening biochemical marker with significant increase in all the cardiac cases ranging from 291 IU/l to 586.4 IU/l.

Evaluating anemia using contrast-enhanced spectral detector CT of the chest in a large cohort of 522 patients

ObjectivesThe blood of patients with anemia demonstrates distinctly lower attenuation in unenhanced CT images. However, the frequent usage of intravenous contrast hampers evaluation of anemia. Spectral detector computed tomography (SDCT) allows for reconstruction of virtual non-contrast images (VNC) from contrast-enhanced data (CE). The purpose of this study was to evaluate whether VNC allow for prediction of anemia.MethodsFive hundred twenty-two patients with CE-SDCT of the chest and accessible serum hemoglobin (HbS) were retrospectively included. Patients were assigned to three groups (severe anemia, moderate/mild anemia, and healthy) based on recent lab tests (≤ 7 days) for HbS following gender and the WHO definition of anemia. CT attenuation was determined using two ROI in the left ventricular lumen and one ROI in the descending thoracic aorta. ROI were placed on CE and copied to VNC. ANOVA, linear regression, and receiver operating characteristics were used for statistic evaluation.ResultsAverage HbS was 11.6 ± 2.4 g/dl. Attenuation on VNC showed significant differences between healthy patients, patients with mild/moderate anemia, and severely anemic patients (all p ≤ 0.05). Applying cutoffs of 39.2/37.6 HU and 33.6/32.7 HU allowed to differentiate between healthy, mild/moderately, and severely anemic men/women (AUC 0.857/0.833 and 0.879/0.932). A linear relationship between HbS and attenuation on VNC was established (r2 = 0.54, HbS = − 0.875 + 0.329 × HU).ConclusionsAn approximation of HbS and presence of anemia can be conducted based on simple attenuation measurements in contrast-enhanced SDCT examinations enabled by VNC imaging.Key Points• While the attenuation of blood is a previously described biomarker for anemia in non-contrast images, virtual non-contrast images from spectral detector CT circumvent this limitation and allow for diagnosis of anemia in contrast-enhanced scans.• Attenuation of blood in virtual non-contrast images derived from spectral detector CT shows a moderate correlation to serum hemoglobin levels.• Presence of anemia be estimated in virtual non-contrast images using proposed cutoffs of 39.2 HU and 37.6 HU for men and women, respectively, to differentiate between healthy and anemic patients.

Evaluation of cancer-derived myocardial impairments using a mouse model.

Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mice, decreased heart weight and myocardial volume, and dilated left ventricular lumen, and atrophied cardiomyocytes were noted. The cardiomyocytes also showed accumulated 8-hydroxydeoxyguanosine, decreased leucine zipper and EF-hand-containing transmembrane protein-1, and increased microtubule-associated protein light chain3-II. Levels of tumor necrosis factor-α and high-mobility group box-1 proteins in the myocardium were increased, and nuclear factor κB, a signaling molecule associated with these proteins, was activated. When rat cardiomyoblasts (H9c2 cells) were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state. These results are in good agreement with those previously reported on cancerous myocardial damage. The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage.

Abstract 287: Transgenic Overexpression of Dimethylarginine Dimethylaminohydrolase 1 Protects From Angiotensin II - Induced Cardiac Hypertrophy and Vascular Remodeling

Background: Dimethylarginine dimethylaminohydrolase 1 (DDAH1) hydrolyzes the endogenous inhibitor of nitric oxide synthases asymmetric dimethylarginine (ADMA). DDAH1 is also suggested to have ADMA-independent effects. DDAH1 overexpression lowers ADMA levels and protects from renal interstitial fibrosis and vascular oxidative stress in angiotensin-II-induced hypertension. The current study was designed to test the hypothesis that DDAH1 overexpression protects from angiotensin II-induced cardiac hypertrophy and vascular remodeling. Methods: Angiotensin II (AngII) was infused in the doses of 0.75 and 1.5 mg/kg/day, respectively, in DDAH1 transgenic mice (TG) and wild type (WT) littermates via osmotic minipumps. Echocardiography was performed in the first and fourth week after start of the infusion. Systolic blood pressure was measured by the tail-cuff method. Cardiac hypertrophy and vascular remodeling was assessed by histology after 4 weeks of AngII infusion. Results: TG mice had decreased plasma and tissue ADMA. Infusion of Ang II resulted in an increase in systolic blood pressure, which was similar between TG and WT mice at week 1, however, TG mice were protected from a further increase in blood pressure. After 4-weeks infusion of AngII TG mice had significantly higher left ventricular lumen to wall ratio, smaller size of cardiomyocytes and reduced myocardial collagen expression compared to WT littermates. TG mice had lower left ventricular posterior wall thickness in systole and diastole as compared to WT controls. The vasomotor function of aortic rings in response to acetylcholine was improved in the TG mice as compared to the WT mice. TG mice had less aortic hypertrophy and fibrosis and more elastin in aorta as compared to WT mice. Aortic infiltration of CD45 + , CD3 + , CD8 + and CD4 + T-cells was significantly lower in TG than in WT mice. Conclusion: This study shows that upregulation of DDAH1 protects from AngII-induced cardiac hypertrophy and vascular remodeling. Upregulation of DDAH1 might be a potential therapeutic approach for protection from AngII – induced end organ damage. We are currently investigating, whether protective effects of DDAH1 are ADMA-dependent or ADMA-independent.

Image quality in coronary computed tomography angiography: influence of adaptive statistical iterative reconstruction at various radiation dose levels.

Background Computed tomography (CT) technology is rapidly evolving and software solution developed to optimize image quality and/or lower radiation dose. Purpose To investigate the influence of adaptive statistical iterative reconstruction (ASIR) at different radiation doses in coronary CT angiography (CCTA) in detailed image quality. Material and Methods A total of 160 CCTA were reconstructed as follows: 55 scans with filtered back projection (FBP) (650 mA), 51 scans (455 mA) with 30% ASIR (ASIR30), and 54 scans (295 mA) with 60% ASIR (ASIR60). For each reconstruction, subjective image quality was assessed by five independent certified cardiologists using a visual grading analysis (VGA) with five predefined image quality criteria consisting of a 5-point scale. Objective measures were contrast, noise, and contrast-to-noise ratio (CNR). Results The CTDIvol resulted in 10.3 mGy, 7.4 mGy, and 4.6 mGy for FBP, ASIR30, and ASIR60, respectively. Homogeneity of the left ventricular lumen was the sole aspect in which reconstruction algorithms differed with a decreasing effect for ASIR60 compared to FBP (estimated odds ratio [OR] = 0.49 [95% confidence interval (CI) = 0.32-0.76; P = 0.001]). Decreased sharpness and spatial- and low-contrast resolutions were observed when using ASIR instead of FBP, but differences were not statistically significant. Concerning objective measurements, noise increased significantly for ASIR30 (OR = 1.08; 95% CI = 1.02-1.14; P = 0.006) and ASIR60 (OR = 1.06; 95% CI = 1.01-1.12; P = 0.034) compared to FBP. Conclusion ASIR significantly decreased the subjectively assessed homogeneity of the left ventricular lumen and increased the objectively measured noise compared to FBP. Considering these results, ASIR at a reduced radiation dose should be implemented with caution.

Abstract 382: Transgenic Overexpression of Dimethylarginine Dimethylaminohydrolase 1 Protects From Angiotensin II-induced Cardiac Hypertrophy

Background: ADMA (asymmetric dimethylarginine) is an endogenous inhibitor of nitric oxide synthase. ADMA can be metabolized to citrulline by dimethylarginine dimethylaminohydrolase (DDAH). DDAH1 overexpression lowers ADMA and protects from angiotensin II - induced renal interstitial fibrosis and vascular oxidative stress. The goal of the current study was to test the hypothesis that transgenic overexpression of DDAH1 protects from angiotensin II-induced cardiac hypertrophy. Methods and Results: DDAH1 transgenic mice grew and developed normally and had decreased plasma ADMA levels. Angiotensin II was infused for four weeks in the dose of 0.75 mg/kg/day in DDAH1 transgenic mice and wild type littermates via osmotic minipumps. Echocardiography was performed in the first and fourth week after start of the infusion on anaesthetized mice. After 4 weeks of angiotensin II infusion wild type mice developed cardiac hypertrophy. The DDAH1 transgenic mice had higher left ventricular lumen to wall ratio compared to the wild type mice (1.76 ± 0.18 vs 1.15 ± 0.22, P&lt;0.01). They also had lower left ventricular posterior wall thickness in systole and diastole as compared to the wild type controls (1.18 ± 0.03 mm vs 1.95 ± 0.16 mm, P&lt;0.001 and 0.81 ± 0.03 mm vs 1.62 ± 0.25 mm, P&lt;0.001, respectively). Conclusion: We demonstrated that upregulation of DDAH1 protects from angiotensin II-induced cardiac hypertrophy. Our findings suggest that ADMA plays a role in angiotensin II - induced myocardial remodeling. Upregulation of DDAH1 might be a potential approach for protection from angiotensin II - induced end organ damage.

Self-gated fetal cardiac MRI with tiny golden angle iGRASP: A feasibility study.

To develop and assess a technique for self-gated fetal cardiac cine magnetic resonance imaging (MRI) using tiny golden angle radial sampling combined with iGRASP (iterative Golden-angle RAdial Sparse Parallel) for accelerated acquisition based on parallel imaging and compressed sensing. Fetal cardiac data were acquired from five volunteers in gestational week 29-37 at 1.5T using tiny golden angles for eddy currents reduction. The acquired multicoil radial projections were input to a principal component analysis-based compression stage. The cardiac self-gating (CSG) signal for cardiac gating was extracted from the acquired radial projections and the iGRASP reconstruction procedure was applied. In all acquisitions, a total of 4000 radial spokes were acquired within a breath-hold of less than 15 seconds using a balanced steady-state free precession pulse sequence. The images were qualitatively compared by two independent observers (on a scale of 1-4) to a single midventricular cine image from metric optimized gating (MOG) and real-time acquisitions. For iGRASP and MOG images, good overall image quality (2.8 ± 0.4 and 2.6 ± 1.3, respectively, for observer 1; 3.6 ± 0.5 and 3.4 ± 0.9, respectively, for observer 2) and cardiac diagnostic quality (3.8 ± 0.4 and 3.4 ± 0.9, respectively, for observer 1; 3.6 ± 0.5 and 3.6 ± 0.9, respectively, for observer 2) were obtained, with visualized myocardial thickening over the cardiac cycle and well-defined myocardial borders to ventricular lumen and liver/lung tissue. For iGRASP, MOG, and real time, left ventricular lumen diameter (14.1 ± 2.2 mm, 14.2 ± 1.9 mm, 14.7 ± 1.1 mm, respectively) and wall thickness (2.7 ± 0.3 mm, 2.6 ± 0.3 mm, 3.0 ± 0.4, respectively) showed agreement and no statistically significant difference was found (all P > 0.05). Images with iGRASP tended to have higher overall image quality scores compared with MOG and particularly real-time images, albeit not statistically significant in this feasibility study (P > 0.99 and P = 0.12, respectively). Fetal cardiac cine MRI can be performed with iGRASP using tiny golden angles and CSG. Comparison with other fetal cardiac cine MRI methods showed that the proposed method produces high-quality fetal cardiac reconstructions. 2 Technical Efficacy: Stage 1 J. MAGN. RESON. IMAGING 2017;46:207-217.

Anatomopathological staging of feline hypertrophic cardiomyopathy through quantitative evaluation based on morphometric and histopathological data

Diagnosis of feline hypertrophic cardiomyopathy (HCM) is both clinical and anatomopathological. Since standardized echocardiographic parameters have previously been established for its diagnosis and classification, the aim of the present study is to provide an original, complete and repeatable quantitative anatomopathological evaluation of this myocardial disease. Since ES-HCM is a clearly defined clinicopathological entity of feline HCM, the present study also aims to investigate its temporal evolution. The hearts of 21 cats with previous diagnosis or suspicion of HCM and 6 control animals were submitted for morphometric and histopathological investigations. The proposed quantitative assessment of gross and histopathological features of HCM appears to be original and repeatable. Correlations between morphometric data allow to establish that the progression to the end-stage phenotypes, primarily characterized by increase in left ventricular fibrous tissue deposition, is accompanied by dilation of left ventricular lumen (P=0.0004) and left atrium (P=0.0017) and increase in intramural coronary arteriosclerosis (P=0.0293).

Rigor mortis at the myocardium investigated by post-mortem magnetic resonance imaging

IntroductionPost-mortem cardiac MR exams present with different contraction appearances of the left ventricle in cardiac short axis images. It was hypothesized that the grade of post-mortem contraction may be related to the post-mortem interval (PMI) or cause of death and a phenomenon caused by internal rigor mortis that may give further insights in the circumstances of death. Method and materialsThe cardiac contraction grade was investigated in 71 post-mortem cardiac MR exams (mean age at death 52y, range 12–89y; 48 males, 23 females). In cardiac short axis images the left ventricular lumen volume as well as the left ventricular myocardial volume were assessed by manual segmentation. The quotient of both (LVQ) represents the grade of myocardial contraction. LVQ was correlated to the PMI, sex, age, cardiac weight, body mass and height, cause of death and pericardial tamponade when present. In cardiac causes of death a separate correlation was investigated for acute myocardial infarction cases and arrhythmic deaths. ResultsLVQ values ranged from 1.99 (maximum dilatation) to 42.91 (maximum contraction) with a mean of 15.13. LVQ decreased slightly with increasing PMI, however without significant correlation. Pericardial tamponade positively correlated with higher LVQ values. Variables such as sex, age, body mass and height, cardiac weight and cause of death did not correlate with LVQ values. There was no difference in LVQ values for myocardial infarction without tamponade and arrhythmic deaths. ConclusionBased on the observation in our investigated cases, the phenomenon of post-mortem myocardial contraction cannot be explained by the influence of the investigated variables, except for pericardial tamponade cases. Further research addressing post-mortem myocardial contraction has to focus on other, less obvious factors, which may influence the early post-mortem phase too.

Hydrogen sulfide provides cardioprotection against myocardial/ischemia reperfusion injury in the diabetic state through the activation of the RISK pathway.

BackgroundCoronary artery disease remains the principal cause of death in patients with diabetes mellitus. Diabetic mice display exacerbated injury following myocardial ischemia-reperfusion (MI/R) and are resistant to most therapeutic interventions. We have reported that sodium sulfide (Na2S) therapy confers cardioprotection during MI/R in non-diabetic mice. Here we tested the hypothesis that Na2S therapy would limit the extent of myocardial injury following MI/R when administered at the time of reperfusion.Methods and resultsDiabetic mice (db/db, 12 weeks of age) were subjected to transient myocardial ischemia for a period of 30 minutes followed by reperfusion up to 24 hours. Na2S (0.05 to 1 mg/kg) or saline (vehicle) was administered into the left ventricular lumen at the time of reperfusion. Na2S therapy significantly decreased myocardial injury in the db/db diabetic mouse, as evidenced by a reduction in infarct size and circulating troponin-I levels. The reduction in myocardial injury was also associated with a reduction in oxidative stress and a decrease in cleaved caspase-3 expression. In an effort to evaluate the signaling mechanism responsible for the observed cardioprotection, additional groups of mice were sacrificed during early reperfusion. Hearts were excised and processed for Western blot analysis. These studies revealed that Na2S therapy activated the Erk1/2 arm of the Reperfusion Injury Salvage Kinase (RISK) pathway.ConclusionThese findings provide important information that myocardial Erk1/2 activation by Na2S therapy following MI/R sets into motion events, which ultimately lead to cardioprotection in the setting of diabetes.

Functional imaging of murine hearts using accelerated self-gated UTE cine MRI.

We introduce a fast protocol for ultra-short echo time (UTE) Cine magnetic resonance imaging (MRI) of the beating murine heart. The sequence involves a self-gated UTE with golden-angle radial acquisition and compressed sensing reconstruction. The self-gated acquisition is performed asynchronously with the heartbeat, resulting in a randomly undersampled kt-space that facilitates compressed sensing reconstruction. The sequence was tested in 4 healthy rats and 4 rats with chronic myocardial infarction, approximately 2months after surgery. As a control, a non-accelerated self-gated multi-slice FLASH sequence with an echo time (TE) of 2.76ms, 4.5 signal averages, a matrix of 192×192, and an acquisition time of 2min 34s per slice was used to obtain Cine MRI with 15 frames per heartbeat. Non-accelerated UTE MRI was performed with TE=0.29ms, a reconstruction matrix of 192×192, and an acquisition time of 3min 47s per slice for 3.5 averages. Accelerated imaging with 2×, 4× and 5× undersampled kt-space data was performed with 1min, 30 and 15s acquisitions, respectively. UTE Cine images up to 5× undersampled kt-space data could be successfully reconstructed using a compressed sensing algorithm. In contrast to the FLASH Cine images, flow artifacts in the UTE images were nearly absent due to the short echo time, simplifying segmentation of the left ventricular (LV) lumen. LV functional parameters derived from the control and the accelerated Cine movies were statistically identical.