Left Ventricular Posterior Wall Dimension Research Articles

Perceval sutureless bioprosthesis versus Perimount sutured bioprosthesis for aortic valve replacement in patients with aortic stenosis: a retrospective, propensity-matched study

BackgroundRapid-deployment aortic valve replacement (RDAVR) is an alternative to conventional AVR (cAVR) for aortic stenosis. Benefits include a reduction in operative times, facilitation of minimal access surgery and superior haemodynamics compared to conventional valves. However, further evidence is required to inform guidelines, preferably in the form of propensity-matched studies that include mid-term follow-up data.MethodsThis was a single-centre, retrospective, propensity-matched cohort study comparing the Perceval and conventional Perimount Magna Ease valve for short- and mid-term clinical parameters and size-matched mid-term echocardiographic parameters (n = 102 in both groups) from 2014 to 2020. Data were extracted from a nationally managed dataset.ResultsThere were no demographic differences between the matched groups. The Perceval group had shorter cross-clamp time (Perceval 62 [49–81] minutes; Perimount 79 [63–102] minutes, P < 0.001), shorter bypass time (Perceval 89 [74–114] minutes; Perimount 104 [84–137] minutes, P < 0.001), and more frequent minimally-invasive approaches (Perceval 28%; Perimount 5%, P < 0.001). Size-matched haemodynamics showed initially higher gradients in the Perceval group, but haemodynamics equalised at 12 + months. The Perceval group had a more favourable % change in the left ventricular posterior wall dimension at 2 + years (Perceval − 4.8 ± 18; Perimount 17 ± 2).ConclusionsThe Perceval facilitated shorter operations, which may benefit intermediate-high-risk, elderly patients with comorbidities requiring concomitant procedures. It also facilitated minimally invasive surgery. Size-matched haemodynamic performance was similar at mid-term follow-up, with the Perceval possibly better facilitating regression of left ventricular hypertrophy.

Global Profile of tRNA-Derived Small RNAs in Pathological Cardiac Hypertrophy Plasma and Identification of tRF-21-NB8PLML3E as a New Hypertrophy Marker.

It remains unclear whether transfer RNA-derived small RNAs (tsRNAs) play a role in pathological cardiac hypertrophy (PCH). We aimed to clarify the expression profile of tsRNAs and disclose their relationship with the clinical phenotype of PCH and the putative role. Small RNA sequencing was performed on the plasma of PCH patients and healthy volunteers. In the larger sample size and angiotensin II (Ang II)-stimulated H9c2 cells, the data were validated by real-time qPCR. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were examined in Ang II-stimulated H9c2 cells. The potential role of tsRNAs in the pathogenesis of PCH was explored by bioinformatics analysis. A total of 4185 differentially expressed tsRNAs were identified, of which four and five tsRNAs were observed to be significantly upregulated and downregulated, respectively. Of the five downregulated tsRNAs, four were verified to be significantly downregulated in the larger sample group, including tRF-30-3JVIJMRPFQ5D, tRF-16-R29P4PE, tRF-21-NB8PLML3E, and tRF-21-SWRYVMMV0, and the AUC values for diagnosis of concentric hypertrophy were 0.7893, 0.7825, 0.8475, and 0.8825, respectively. The four downregulated tsRNAs were negatively correlated with the left ventricular posterior wall dimensions in PCH patients (r = -0.4227; r = -0.4517; r = -0.5567; r = -0.4223). The levels of ANP and BNP, as well as cell size, were decreased in Ang II-stimulated H9c2 cells with 21-NB8PLML3E mimic transfection. Bioinformatics analysis revealed that the target genes of tRF-21-NB8PLML3E were mainly enriched in the metabolic pathway and involved in the regulation of ribosomes. The plasma tRF-21-NB8PLML3E might be considered as a biomarker and offers early screening potential in patients with PCH.

Longitudinal Changes in Cardiac Structure and Function in Pediatric Kidney Transplant Recipients.

Cardiovascular disease results in increased morbidity and mortality in pediatric kidney transplant recipients. Longitudinal changes in cardiac structure and function and the association with blood pressure control over time in pediatric kidney transplant recipients are unknown. To determine the influence of blood pressure control on cardiac changes following pediatric kidney transplant, we conducted a retrospective cohort study of children who received their first kidney transplant at the Hospital for Sick Children from 2004 to 2015. Children were followed until transfer to adult care or censoring in July 2018. Cardiac structure and function parameters were collected from clinical echocardiograms and assessed using standardized scores. Blood pressure control was determined by systolic blood pressure Z scores (above or below the 90th percentile) in combination with antihypertensive medications. A segmented mixed-effects model assessed Z scores of interventricular septum thickness, left ventricular end-diastolic dimension, and left ventricular posterior wall dimension. Of 142 children included, 58% were men, mean age at transplant was 11 (±4.5) years, and average follow-up time was 4 (±3) years. All cardiac structural Z scores improved during follow-up. Interventricular septum thickness normalized at 4.0 years post-transplant. Left ventricular end-diastolic dimension normalized at 1.5 years post-transplant. Left ventricular posterior wall dimension normalized at 6.3 years post-transplant. Left ventricular mass index showed sustained improvement up to 12 years post-transplant. Individuals with uncontrolled blood pressure had increased left ventricular mass (β=2.97 [95% CI, 0.77-5.16]). Cardiac structural abnormalities improve following kidney transplantation and normalize within 7 years, especially with controlled blood pressure. Strict blood pressure control is critical after pediatric kidney transplantation.

Remodeling Process in the Right and Left Atria and Ventricles Following Percutaneous Closure of the Atrial Septal Defect in Children and Adolescents: A Mid-term Study

Background: Atrial septal defect and its closure can lead to changes in the right and left cardiac cavities' function and size. In this study, Z-scores of the cardiac chambers and the heart function were assessed, and the important complications were mentioned. Methods: This interventional cross-sectional study was done on patients who had atrial septal defect closure aged younger than 18 years. All patients were recruited for transthoracic echocardiography. About half of the patients were randomly selected. The information of angiography and its side effects belong to all patients, but the echocardiographic parameters and Z-scores belong only to the selected group. Results: A total of 370 patients underwent the atrial septal defect closure, of whom 150 patients participated in the study. The patients' average age and weight were 9.25 ± 3.44 years and 15.12 ± 11.83 kg, respectively, and the mean follow-up time was 2.56 years. Z-scores of the interventricular septal dimension in diastole, the left ventricular posterior wall dimension in diastole, the left ventricular internal dimension in systole, and Z-scores of the size of the right atrium, right ventricle, pulmonary valve annulus, and the main pulmonary artery were more than Z-scores of the normal population. Furthermore, Z-scores of the E/A and the Eat/Aat of the tricuspid valve were less than their peers. Besides, the correlation between Z-scores and the atrial septal defect size and weight of the patients was assessed, which was statistically significant, and patients who underwent atrial special defect closure at the age of fewer than three years and less than 15 kg had more normal cardiac Z-scores. Conclusions: Z-scores of the cardiac chambers and pulmonary artery were more than normal after successful closure of the atrial septal defect in the mid-term follow-up.

X-linked creatine transporter deficiency results in prolonged QTc and increased sudden death risk in humans and disease model

PurposeCreatine transporter deficiency (CTD) is a rare X-linked disorder of creatine transport caused by pathogenic variants in SLC6A8 (Xq28). CTD features include developmental delay, seizures, and autism spectrum disorder. This study was designed to investigate CTD cardiac phenotype and sudden death risk. MethodsWe performed a cross-sectional analysis of CTD males between 2017 and 2020. Subjects underwent evaluation with electrocardiogram (ECG), echocardiography, and ambulatory ECG with comparable analysis in creatine transporter deficient mice (Slc6a8−/y) using ECG, echocardiography, exercise testing, and indirect calorimetry. ResultsEighteen subjects with CTD (18 males, age 7.4 [3.8] years) were evaluated: seven subjects (39%) had QTc ≥ 470 milliseconds: 510.3±29.0 vs. 448.3 ± 15.9, P < 0.0001. The QTc ≥ 470 milliseconds cohort had increased left ventricular internal dimension (diastole) ([LVIDd] Z-score: 0.22 ± 0.74, n = 7 vs. −0.93 ± 1.0, n = 11, P = 0.0059), and diminished left ventricular posterior wall dimension (diastole) ([LVPWDd, in mm]: 5.0 ± 0.6, n = 7 vs. 5.7 ± 0.8, n = 11, P = 0.0183), when compared to subjects with normal or borderline QTc prolongation. Similar ECG and echocardiographic abnormalities were seen in Slc6a8−/y mice. Additionally, Slc6a8−/y mice had diminished survival (65%). ConclusionProlonged QTc and abnormal echocardiographic parameters consistent with developing cardiomyopathy are seen in some male subjects with CTD. Slc6a8−/y mice recapitulated these cardiac abnormalities. Male CTD subjects may be at increased risk for cardiac dysfunction and sudden death.

Early Prediction of Left Ventricular Reverse Remodeling in First-Diagnosed Idiopathic Dilated Cardiomyopathy: A Comparison of Linear Model, Random Forest, and Extreme Gradient Boosting.

Introduction: Left ventricular reverse remodeling (LVRR) is associated with decreased cardiovascular mortality and improved cardiac survival and also crucial for therapeutic options. However, there is a lack of an early prediction model of LVRR in first-diagnosed dilated cardiomyopathy.Methods: This single-center study included 104 patients with idiopathic DCM. We defined LVRR as an absolute increase in left ventricular ejection fraction (LVEF) from >10% to a final value >35% and a decrease in left ventricular end-diastolic diameter (LVDd) >10%. Analysis features included demographic characteristics, comorbidities, physical sign, biochemistry data, echocardiography, electrocardiogram, Holter monitoring, and medication. Logistic regression, random forests, and extreme gradient boosting (XGBoost) were, respectively, implemented in a 10-fold cross-validated model to discriminate LVRR and non-LVRR, with receiver operating characteristic (ROC) curves and calibration plot for performance evaluation.Results: LVRR occurred in 47 (45.2%) patients after optimal medical treatment. Cystatin C, right ventricular end-diastolic dimension, high-density lipoprotein cholesterol (HDL-C), left atrial dimension, left ventricular posterior wall dimension, systolic blood pressure, severe mitral regurgitation, eGFR, and NYHA classification were included in XGBoost, which reached higher AU-ROC compared with logistic regression (AU-ROC, 0.8205 vs. 0.5909, p = 0.0119). Ablation analysis revealed that cystatin C, right ventricular end-diastolic dimension, and HDL-C made the largest contributions to the model.Conclusion: Tree-based models like XGBoost were able to early differentiate LVRR and non-LVRR in patients with first-diagnosed DCM before drug therapy, facilitating disease management and invasive therapy selection. A multicenter prospective study is necessary for further validation.Clinical Trial Registration:http://www.chictr.org.cn/usercenter.aspx (ChiCTR2000034128).

The crosstalk of HDAC3, microRNA-18a and ADRB3 in the progression of heart failure

BackgroundHeart failure (HF) is a clinical syndrome characterized by left ventricular dysfunction or elevated intracardiac pressures. Research supports that microRNAs (miRs) participate in HF by regulating targeted genes. Hence, the current study set out to study the role of HDAC3-medaited miR-18a in HF by targeting ADRB3.MethodsFirstly, HF mouse models were established by ligation of the left coronary artery at the lower edge of the left atrial appendage, and HF cell models were generated in the cardiomyocytes, followed by ectopic expression and silencing experiments. Numerous parameters including left ventricular posterior wall dimension (LVPWD), interventricular septal dimension (IVSD), left ventricular end diastolic diameter (LVEDD), left ventricular end systolic diameter (LVESD), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LEVDP), heart rate (HR), left ventricular pressure rise rate (+ dp/dt) and left ventricular pressure drop rate (-dp/dt) were measured in the mice. In addition, apoptosis in the mice was detected by means of TUNEL staining, while RT-qPCR and Western blot analysis were performed to detect miR-18a, HDAC3, ADRB3, cMyb, MMP-9, Collagen 1 and TGF-β1 expression patterns. Dual luciferase reporter assay validated the targeting relationship between ADRB3 and miR-18a. Cardiomyocyte apoptosis was determined by means of flow cytometry.ResultsHDAC3 and ADRB3 were up-regulated and miR-18a was down-regulated in HF mice and cardiomyocytes. In addition, HDAC3 could reduce the miR-18a expression, and ADRB3 was negatively-targeted by miR-18a. After down-regulation of HDAC3 or ADRB3 or over-expression of miR-18a, IVSD, LVEDD, LVESD and LEVDP were found to be decreased but LVPWD, LVEF, LVFS, LVSP, + dp/dt, and −dp/dt were all increased in the HF mice, whereas fibrosis, hypertrophy and apoptosis of HF cardiomyocytes were declined.ConclusionCollectively, our findings indicate that HDAC3 silencing confers protection against HF by inhibiting miR-18a-targeted ADRB3.

P2545Long-term use of anabolic-androgenic steroids in male weightlifters is associated with left ventricular systolic dysfunction

Abstract Background Illicit use of anabolic-androgenic steroids (AAS) is widespread and has adverse psychological and cardiovascular effects. Few well-powered studies have explored the effect of long-term AAS-use on left ventricular systolic function. Purpose To explore the relationship between long-term use of AAS and left ventricular mass and systolic function. Methods We included male weightlifters with a history of &gt;1 year of cumulative AAS-use and male weightlifters unexposed to AAS. We performed echocardiography in all and assessed left ventricular mass using 2D echocardiographic linear measurements and Cube formula, left ventricular ejection fraction (EF) ad modum Simpson, and left ventricular global longitudinal strain (GLS) by speckle-tracking echocardiography. Results We recruited 100 male weightlifters, 58 of whom were previous or current AAS-users with mean±SD AAS-use of 10.4±7.0 years, and 42 unexposed weightlifters. There were no difference in age (35.5±9.2 vs. 35.3±7.5 years, p=0.8) nor body mass index (BMI) (BMI 31.4±5.0 vs. 30.1±3.5, p=0.6) between AAS-exposed and unexposed weightlifters. Compared with unexposed weightlifters, AAS-exposed weightlifters demonstrated thicker interventricular septum (11.2±2.4 vs. 9.2±1.3 mm, p&lt;0.001), thicker left ventricular posterior wall dimension (10.1±2.1 vs. 8.9±1.3 mm, p&lt;0.001), and higher left ventricular mass index (99.7±25.4 vs. 78.4±12.1 g/m2, p&lt;0.001). Both left ventricular EF and left ventricular GLS were decreased in AAS-exposed weightlifters compared with unexposed weightlifters (49±9 vs. 53±6%, p=0.02, and −15.6±2.6 vs. −18.3±2.1%, p&lt;0.001) (Figure). Conclusion AAS use in male weightlifters was associated with increased left ventricular mass and impaired left ventricular systolic function. Our results suggest considerable adverse cardiac effects of AAS use, but the results need confirmation in prospective observational trials.

Abstract 894: Inhibition of Long Noncoding RNA lncExACT1 Induces Physiological Cardiac Hypertrophy and Protects Against Pathological Hypertrophy

Long noncoding-RNAs (lncRNAs) are critical regulators of cardiac development as well as pathological hypertrophy and heart failure (HF). However, their roles in exercise-induced physiological hypertrophy are unclear. Here, we used RNAseq to identify a novel class of cardiac lncRNAs that are dynamically regulated by exercise. We call these l ong n on c oding Ex ercise A ssociated C ardiac T ranscripts (lncExACTs). Among them, lncExACT1, a highly conserved lncRNA, is down-regulated in exercised hearts but upregulated in transverse aortic constriction (TAC)-induced pathological hypertrophy and HF. In primary neonatal cardiomyocytes (CMs), transfection of LNA antisense oligonucleotide complementary to lncExACT1 (GapmeR) was sufficient to inhibit lncExACT1 expression and increase CM size with a gene expression pattern consistent with physiological hypertrophy (increased PCG1α and α/βMHC ratio, all p &lt;0.05 vs . control). In contrast, lentiviral overexpression of lncExACT1 in primary CMs induced a pathological gene expression pattern (decreased PCG1α and β/αMHC ratio, with increased ANP and BNP, all p &lt;0.05 vs . control). In vivo, GapmeR treatment for two weeks reduced cardiac lncExACT1 expression (0.5-fold at 2 weeks), increased ventricular wall thickness and fractional shortening (FS, p =0.034 vs . control), increased heart weight to tibial length ratio (HW/TL) and α/βMHC. In contrast, injection of AAV9-lncExACT1 increased cardiac lncExACT1 (6-fold at 5 weeks) increased HW/TL as well as βMHC and ANP. Further, lncExACT1 acted as a sponge for microRNA-222 (a microRNA we previously reported is necessary for physiological cardiac growth) thereby increasing expression of microRNA-222 targets, including p27, a cell cycle inhibitor protein. Moreover, GapmeR injection reduced TAC-induced increase of interventricular septal end diastole (IVSd) and left Ventricular Posterior Wall Dimensions (LVPWd) without affecting FS. We conclude that inhibition of lncExACT1 is sufficient to induce physiological hypertrophy and protect against pathological hypertrophy, while induction of lncExACT1 promotes pathological hypertrophy. lncExACT1 appears to mediate these effects, at least in part, by acting as competing endogenous RNA for microRNA-222.

Echocardiographic study of healthy Indian Spitz dogs with normal reference ranges for the breed.

Aim:The present study was aimed to determine the normal reference values of M-mode echocardiographic measurements in healthy Indian Spitz dogs and evaluate the influence of gender and body weight on these measurements.Materials and Methods:M-mode echocardiography was performed in twenty-four clinically healthy conscious Indian Spitz dogs, aged 3-5 years and weighing 7-18 kg. Measurements were made from the right parasternal long axis left ventricular outflow tract view of the heart. The parameters recorded were: Left ventricular internal dimension, interventricular septal thickness and left ventricular posterior wall thickness during diastole and systole, left atrial diameter, aortic root diameter, left ventricular systolic functional parameters, and indices and mitral valve parameters.Results:M-mode echocardiographic measurements in healthy Indian Spitz dogs were standardized. Gender had no influence on echocardiographic measurements except mitral valve excursion amplitude and time interval between onset and end of mitral valve closure, which were significantly (p<0.05) higher in females than males. Left ventricular internal dimension at end-diastole, left ventricular internal dimension at end-systole, left ventricular posterior wall dimension at end-systole, end-diastolic volume, end-systolic volume, stroke volume, cardiac output, left ventricular ejection time, and mitral valve excursion amplitude correlated significantly (p<0.05) with body weight in Indian Spitz dogs.Conclusion:Data obtained in the present study can be used as breed-specific reference values for cardiac disease diagnosis as well as for future studies in Indian Spitz dogs.

Association of insulin growth factor-1 and growth hormone levels in elderly renal transplant recipients with cardiac dysfunction

Insulin growth factor-1 (IGF-1) and growth hormone (GH) have cardiac protective effects through many mechanisms; they can directly oppose endothelial dysfunction in a number of ways. Many studies assessed the effect of GH or IGF-like growth factor 1 in patients with cardiac dysfunction, but no previous study assessed the GH and insulin-like growth factor-1 in renal transplant recipients with and without cardiac dysfunction, especially elderly. Eighty patients with renal transplantation and age limit above 75 years. They were subdivided into two groups according to the presence or absence of cardiac dysfunction based on medical history, clinical findings, electrocardiogram, and echocardiography. Serum GH and insulin-like growth factor-1 were studied by immunoradiometric assay. The echocardiography study was performed. M-mode two-dimensional and Doppler measurements were taken to obtain the four- and five-chamber views, chambers' dimensions, left ventricular end-diastolic dimensions, left ventricular end-systolic dimensions, septal wall thickness (SWT), distance between leading edges of the endocardial and pericardial echoes of left ventricular posterior wall (posterior wall thickness), aortic root and left atrial dimensions (LAD), fractional shortening and ejection fraction. IGF-1 is lower in patients with cardiac dysfunction with renal transplantation with mean value of 61 ± 30.05 than those control group with mean value 145.52 ± 70.5. Level of human growth factor is higher in patients with dysfunction with renal transplantation with mean value 2.62 ± 3.05 than those control group after renal transplantation with mean value 0.85 ± 0.9. No correlations were found between IGF-1 and various echocardiographic parameters. Only SWT and LAD were negatively correlated with GH, r = -0.08, P <0.02, r = -0.37, P <0.03, respectively. No correlation was found between IGF-1 and various echocardiographic parameters. Only SWT and LAD were negatively correlated with GH.

Single-Stranded DNA-Binding Protein 1 Abrogates Cardiac Fibroblast Proliferation and Collagen Expression Induced by Angiotensin II.

Angiotensin II (Ang II), an effective component of renin-angiotensin system, plays a pivotal role in cardiac fibrosis, which may further contribute to heart failure. Single-stranded DNA-binding protein 1 (SSBP1), a DNA damage response protein, regulates both mitochondrial function and extracellular matrix remodeling. In this study, we aim to investigate the role of SSBP1 in cardiac fibrosis that is induced by Ang II. We infused C57BL/6J mice with vehicle or Ang II and valsartan using implanted osmotic mini-pumps. Moreover, heart function was examined by echocardiography and cardiac fibrosis was analyzed via picrosirus red staining. The expression of COL1A1, COL3A1, SSBP1, p53, Nox1, and Nox4 was analyzed via qRT-PCR and/or immunoblots. The SSBP1 expression was manipulated via SSBP1 shRNA and pcDNA3.1/SSBP1 plasmids, while the p53 expression was enhanced via AdCMV-p53 infection. The exposure to Ang II increased the mouse heart weight, systolic blood pressure, interventricular septal thickness diastolic (IVSTD) and left ventricular end posterior wall dimension diastolic (LVPWD), which were counteracted by valsartan. While cardiac fibrosis was induced with Ang II treatment, it was relieved using valsartan. Furthermore, Ang II treatment caused mitochondrial dysfunction, oxidative stress, and down-regulated SSBP1 expression. The knockdown of SSBP1 increased cardiac fibroblast proliferation, collagen expression, and decreased p53 expression, which was impeded via SSBP1 overexpression. Moreover, the forced expression of p53 abated the fibroblast proliferation and collagen expression that was induced by Ang II. To summarize, SSBP1 was down-regulated by Ang II and implicated in cardiac fibroblast proliferation and collagen expression partly via the p53 protein.

Switch to agalsidase alfa after shortage of agalsidase beta in Fabry disease: a systematic review and meta-analysis of the literature.

In 2009, the agalsidase beta shortage resulted in switching to agalsidase alfa treatment for many Fabry disease patients, offering the unique opportunity to compare the effects of the two drugs. Because single studies describing effects of switching on the disease course are limited and inconclusive, we performed a systematic review and meta-analysis of existing data. Relevant studies were identified in the PubMed, Cochrane, ISI Web, and SCOPUS databases from July 2009 to September 2015. The following parameters were analyzed: clinical events, changes in organ function or structure, disease-related symptoms, lyso-Gb3 plasma levels, and adverse effects. The nine studies (217 patients) included in our systematic review showed only marginal differences in most of the evaluated parameters. Seven of these studies were included in the meta-analysis (176 patients). The pooled incidence rate of major adverse events was reported for five studies (150 patients) and was equal to 0.04 events per person-year. No significant change was observed after the shift in glomerular filtration rate, whereas left ventricular mass index, left ventricular posterior wall dimension, and ejection fraction were significantly reduced over time. Our data showed that the switch to agalsidase alfa was well tolerated and associated with stable clinical conditions.Genet Med 19 3, 275-282.

Congenital Giant Left Atrium with Severe Mitral Valve Regurgitation.

A three-month-old male infant presented to the Royal Hospital, Muscat, Oman in April 2014 following two episodes of pneumonia. On presentation, the patient was not dysmorphic; however, he was tachycardic and tachypnoeic with severe respiratory distress. A pansystolic murmur was heard in his apex, radiating to the axilla. A chest examination showed bilateral wheezing and scattered crepitations. An abdominal examination revealed a soft abdomen with hepatomegaly (liver span of 12 cm), situated 4 cm below the right costal margin. Echocardiography and an angiographic volume-rendered reconstructed computed tomograph showed a giant left atrium measuring 7.4 × 4.7 cm [Figure 1]. The atrium had severe mitral valve regurgitation from poor coaptation of the mitral valve leaflets due to annulus dilation of 22 mm. The mitral valve apparatus and left atrial appendage were normal, excluding the associated left atrial appendage aneurysm. There was mild tricuspid valve regurgitation with a peak gradient of 90 mmHg (systemic blood pressure: 80/55 mmHg), indicating severe pulmonary hypertension. The left ventricle was moderately dilated—the left ventricular posterior wall dimension in diastole was 4 mm; the interventricular septum dimension in diastole was 4 mm; the left ventricular end diastolic dimension was 40 mm; and the left ventricular end systolic dimension was 18 mm. Normal ventricular systolic function was noted (ejection fraction: 62%). The right ventricle was compressed by the dilated left ventricle, with severe compression of the right atrium secondary to the dilated left atrium. The inferior vena cava and hepatic veins were dilated; however, the superior vena cava was compressed by the dilated left atrium with a mean gradient of 8 mmHg at its midportion. The dilated pulmonary veins drained normally to the left atrium. No intracardiac vegetation or thrombi were seen. These findings were confirmed by cardiac computed tomography (CT) angiography; severe compression of the left main bronchus was also observed [Figure 2]. The CT angiography also revealed a left atrial volume of 84 mL compared to a left ventricular volume of 10 mL. A chest radiograph of the infant revealed a persistent left-sided lung opacity [Figure 3]. Further abdominal ultrasonography and CT findings indicated eventration of the left hemidiaphragm with a raised spleen position corresponding to the opaque shadow seen on the chest radiograph. A diagnosis of a congenital giant left atrium (CGLA) was made. Figure 1A & B: A: Four chamber echocardiograph showing a giant congenital left atrium (white arrow) severely compressing the right atrium (red arrow) in a three-month-old male infant. B: Volume-rendered reconstructed computed tomography angiograph showing the giant ... Figure 2A & B: A: Axial computed tomography (CT) angiograph showing a giant congenital left atrium (black arrow) with left upper lobe and segmental right lower lobe atelectasis (red arrows) in a three-month-old male infant. B: Maximum-intensity CT angiograph projection ... Figure 3: Frontal chest radiograph of a three-month-old male infant with congenital giant left atrium showing a persistent left-sided lung opacity (arrow). This was determined by ultrasonography and computed tomography to be a raised spleen caused by eventration ... Despite cardiac anti-failure medications and inotropic support, a high-risk operation was performed to repair the mitral valve due to the cardiac findings and prolonged intubation. A posterior annuloplasty and a posterior left atrial wall excision were also carried out concurrently. The diagnosis of CGLA was confirmed during the course of the surgery. Following the operation, the left atrial dilation improved and the right ventricular systolic pressure decreased to 30 mmHg (estimated from the tricuspid valve regurgitation jet). Unfortunately, the moderate mitral valve regurgitation continued postoperatively and the infant died two weeks later due to severe cardiorespiratory compromise.

IGF-1 ENGINEERED HUMAN CARDIAC STEM CELLS PROMOTE REPAIR OF ISCHEMIC MYOCARDIUM BY IMPROVING TRANSPLANT CELL SURVIVAL AND REDUCING MYOCARDIAL APOPTOSIS

the need for comprehensive long-term follow up studies. METHODS: The Canadian Registry of Atrial Fibrillation (CARAF) enrolled patients from 7 centres in Canada at the time of first electrocardiographic diagnosis of AF. Comprehensive clinical and echocardiographic data were collected and patients were followed annually, documenting clinical outcomes, recurrence of PAF, and progression to CAF. Univariate and multivariable Cox proportionate hazards analyses were performed to model the association between baseline clinical, electrocardiographic, and echocardiographic variables and outcomes of stroke and death in patients with AF. RESULTS: A total of 897 patients with non-surgical paroxysmal AF (PAF) were included in the analysis. The medial follow-up time was 8.89 years (interquartile range of 5 to 9.12 years). A total of 268 deaths and 84 strokes occurred during the follow-up period. Univariate analyses identified 13 risk factors that were independently associated with risk of death and 9 risk factors that were independently associated with risk of stroke. Of these risk factors, history of cardiomyopathy, presence of congestive heart failure (CHF), severe mitral regurgitation (MR) and older age had the highest hazard ratios (HR) for occurrence of death (HR 1⁄42.74, 2.61, 2.11 and 2.10, respectively (p<0.001)). The factors were also statistically associated with death in multivariate analysis. Presence of moderate to severe mitral stenosis (MS), cardiomyopathy, increase in left ventricular (LV) posterior wall dimension, CHF and age were highly associated with occurrence of stroke (HR1⁄4 3.99, 3.23, 2.51, 1.94 and 1.73, respectively (p<0.03)). In multivariable analysis, MS, age, And LV posterior wall dimension were associated with stroke. CONCLUSION: In patients with diagnosis of PAF, there are various clinical and echocardiographic risk factors that are independently associated with higher risk of poor outcomes such as death and stroke.

ISOLATION AND RECOVERY OF HUMAN CARDIAC STEM CELLS FROM CRYOPRESERVED CARDIAC TISSUE

the need for comprehensive long-term follow up studies. METHODS: The Canadian Registry of Atrial Fibrillation (CARAF) enrolled patients from 7 centres in Canada at the time of first electrocardiographic diagnosis of AF. Comprehensive clinical and echocardiographic data were collected and patients were followed annually, documenting clinical outcomes, recurrence of PAF, and progression to CAF. Univariate and multivariable Cox proportionate hazards analyses were performed to model the association between baseline clinical, electrocardiographic, and echocardiographic variables and outcomes of stroke and death in patients with AF. RESULTS: A total of 897 patients with non-surgical paroxysmal AF (PAF) were included in the analysis. The medial follow-up time was 8.89 years (interquartile range of 5 to 9.12 years). A total of 268 deaths and 84 strokes occurred during the follow-up period. Univariate analyses identified 13 risk factors that were independently associated with risk of death and 9 risk factors that were independently associated with risk of stroke. Of these risk factors, history of cardiomyopathy, presence of congestive heart failure (CHF), severe mitral regurgitation (MR) and older age had the highest hazard ratios (HR) for occurrence of death (HR 1⁄42.74, 2.61, 2.11 and 2.10, respectively (p<0.001)). The factors were also statistically associated with death in multivariate analysis. Presence of moderate to severe mitral stenosis (MS), cardiomyopathy, increase in left ventricular (LV) posterior wall dimension, CHF and age were highly associated with occurrence of stroke (HR1⁄4 3.99, 3.23, 2.51, 1.94 and 1.73, respectively (p<0.03)). In multivariable analysis, MS, age, And LV posterior wall dimension were associated with stroke. CONCLUSION: In patients with diagnosis of PAF, there are various clinical and echocardiographic risk factors that are independently associated with higher risk of poor outcomes such as death and stroke.

Effect of type 2 diabetes on the left ventricular diastolic dysfunction in patients with chronic kidney disease, 3 and 4 stages

Patients with chronic kidney disease (CKD) and coexisting diabetes mellitus (DM) are likely to have cardiological complications. We assessed whether patients with moderate kidney dysfunction, with coexisting type 2 DM and preserved left ventricular (LV) systolic function, demonstrate a more advanced LV diastolic dysfunction. The study group consisted of 58 ambulatory patients with CKD, stages 3 and 4. The patients were assigned to groups based on the presence of type 2 DM. The first group (DM+) consisted of 21 patients with type 2 DM while second one (DM−) consisted of 37 patients without type 2 DM. Standard echocardiography was performed in all patients with tissue Doppler echocardiography for evaluation of the systolic velocity and both diastolic velocities of LV. The following laboratory parameters were measured: serum creatinine concentration, estimated glomerular filtration rate, and the levels of urea, phosphorus, calcium, parathormone, platelets count, hemoglobin level and N-terminal pro-B-type natriuretic peptide levels. LV diastolic dysfunction was defined as EmLV less than 8 cm/s. Patients in DM+ group, as compared to patients in DM− group, were characterized by higher values of left and right ventricular end-diastolic dimension, left atrial diastolic dimension, interventricular septal diastolic diameter, LV posterior wall dimension at diastole and of LV mass index, smaller LV ejection fraction and LV fractional shortening. In tissue Doppler echocardiography patients of DM+ group, as compared to patients of DM− group, did not differ in value of EmLV (7.4 ± 2.4 cm/s vs. 7.6 ± 2.1 cm/s, P = .723), respectively, and were characterized by similar estimated LV diastolic filling pressure as indicated by E /EmLV (10.1 ± 3.7 vs. 8.8 ± 2.6, P = .119). CKD patients in the moderate stage, with coexisting type 2 DM were not characterized by higher risk of developing LV diastolic dysfunction.

The association of cardiac ventricular hypertrophy with congenital hyperinsulinism

Ventricular hypertrophy (VH) has been observed in children with congenital hyperinsulinism (CHI), a condition of hypoglycaemia characterised by dysregulated insulin secretion, but the prevalence is not known. Cardiac assessment was performed in children (n=49) with CHI at diagnosis and follow-up. Two dimensional and Doppler echocardiography studies were used to assess cardiac structures, while M-mode study was used to measure left ventricular (LV) dimensions, subsequently converted to Z scores. Where possible, LV hypertrophy was confirmed by LV mass index (g/m(2.7)) >95th centile. Cardiac structural lesions were found in 14 (28%) children. At initial echocardiography, VH was present in 31 (65%) children with median (range) LV posterior wall dimension in diastole Z scores of +1.6 (-2.4 to +5.8) and interventricular septal wall dimension in end diastole Z scores of +1.9 (-1.7 to +17.2). At follow-up echocardiography, performed after an interval of 178 (45-390) days, VH persisted in 16 (33%) children. In regression analysis, the presence of VH (odds ratio (95% confidence intervals) 1.1 (1.0-1.2), P=0.04) at initial echocardiography was correlated with maximum glucose requirement at diagnosis, indicating that severity of CHI at presentation may play a role in the pathogenesis of VH. A significant proportion of children with CHI have cardiac structural lesions. A majority also have VH, which may be associated with the severity of CHI at diagnosis. VH may persist in some children, which requires careful long-term cardiac review.

Derivation of Transthoracic Echocardiographic Reference Ranges for Left Ventricular, Left Atrial and Aortic Root M-Mode Dimensions in Preterm Infants

Background: M-mode measurement of left heart dimensions is routine in transthoracic echocardiography. Reference ranges are well defined in adults and paediatric patients. No such data have been published in preterm neonates. Methods: All echocardiographic studies performed in Monash Newborn between 3rd December 2007 and 2nd December 2010 were identified. Infants with congenital heart disease, a greater than small sized patent ductus arteriosus or technically inadequate M-mode images were excluded. M-mode left ventricular, left atrial and aortic root measurements were made retrospectively by an experienced cardiac sonographer. Analysis was limited to infants with a birth or current weight ≤3.5 kg and ≤45 completed weeks of corrected gestational age (cGA) at the time of echocardiography. Analysis was performed in SPSS. Regression curves were modelled with respect to weight and cGA and reference curves for ±1 and ±2 standard deviations calculated using the method of Altman (Statistics in Medicine, 1993). Results: 234 studies were identified, mean GA at birth 30 weeks, birth weight 1.5 ± 0.9 kg. All measured parameters increased with weight and cGA (all P < 0.001). Standard deviation increased, but did not reach statistical significance over the given weight and cGA range. Examples for Left ventricular end diastolic dimension (LVEDd), posterior wall and aortic root dimensions below. Conclusions: The derivation of reference ranges for left ventricular dimensions in preterm infants will permit better recognition of abnormalities and better description and documentation of change with the opportunity to calculate Z scores.

Long-Term Efficacy of Deferasirox in Preventing Cardiovascular Complications in the Iron-Overloaded Gerbil

Iron-induced cardiovascular disease is the leading cause of death in iron-overloaded patients. Deferasirox is a novel tridentate oral chelator that exhibits a half-life suitable for once-daily dosing; however, little is known regarding the effectiveness of this agent in preventing iron-induced cardiovascular disease. Adult male Mongolian gerbils were randomly divided into 3 groups: control, iron overload, and iron overload followed by deferasirox treatment. Iron-overloaded animals received iron dextran 100 mg/kg intraperitoneally (ip)/5 days for 10 weeks, while deferasirox was given 100 mg/kg per d orally (po) for 9 months post iron loading. Cardiac and aortic iron levels were determined by inductively coupled plasma atomic emission spectrometry. Gerbil electro- and echocardiograms were obtained in anesthetized animals at regular intervals. Compared to control animals, iron concentration was 3.3- and 2.4-fold higher in iron-overloaded heart and aorta, respectively (P < .05). Deferasirox treatment reduced cardiac and aortic iron levels by 32% and 35%, respectively (P < .05). These results were consistent with the decrease in cellular iron deposition observed with Prussian Blue iron staining. Iron-overloaded gerbils were found to exhibit frequent arrhythmias including premature ventricular contractions, supraventricular tachycardia, and recurrent ventricular tachycardia. In addition, echocardiographic assessment demonstrated iron overload-associated increase in left ventricular dimensions including left ventricular posterior wall dimension (LVPWd: 49%), left ventricular internal dimension (LVIDd: 26%), and left ventricular septum thickness (LVSd: 42%). These parameters were significantly reduced with deferasirox treatment (LVPWd: 23%, LVIDd: 24%, and LVSd: 27%). Iron overload was also associated with reduced ejection fraction (EF: by 30%) and fractional shortening (FS: by 23%) in comparison with controls (P < .05). With deferasirox treatment, these values were higher (EF: by 30%, FS: by 28%) compared to iron-overloaded group. These findings suggest that deferasirox may be useful for attenuating iron-induced changes in cardiac structure and function.