Left Ventricular Posterior Wall Thickness At End-diastole Research Articles

Association between systemic inflammatory response index and left ventricular remodeling and systolic dysfunction in atrial fibrillation patients

BackgroundCardiac remodeling and dysfunction can be caused by atrial fibrillation (AF). The aim of this research is to investigate the relationship between the systemic inflammatory response index (SIRI) and left ventricular (LV) remodeling and systolic function in individuals with AF.Methods416 patients with AF who were admitted to the Second Department of Cardiology in the East Ward of the Qingdao Municipal Hospital between January 2020 and May 2022 were included in the present retrospective research. The relationship between SIRI and various cardiac parameters was analyzed. The patients’ left atrial (LA) enlargement and left ventricular (LV) hypertrophy and systolic dysfunction were evaluated. SIRI was calculated by the formula: neutrophil × monocyte/lymphocyte.ResultsSIRI significantly correlated with LV end-diastolic diameter (LVDd), LV posterior wall thickness at end-diastole (LVPWTd), interventricular septal thickness at end-diastole (IVSTd), LV mass index (LVMI), LV ejection fraction (LVEF), LA diameter (LAD), C-reactive protein (CRP), and N-terminal pro-B-type natriuretic peptide (NT-proBNP) in patients with AF. In multivariate linear regression analyses, SIRI was discovered to be significantly related to LVMI (ln-transformed) (p = 0.025), LVEF (ln-transformed) (p = 0.005), and LAD (ln-transformed) (p = 0.007). In multivariate logistic regression, the highest quartile of SIRI (SIRI > 1.62) was significantly associated with LV hypertrophy (p = 0.026), impaired LV systolic function (p = 0.002), and LA enlargement (p = 0.025).ConclusionsSIRI was significantly associated with LV remodeling and systolic function impairment in patients with AF. SIRI may serve as a reliable and convenient inflammatory biomarker for detecting impaired cardiac structure and systolic function in patients with AF.

Cardiomyocyte ZKSCAN3 regulates remodeling following pressure-overload.

Autophagy is important for protein and organelle quality control. Growing evidence demonstrates that autophagy is tightly controlled by transcriptional mechanisms, including repression by zinc finger containing KRAB and SCAN domains 3 (ZKSCAN3). We hypothesize that cardiomyocyte-specific ZKSCAN3 knockout (Z3K) disrupts autophagy activation and repression balance and exacerbates cardiac pressure-overload-induced remodeling following transverse aortic constriction (TAC). Indeed, Z3K mice had an enhanced mortality compared to control (Con) mice following TAC. Z3K-TAC mice that survived exhibited a lower body weight compared to Z3K-Sham. Although both Con and Z3K mice exhibited cardiac hypertrophy after TAC, Z3K mice exhibited TAC-induced increase of left ventricular posterior wall thickness at end diastole (LVPWd). Conversely, Con-TAC mice exhibited decreases in PWT%, fractional shortening (FS%), and ejection fraction (EF%). Autophagy genes (Tfeb, Lc3b, and Ctsd) were decreased by the loss of ZKSCAN3. TAC suppressed Zkscan3, Tfeb, Lc3b, and Ctsd in Con mice, but not in Z3K. The Myh6/Myh7 ratio, which is related to cardiac remodeling, was decreased by the loss of ZKSCAN3. Although Ppargc1a mRNA and citrate synthase activities were decreased by TAC in both genotypes, mitochondrial electron transport chain activity did not change. Bi-variant analyses show that while in Con-Sham, the levels of autophagy and cardiac remodeling mRNAs form a strong correlation network, such was disrupted in Con-TAC, Z3K-Sham, and Z3K-TAC. Ppargc1a also forms different links in Con-sham, Con-TAC, Z3K-Sham, and Z3K-TAC. We conclude that ZKSCAN3 in cardiomyocytes reprograms autophagy and cardiac remodeling gene transcription, and their relationships with mitochondrial activities in response to TAC-induced pressure overload.

Percentile curves of normal echocardiographic measurements values for left heart structures in 1570 Han Chinese preterm and term infants.

This study was designed to evaluate echocardiographic measurements in Han Chinese preterm and term infants and to build percentile curves of normal echocardiographic measurements values related to the weight. From December 2014 to December 2021, a total of 797 male infants and 773 female infants born in * were included in the study. The echocardiographic measurements of each subject were as follows: left ventricular internal diameter at end-diastole (LVIDd), left ventricular internal diameter at end-systole (LVIDs), left ventricular posterior wall thickness at end-diastole (LVPWd), left ventricular posterior wall thickness at end-systole (LVPWs), interventricular septal thickness at end-diastole (IVSd), interventricular septal thickness at end-systole (IVSs), ascending aorta diameter (AO), left atrium (LA) dimension, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS) and left ventricular mass (LVM). The correlations between echocardiography measurements and birth weight (BW), length (L), gestational age (GA), and body surface area (BSA) were analyzed. There was a good correlation between the echocardiographic measurements and birth weight and percentile curves of the echocardiographic measurements were established according to different birth weight. The echocardiographic measurements were not affected by gender. However, LVEF and LVFS did not change with BW or gender. The percentile curves of normal values make it possible to classify echocardiographic measurements for left heart structures and function as normal or abnormal and is helpful for the diagnosis of neonatal heart disease in preterm and term infants.

Effects of Yixintai Pills on Myocardial Cell Apoptosis in Rats With Adriamycin-Induced Heart Failure.

To study the effects of Yixintai pills on myocardial cell apoptosis in rats with adriamycin (ADR)-induced heart failure (HF) and the mechanism of action. Sixty healthy male Wistar rats randomly were divided into Control, Model, Captopril, and Yixintai pill groups. A rat model of ADR-induced HF was constructed by intraperitoneal injection of ADR (2.5 mg/kg). The control group was given an equal volume of normal saline; the Yixintai pill and Captopril groups were given corresponding mediations (5 mg/kg) by lavage. After 4 weeks of treatment, fasting blood was collected to detect the contents of plasma rennin activity (PRA), angiotensin II (AngII), and aldosterone (ALD). B ultrasound was used to detect the heart structure, and the heart weight/body weight (HW/BW) ratio was calculated. The pathology of myocardial tissues was observed by HE staining. The apoptosis of myocardial cells was detected by TUNEL assay. The expression levels of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in serum were analyzed by ELISA, and the protein expression levels of protein kinase B (Akt), phosphorylated (p)-Akt, glycogen synthase kinase-3β (GSK-3β) and p-GSK-3β in myocardial tissues were measured by Western blotting. Compared with the Control group, the PRA, AngII, ALD, left ventricular posterior wall thickness at end-systole (LVPWs), left ventricular posterior wall thickness at end-diastole (LVPWd), interventricular septal thickness at end-systole (IVSs), interventricular septal thickness at end-diastole (IVSd), HW/BW, TNF-α and IL-6 of model group increased significantly (P < .05). PRA, AngII, ALD, LVPWs, LVPWd, IVSs, IVSd, HW/BW, TNF-α and IL-6 of the Yixintai pill and Captopril groups were significantly lower than those of the Model group (P < .05). There were no significant differences in the indices between the Yixintai pill and Captopril groups (P > .05). In the Model group, lamellar necrosis, vacuolar degeneration, increased myocardial fibers and lamellar dissolution of myocardial cells were found in myocardial tissues. However, the myocardial cells of the Control group were neatly arranged and clearly structured, and only a few ones underwent fibrosis. There were mild myocardial fibrosis and vacuolar degeneration in the Yixintai pill and Captopril groups, and the degeneration and hyperplasia of myocardial fibers were obviously relieved. Compared with the Control group, the apoptosis index (AI) of the Model group increased significantly (P < .05). The AI values of the Yixintai pill and Captopril groups were significantly lower than those of the Model group (P < .05). Compared with the Control group, the expression levels of p-Akt and p-GSK-3β in the Model group decreased significantly (P < .05). The expression levels of p-Akt and p-GSK-3β in the Yixintai pill and Captopril groups were significantly higher than those of the Model group (P < .05), whereas the former 2 groups had similar results (P > 0.05). Yixintai pills may inhibit myocardial cell apoptosis and ventricular remodeling in rats by up-regulating PI3K/Akt/GSK-3β signal, thus protecting the heart function.

Glypican‐1 and Remodeling Cardiac Hypertrophy.

Heart failure impacts about 5.7 million people in the U.S. alone and the clinical signs often arise from changes in heart function. Cardiac hypertrophy is a known contributor to impaired cardiac contractility and ejection fraction. The heart deals with a working relationship with volume and pressure and thus mechanosensitive proteins may play a role on heart function. This study investigates the role of heparan sulfate proteoglycans, specifically syndecan1 (Sdc1) and glypican1 (Gpc1) on heart function and hypertrophy. We investigated if global deletion of Gpc1 and Sdc1 in mice alters heart histological features and thus cardiac function. Global male knockout mice for Sdc1 (Sdc1KO) and Gpc1 (Gpc1KO) were used and compared to its respective controls C57B6 and CD1 (7 weeks old). Left ventricular posterior wall thickness at end diastole (LVPWd), interventricular septal thickness at end of diastole (IVSTd) and left ventricular internal diameter in diastole (LVIDd) and myocyte cross‐sectional area in the left ventricle were assessed by transmission microscopy using hematoxylin &amp; eosin (H&amp;E) staining. Collagen deposition was assessed by Masson’s Trichrome staining. No differences in heart dimensions (LVPWd, IVSTd, LVIDd) were found between C57B6 and Sdc1KO. IVSTd and LVPWd was increased in Gpc1KO compared to CD1 (IVSTd: 1.15 mm for Gpc1KO and 1.03 mm for CD1; LVPWd: 0.75 mm for Gpc1KO and 0.64 mm for CD1). Both knock out lines showed decreased myocyte cross‐sectional area in the left ventricle size compared to its control (203.86 μm2 for Gpc1KO, 248.43 μm2 for CD1, 194.64 μm2 for Sdc1KO, and 239.02 μm2 for C57B6). Blind scoring of collagen staining showed that there was not a significant difference in collagen deposition between Gpc1KO and CD1 (1.14 for Gpc1KO and 0.99 for CD1). Taking together, these findings indicate that Sdc1KO and Gpc1KO show alterations in cardiac histological features. Our data raises the possibility of heparan sulfate proteoglycans being involved in cardiomyocyte proliferation or development. Particularly, Gpc1KO show the unique characteristic of having a hypertrophic heart without collagen deposition. Heparan sulfate proteoglycans may play a key role in cardiac function and we speculate that they may be involved in heart disease progression.Support or Funding InformationDepartment of Anesthesiology, College of Medicine, University of Arizona, Tucson

Echocardiographic and biochemical profile in children with celiac disease

Background: A number of heart diseases such as autoimmune myocarditis, cardiomyopathy, and ischemic heart disease are recently being reported among celiac patients. Studies have also demonstrated subclinical cardiac dysfunction and clustering of many traditional cardiovascular risk factors in children with celiac disease. Objective: The present study was conducted for echocardiographic and biochemical assessment of children with celiac disease. Materials and Methods: A cross-sectional observational study was conducted among 36 children (aged 1–16 years) who were newly diagnosed with celiac disease and age- and sex-matched controls. Venous blood samples were assessed for serum C-reactive protein (CRP), folic acid, Vitamin B12, and homocysteine levels, and fasting lipid profile including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) levels using appropriate methods. Echocardiographic parameters were measured by M-mode ultrasonography measuring left atrial dimension (LAD), left ventricular end-diastolic dimension (LVEDD), right ventricular diastolic diameter (RVDD), interventricular septal thickness at end-diastole (IVSd), left ventricular posterior wall thickness at end-diastole (LVPWd), aortic root dimension (ARD), and ejection fraction (EF). Results: Among the echocardiographic parameters, EF was significantly lower while other parameters such as LAD, LVEDD, RVDD, IVSd, LVPWd, and ARD showed no significant increase among the cases. Significantly lower levels of TC, HDL-C, and LDL-C with normal TG, CRP, Vitamin B12, and folic acid levels with significantly increased serum homocysteine levels were noted among cases. Conclusion: A significant difference in EF and the presence of biochemical risk factors for cardiovascular diseases warrants further detailed evaluation and follow-up with regular monitoring of cardiac functions.

Abstract 524: Activated Fms-like Tyrosine Kinase 3 Receptor Prevents Ventricular Remodeling Induced by Ang Ii Through the Attenuation of Autophagy

Aim: FMS-like tyrosine kinase 3 (Flt3) is a receptor tyrosine kinase. This study was to determine whether activation Flt3 could regulate autophagy ameliorate AngII-induced heart cardiac remodeling and to elucidate the mechanisms of action. Methods: In vivo cardiac remodeling was induced in male C57BL/6 mice by implanting subcutaneously osmotic minipumps releasing Angiotensin II (Ang II) for 28 days (1100ng/kg/min). Flt3 ligand (FL) was administered intraperitoneally (5μg/mouse/2days). Heart hypertrophy, fibrosis and function were evaluated based on echocardiography, histological and biochemical measurements. In vitro, hypertrophy was induced by Ang II on adenovirus vector-mediated overexpression Flt3 receptor in H9c2 cells, and NRCMs. Crystal violet staining, flow cytometry and TUNEL were used for in vitro experiments. The levels of signaling proteins were measured using western blotting, while the expression of the relevant genes was analyzed using real-time qRT-PCR. Results: Echocardiography demonstrated that Ang II induced marked damaged heart function, while cardiac Flt3 receptor activation significantly decrease left ventricular internal dimension at end-diastole (LVIDd), left ventricular posterior wall thickness at end-diastole (LVPWd), and increase ejection fraction (EF%) and fractional shortening (FS%). FL-treated mice showed a significant attenuation of cardiac hypertrophy, ratios of heart weight/body weight (HW/BW) and heart weight/tibia length (HW/TL), as well as cardiac fibrosis and apoptosis. Additionally, the autophagic levels in cardiomyocytes of FL-treated mice were distinctly decreased as evidenced by expression of LC3 in immunohistochemical staining and western blotting. In H9c2 cells with adenovirus vector-mediated overexpression of Flt3 and neonatal rat cardiomyocytes, FL treatment significantly decrease the cell size, apoptosis and autophagy induced by Ang II. Additionally, using rapamycin or metformin, respectively canceled FL protective effects. Conclusion: Flt3 activation suppresses Ang II-induced cardiac hypertrophy and apoptosis via AMPK /mTOR/ FOXO3a autophagy signaling pathway. These results provide evidence supporting Flt3 as a novel therapeutic target in cardiac remodeling.

Abstract P2-11-18: The use of consomic animal models to identify genetic factors that modulate radiation-induced cardiac toxicity

Abstract Purpose/Objectives: Radiation therapy is used by more than 50% of breast cancer patients, but radiation doses can be limited by normal tissue side effects. For example, breast cancer radiation therapy can improve breast cancer-specific survival, but increase cardiac deaths in those with left-sided cancers. Identifying genetic factors that can enhance tumor radiation sensitivity while decreasing normal tissue toxicities has the potential to improve the therapeutic ratio of radiation therapy – leading to more cures and less long-term toxicities. The use of animal models with differing genetic backgrounds to assess radiation toxicity, followed by genetic mapping of radiosensitivity phenotypes, has the potential to identify new targets that can predict cardiac toxicity from radiation therapy. This project examines how genetic host factors alter normal tissue toxicity risks from breast cancer radiation. Materials/Methods: Inbred female SS rats and SS.BN3 consomic rats, that are genetically identical to SS rats except that chromosome 3 is inherited from the BN strain, have previously been shown to exhibit different vascular dynamics and breast tumor growth. For this study, adult female SS and SS.BN3 rats received image-guided whole heart radiation to a dose of 21 Gy (3 fields, AP and 2 laterals). Cardiac troponin was serially measured at 2, 6, and 12 weeks, and echocardiograms with strain analysis were performed at baseline and 3 months. The Student's t-test was used to compare values. Results: The SS female rats exhibited enhanced cardiac toxicity compared to SS.BN3 rats, with cardiac troponin levels elevated at 12 weeks (0.32 ng/ml vs.0.08 ng/ml for SS vs. SS.BN3, p=0.01), and moderate to severe pericardial effusions seen in 6 of 9 SS rats vs. 2 of 7 SS.BN3 rats. At 3 months post-radiation, echocardiograms revealed increased left ventricular posterior wall thickness at end diastole (LVPWd) in SS vs. SS.BN3 rats (0.25 vs. 0.20 cm, p=0.002) and increased left ventricular mass (LVM) in SS vs. SS.BN3 rats (1.54 vs. 1.28 g, p&amp;lt;0.001). Taken together, the SS female rats are more sensitive to cardiac irradiation than SS.BN3. Conclusions: These results demonstrate that genetic variant on rat chromosome 3 alter the radiosensitivity to single fraction cardiac radiation therapy. Gene expression analysis and genetic mapping will be performed to identify the causative target(s). These models will also be expanded to test whether similar results are seen with fractionated cardiac radiation therapy. This project has the potential to enhance the effectiveness and toxicity profile of radiation therapy in breast cancer. Citation Format: Bergom C, Schlaak R, Frei A, Fish BL, Harmann L, Gasperetti T, Schottstaedt AM, Flister MJ, Medhora M, Strande JL. The use of consomic animal models to identify genetic factors that modulate radiation-induced cardiac toxicity [abstract]. In: Proceedings of the 2017 San Antonio Breast Cancer Symposium; 2017 Dec 5-9; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2018;78(4 Suppl):Abstract nr P2-11-18.

Echocardiographic reference ranges in older children and adolescents in sub-Saharan Africa

BackgroundEchocardiographic reference ranges are important to identify abnormalities of cardiac dimensions. Reference ranges for children in sub-Saharan Africa have not been established. The aim of this study was to establish echocardiographic z-score references for Black children in sub-Saharan Africa. Methods282 healthy subjects aged 6–16years (143 [51%] males) with no known history of cardiac disease were enrolled in the study in Harare, Zimbabwe between 2014 and 2016. Standard M-mode echocardiography was performed and nine cardiac chamber dimensions were obtained. Two non-linear statistical models (gamma weighted model and cubic polynomial model) were tested on the data and the best fitting model was used to calculate z-scores of these cardiac chamber measures. The reference ranges are presented on scatter plots against BSA. ResultsNormative data for the following cardiac measures were obtained and z-scores calculated: right ventricular diameter at end diastole (RVEDD); left ventricular diameter at end diastole (LVEDD) and systole (LVESD); interventricular septal wall thickness at end diastole (IVSd) and systole (IVSs); left ventricular posterior wall thickness at end diastole (LVPWd) and systole (LVPWs); left atrium diameter at end systole (LA) and tricuspid annular plane systolic excursion (TAPSE). Girls had higher values for BMI and heart rate than boys (p=0.048 and p=0.001, respectively). Mean interventricular septal and left ventricular posterior walls thickness was higher than published normal values in predominantly Caucasian populations. ConclusionThese are the first echocardiographic reference ranges for children from sub Saharan Africa and will allow accurate assessment of cardiac dimensions in clinical practice.

Obesity and left ventricular mass in children

Background Obesity has negative effects on cardiac function during growth leading to increased heart size and mass, as a result of higher stroke volume and cardiac output.Objective To assess for a relationship between obesity and left ventricular mass (LVM) in children, as well as to assess for a correlation between the duration of obesity and LVM.Methods This cross-sectional study was conducted from October 2011 until February 2012 in Medan and included 30 obese and 30 normal weight children, aged 6 to 13 years. All subjects underwent complete echocardiography examinations to assess LVM and other left ventricular parameters. The Devereux formula was used to measure LVM.Results During the study, 65 children underwent echocardiography, but 5 were subsequently excluded. The left ventricular dimensions in the obese group were significantly higher compared to normal weight group with regards to interventricular septum at end diastole (IVSd), interventricular septum at end systole (IVSS), left ventricular internal diameter at end diastole (LVIDd), left ventricular internal diameter at end systole (LVIDs), left ventricular posterior wall thickness at end diastole (LVPWd), left ventricular mass (LVM), and left ventricular mass index (LVMI) (P=0.0001). Duration of obesity and LVM had a moderate, positive correlation (r=0.407).Conclusion There is significantly higher LVM in the obese group than in the normal weight group. The duration of obesity had a moderate, positive correlation to LVM.

Abstract 30: 4-PBA Prevents TAC-induced Myocardial Hypertrophy and Interstitial Fibrosis by Attenuating ER Stress in Mice

Background: Recently, 4-phenylbutyric acid (4-PBA) has been recognized as a potent ER stress inhibitor and a histone deacetylase inhibitor, but its therapeutic effect in cardiovascular diseases is still not fully understood. Our previous study indicated that attenuation of ER stress by administration of low dosage of 4-PBA (20 mg/kg/d) prevented post-infarction-induced cardiac rupture and remodeling through modulating both cardiac apoptosis and fibrosis in the mouse model of myocardial infarction. However, little is known whether the administration of 4-PBA is effective for hypertrophic heart disease. The aim of this study is therefore to test the therapeutic effect of 4-PBA on pressure-overload induced myocardial hypertrophy. Methods and Results: Transverse aortic constriction (TAC) was used to produce pressure-overload in C57BL/6 male mice for 4 weeks. After surgery, 4-PBA (20mg/kg/d) or 0.9% NaCL was intraperitoneally injected daily. At the end of 4 weeks, the survivals were underwent high-resolution echocardiographic imaging observation. The results showed that the left ventricular posterior wall thickness at end systole (LVPWs) and left ventricular posterior wall thickness at end diastole (LVPWd) were increased in TAC group. Administration of 4-PBA ameliorated this hypertrophic effect. Autopsy also confirmed the anti-hypertrophic effect of 4-PBA. Masson-staining found that there was no difference in perivascular fibrosis between TAC and TAC+4-PBA groups. However, myocardial interstitial fibrosis and collagen deposition were significant decreased by 4-PBA. We finally detected the ER stress and histone acetylation using western blotting. Our results showed that 4-PBA, at the dosage of 20 mg/kg/day, decreased the expression of CHOP and had no effect on histone 3 acetylation. Conclusion: These findings indicate that attenuating ER stress by 4-PBA maybe a promising therapeutic strategy to prevent pressure-overload induced myocardial hypertrophy and interstitial fibrosis.

Expression of connective tissue growth factor in cardiomyocyte of young rats with heart failure and benazepril intervention

Ventricular remodeling is an important pathologic progress in almost all end stage heart failure (HF), and it is characterized by ventricular thickening and cardiac fibrosis with poor prognosis. The connective tissue growth factor (CTGF), a new growth factor with multi-function, has an important role in fibrosis of tissue and organs. It has been demonstrated that angiotensin-converting enzyme inhibitor (ACEI) can prevent the development of cardiomyocyte from remodeling and improve cardiac function. Researchers try to test the hypothesis that cardiac function improvement attributable to ACEI is associated with inhibiting expression of CTGF in patients with HF. The aim of this study was to observe changes in CTGF expression in cardiomyocyte of young rats with HF and effect of benazepril on CTGF. The animal model of HF was established by constriction of abdominal aorta. Five weeks old rats were randomly divided into 3 groups after 6 weeks of operation: (1) HF group without treatment (n = 15); (2) HF group where rats were treated with benazepril (n = 15); (3) sham-operated group (n = 15) where rats were administered benazepril through direct gastric gavage. After 4 weeks of treatment, the high frequency ultrasound was performed. The expression of CTGF was detected by immunohistochemistry and semi-quantative reverse transcription-polymerase chain reaction. Compared with the sham-operated group, left ventricular diastolic dimension (LVEDD), left ventricular systolic dimension (LVESD), interventricular septal thickness at end-diastole (IVSTd), interventricular septal thickness at end-systole (IVSTs), left ventricular posterior wall thickness at end-diastole (LVPWTd), left ventricular posterior wall thickness at end-systole (LVPWTs), left ventricular relative weight (LVRW), and right ventricular relative weight (RVRW) were all increased (P < 0.01), but ejection fraction (EF) and fractional shortening (FS) were decreased (P < 0.01). CTGF positive cells and expression of CTGF mRNA (0.609 +/- 0.065 vs 0.117 +/- 0.011, P < 0.01) were increased in HF group without treatment. LVESD, IVSTd, IVSTs, LVPWTd, LVPWTs, LVRW and RVRW were all decreased (P < 0.01), but FS and EF were increased (P < 0.01) in cases of HF treated with benazepril when compared with HF group without treatment. LVESD, IVSTd, IVSTs, LVPWTd, LVPWTs, LVRW and RVRW were higher (P < 0.01), EF and FS were lower (P < 0.01), CTGF positive cells and expression of CTGF mRNA were higher (P < 0.01) in HF group treated with benazepril than those of sham-operated group. The expression of CTGF was increased in the cardiomyocyte of young rats with HF and benazepril could prevent left ventricular from remodeling partly and improve cardiac function by inhibiting the expression of CTGF in cardiomyocyte in cases of HF.

M‐MODE ECHOCARDIOGRAPHIC PARAMETERS AND INDICES IN THE NORMAL GERMAN SHEPHERD DOG

M-mode echocardiographic measurements were made from 50 healthy German Shepherd dogs (30 males and 20 females). The dogs were awake and unsedated, in right lateral recumbent position. The following parameters were measured on the echocardiographic images: interventricular septal thickness at end-diastole (IVSd), interventricular septal thickness at end-systole (IVSs), left ventricular internal dimension at end-diastole (LVIDd), left ventricular internal dimension at end-systole (LVIDs), left ventricular posterior wall thickness at end-diastole (LVPWd), left ventricular posterior wall thickness at end-systole (LVPWs), left atrial dimension (LAD), aortic root dimension (AOD), left atrial to aortic root ratio (LAD/AOD), right ventricular internal dimension at end-diastole (RVID), amplitude of mitral valve excursion (DE amplitude), velocity of mitral valve opening (D-E slope), and velocity of mitral valve closure (E-F slope). Fractional shortening (FS) was also calculated. The effect of gender and age on each echocardiographic parameter was analyzed and the relationship between body weight (BW) and each parameter was also investigated. There was a significant relationship between gender and LVPW in systole and diastole and FS. Significant association was also found between BW and IVS, LVID, and LVPW in systole and diastole, FS, LAD, AOD, RVID, DE amplitude, and D-E slope of the mitral valve.

Heart dimensions may influence the occurrence of the heart rate deflection point in highly trained cyclists.

OBJECTIVES: To determine whether the heart rate (HR) response to exercise in 21 highly trained cyclists (mean (SD) age 25 (3) years) was related to their heart dimensions. METHODS: Before...

Changes in left ventricular dimensions after pulmonary artery banding and Jatene operation in children with complete transposition of the great arteries. Echocardiographic study.

Echocardiographic left ventricular (LV) dimensions in patients with complete transposition of the great arteries (TGA's) were measured before and after the Jatene procedure and/or pulmonary artery banding (PAB). The LV posterior wall thickness at end-diastole (LVPWTD) increased from 3.5 +/- 0.4 to 4.9 +/- 0.9 mm (mean +/- 1SD) (p less than 0.01) after PAB, but it did not show a significant change following the Jatene procedure (from 4.5 +/- 1.0 to 5.3 +/- 0.8 mm). The LV end-diastolic internal dimension (LVIDD) increased from 17.7 +/- 4.0 to 22.6 +/- 6.5 mm after PAB (p less than 0.01), but remained unchanged after the Jatene procedure (from 24.5 +/- 5.0 to 25.0 +/- 3.0 mm). The LV shortening fraction (LVSF) decreased from 0.62 +/- 0.10 to 0.47 +/- 0.14 after PAB (p less than 0.01), but remained unchanged after the Jatene procedure (0.40 +/- 0.10 to 0.37 +/- 0.10). the a/b ratio at end-systole: (a/b)s, which indicates the flatness of the LV configuration, increased from 0.27 +/- 0.14 to 0.60 +/- 0.21 after PAB (p less than 0.01) and from 0.61 +/- 0.13 to 0.74 +/- 0.17 after the Jatene procedure (p less than 0.01). The data obtained became stable 1 month after operation. One patient died of low cardiac output with no evidence of myocardial infarction after the Jatene procedure. In this patient, LVPWTD was 5.7 mm, LVIDD was 26 mm, LVSF was 0.71 and the (a/b)s ratio was 0.55.(ABSTRACT TRUNCATED AT 250 WORDS)