Analysis Of Echocardiographic Parameters Research Articles

Realistic Aspects of Cardiac Ultrasound in Rats: Practical Tips for Improved Examination.

Echocardiography is a reliable and non-invasive method for assessing cardiac structure and function in both clinical and experimental settings, offering valuable insights into disease progression and treatment efficacy. The successful application of echocardiography in murine models of disease has enabled the evaluation of disease severity, drug testing, and continuous monitoring of cardiac function in these animals. However, there is insufficient standardization of echocardiographic measurements for smaller animals. This article aims to address this gap by providing a guide and practical tips for the appropriate acquisition and analysis of echocardiographic parameters in adult rats, which may also be applicable in other small rodents used for scientific purposes, like mice. With advancements in technology, such as ultrahigh-frequency ultrasonic transducers, echocardiography has become a highly sophisticated imaging modality, offering high temporal and spatial resolution imaging, thereby allowing for real-time monitoring of cardiac function throughout the lifespan of small animals. Moreover, it allows the assessment of cardiac complications associated with aging, cancer, diabetes, and obesity, as well as the monitoring of cardiotoxicity induced by therapeutic interventions in preclinical models, providing important information for translational research. Finally, this paper discusses the future directions of cardiac preclinical ultrasound, highlighting the need for continued standardization to advance research and improve clinical outcomes to facilitate early disease detection and the translation of findings into clinical practice.

CLINICAL-ANAMNESTIC AND ECHOCARDIOGRAPHIC MARKERS OF NEONATAL SEPSIS AT DIFFERENT GESTATION AGE OF NEWBORN

neonatal sepsis remains one of the leading causes of morbidity and mortality in the neonatal age. The involvement of the myocardium in sepsis remains insufficiently studied, in particular in neonatology, where issues of myocardial dysfunction in neonatal generalized infection seem even more controversial, especially in neonatal sepsis at different gestational terms. Objective. To study specific clinical and anamnestic and echocardiographic parameters in infants depending on gestational age for optimization of the prognosis in neonatal sepsis. Material and research methods. To achieve this goal, we observed 57 newborns with a verified diagnosis of "Neonatal sepsis". Group I (23 patients – 40.3%) included newborns with a gestational age of 37-42 weeks, Group II – 34 premature infants (59.7%) with a gestation of up to 36 weeks. The latter group, depending on the gestational age, was divided into IIA subgroup, which was formed by 21 prematurely born patients with NS with a gestational age of 32-36 weeks, and the IIB subgroup – 13 newborns born before 32 weeks of gestation. Research results. The analysis showed that the severity of the impairment in the general condition of the examined newborns general condition was assessed as severe in 47.8% of newborns of group I, in 88.2% of cases in group II (PI: II <0.05), in 85.7% of representatives of subgroup IIA (PI: IIA <0.05) and in 92.3% of children of subgroup IIB (PI: IIB <0.001). It is shown that every third child (30.4%) of group I, 67.6% of newborns of group II (PI: II <0.05), half (52.4%) of the representatives of subgroup IIA (PII: IIA <0.01) and all seriously ill patients (92.3%) of subgroup IIB (PI: IIB, IIA: IIB <0.05) required cardiopulmonary resuscitation in the delivery room. Thus, in relation to full-term patients, the risk of this significant postnatal factor of emergency is likely to increase: for group II: OR - 4.77 (95% CI 2.63-8.68), RR - 2.17 (95% CI 1.57-3.0), AR = 0.37; and for premature babies with a gestational age of less than 32 weeks (IIB subgroup), respectively: OR – 27.44 (95% CI 11.73-64.19), RR – 7.55 (95% CI 5.58-10.21 ), AR – 0.65. The correlation analysis showed that in premature infants suffering from NS, the increase in the functional capacity of the left ventricular myocardium was associated with the female sex (for EF r = 0.94, P = 0.0001, for FS - r = 0, 94, P = 0.0001) and the number of days of inotropic support (for EF r = 0.68, P = 0.043, for FS - r = 0.71, P = 0.03). Conclusions. The analysis of echocardiographic parameters in the group of premature infants revealed a direct correlation between the ejection fraction and cardiovascular resuscitation immediately after birth (r = 0.64) and the duration of inotropic drugs (r = 0.68).

Abstract 14673: Cardiomyocyte Specific Overexpression of Pellino 1 Reverses Sepsis Induced Cardiac Dysfunction in a Murine Model by Reducing Inflammatory Response and Cardiac Cell Death

Introduction: Sepsis remains a significant cause of mortality in the intensive care unit till today. Recent research suggests nearly one in four deaths in people with heart failure is caused by sepsis. Overexpression of mammalian Pellino-1 (Peli1), a E3 ubiquitin ligase, causes inhibition of apoptosis, oxidative stress, and preservation of cardiac function in a myocardial infarction model. Therefore, in the present study, we explored the possibility to overcome sepsis mediated heart failure by overexpressing Peli1 (AMPEL1Tg/+) in a mouse model of severe sepsis. Methods: C57BL/6J (WT) and AMPEL1 Tg/+ mice were divided into Wild-type sham (WTS), Wild-type Cecal Ligation and Puncture (WTCLP), AMPEL1 Tg/+ sham (AMPEL1 Tg/+ S) and AMPEL1 Tg/+ CLP. Cardiac function (LVEF, FS) by two-dimensional echocardiography was assessed pre-procedure, at 6, and 24 hours post-surgery. Serum IL-6 and TNF-alpha (ELISA) at 6 hours and cardiac apoptosis (TUNEL assay) at 24 hours were measured. Results are expressed as mean ± SEM. Results: Analysis of echocardiographic parameters (EF, FS) preoperatively and among the sham groups were similar however there was significant preservation of post-procedure LVEF (%) in the AMPEL1 Tg/+ CLP at the 6 hour (AMPEL1 Tg/+ :52.7 ± 3.71 vs WT:40.7 ±2.46, p=0.013, n=10-11) and 24-hour time point (AMPEL1 Tg/+ :63.1 ± 1.63 vs WT:49.3 ± 4.41, p=0.002, n=9-11) compared to WT. Similar trend was observed in estimation of FS (%) at 6 hours (AMPEL1 Tg/+ :26.3 ± 2.22 vs WT:19.3 ±1.37, p=0.014, n=10-11) and 24 hours (AMPEL1 Tg/+ :32.4 ± 1.89 vs WT:24.4 ± 2.67, p=0.031, n=9-11). A marked decrease in serum IL-6 (AMPEL1 Tg/+ :259.7 ± 18.70 vs WT:483.2 ± 24.01, p<0.0001, n=6, pg/mL) and TNF-alpha (AMPEL1 Tg/+ :86.89 ± 14.36 vs WT:161.8 ± 20, p=0.012, n=6, pg/mL) was observed in the AMPEL1 Tg/+ CLP at 6 hours. The preserved cardiac function in CLP was further supported by a noticeable decrease in cardiac apoptosis (% TUNEL positive cells) at 24 hours in the AMPEL1 Tg/+ CLP group (4.7 ± 0.94 vs 11.7 ± 2.82, p=0.040, n=6,) compared to WTCLP. Conclusions: Thus, Peli1 overexpression is a novel approach that preserved cardiac function, reduced inflammatory markers, and apoptosis following severe sepsis in a murine genetic model.

Towards standardization of echocardiography for the evaluation of left ventricular function in adult rodents: a position paper of the ESC Working Group on Myocardial Function

Echocardiography is a reliable and reproducible method to assess non-invasively cardiac function in clinical and experimental research. Significant progress in the development of echocardiographic equipment and transducers has led to the successful translation of this methodology from humans to rodents, allowing for the scoring of disease severity and progression, testing of new drugs, and monitoring cardiac function in genetically modified or pharmacologically treated animals. However, as yet, there is no standardization in the procedure to acquire echocardiographic measurements in small animals. This position paper focuses on the appropriate acquisition and analysis of echocardiographic parameters in adult mice and rats, and provides reference values, representative images, and videos for the accurate and reproducible quantification of left ventricular function in healthy and pathological conditions.

Prognostic role of p53 gene polymorphism in risk assessment of anthracycline-induced cardiotoxicity

To study the prognostic significance of polymorphism of the p53 gene (polymorphism Arg72Pro exon 4, rs1042522) on the development of cardiotoxic remodeling of the left ventricle and heart failure. A total of 176 women with breast cancer who received anthracycline antibiotics as part of polychemotherapeutic treatment regimens were examined. Based on the results of the survey, 12 months after the end of polychemotherapy, patients in the remission of the underlying disease were divided into 2 groups: patients with cardiotoxic remodeling (52 patients) and women with preserved heart function (124 patients). All patients before the start of the course of chemotherapy, in the dynamics of treatment with anthracyclines and after therapy with such were carried out the study of echocardiographic parameters. All the patients were taken genetic material, followed by typing alleles of the gene for the protein p53 (rs1042522). Analysis of echocardiographic parameters in patients 12 months after the completion of polychemotherapy in comparison with those before treatment showed a significant difference in the final systolic (33 mm [31; 35] and 28 mm [26; 31], p<0.00001) and terminal diastolic dimensions (51 mm [49; 54.5] and 44 mm [42; 48.5], p=0.0003), as well as a significant decrease in the left ventricular ejection fraction (54.5% [51.5; 58] and 65.5% [62; 70], p<0.00001) in the group of women with developed anthracycline cardiotoxicity. The presence of the Arg/Arg genotype was associated with the development of cardiotoxic myocardial damage during polychemotherapy (OR=3.86, 95% C.I.=1.45-10.26, p=0.005). The Pro/Pro genotype has proved to be a protective factor (OR=0.26, 95% C.I.=0.09-0.69, p=0.015). The conclusion. Predicting the cardiotoxicity of chemotherapy using the polymorphism of the p53 gene is an effective measure of early pre-symptom diagnosis of an increased risk of anthracyclineinduced cardiotoxicity.

Exercise-induced in Secondary Mitral Regurgitation: Analysis of Echocardiographic Parameters at Rest Predicting the Onset of Significant Exercise-induced Mitral Regurgitation

Exercise-induced in Secondary Mitral Regurgitation: Analysis of Echocardiographic Parameters at Rest Predicting the Onset of Significant Exercise-induced Mitral Regurgitation

Preventive use of carvedilol for anthracycline-induced cardiotoxicity: asystematic review and meta-analysis of randomized controlled trials.

Clinical or subclinical cardiotoxicity is aconcern for cancer patients receiving anthracycline-based chemotherapy. Carvedilol is promising for preventing anthracycline-induced cardiotoxicity (AIC). This review appraised the preventive effects of carvedilol against AIC based on randomized controlled trials (RCTs). The Cochrane Collaboration Central Register of Controlled Trials, PubMed, and Embase databases were searched from inception to March27, 2018. RCTs using carvedilol for the prevention of AIC were selected. Risk of bias and methodological quality were assessed. Meta-analysis was conducted, when applicable, for the trial endpoints; otherwise the data were analyzed descriptively. Nine RCTs comprising 717 patients were selected. The risk of bias was unclear and the methodological quality differed substantially. Data pooling of five eligible studies indicated no decreased mortality in patients receiving carvedilol (risk difference = -0.02, 95% CI: -0.07-0.04, p = 0.57, I2 = 44%). The impact on the incidence of left ventricular systolic dysfunction (LVSD) was inconsistently reported but meta-analysis was not applicable due to discordant LVSD definitions. Data pooling of eightstudies and asubgroup analysis indicated ahigher left ventricular ejection fraction (LVEF) with substantial heterogeneity in the carvedilol group (mean difference [MD] = 5.23, 95% CI: 2.20-8.27, p = 0.0007, I2 = 95%, and MD = 4.65, 95% CI: 0.67-8.64, p = 0.02, I2 = 90%, respectively). Further analysis of echocardiographic parameters and biomarkers showed weak evidence of improvement in diastolic function and troponinI level by carvedilol administration. Preventive use of carvedilol in patients undergoing anthracycline-based chemotherapy may be associated with areduced incidence of LVSD, higher LVEF value, better diastolic function, and lower troponinI level. RCTs with larger sample size and longer follow-up are needed to verify these findings.

Assessment of left ventricular filling pressure and its correlation with severity of chronic kidney disease

Aims: This study was aimed to assess the left ventricular filling pressure (LVFP) and its relationship with severity of chronic kidney disease (CKD). Methods: One hundred CKD patients were subjected to standard echocardiography and the new modality of tissue Doppler imaging. The LVFP is calculated with E/e' ratio (early diastolic mitral inflow velocity – E to early diastolic mitral annulus velocity – e'). All these patients were divided into five subgroups depending on their estimated glomerular filtration rate (eGFR: ml/min/body surface area). Results: The analysis of echocardiographic parameters (E and e') showed that in CKD patients, the stage of renal failure was associated with the significant increase in LVFP with P

THE ROLE OF POLYMORPHIC VARIANTS OF NO-SYNTHASE, RECEPTOR ENDOTHELIN-1 AND NADPH-OXIDASE IN THE DEVELOPMENT OF HEART FAILURE RESULTED FROM CHEMOTHERAPY-INDUCED CARDIOTOXICITY

Aim. To study the clinical and genetic aspects of the influence of polymorphic variants of the genes of endothelial NO-synthase (NOS3), the receptor of endothelin-1 type A (EDNRA) and NADPH-oxidase on the development of cardiotoxic remodeling of the left ventricle and heart failure during anthracycline-based regimens for patients with breast cancer.Methods. 176 women with breast cancer receiving anthracycline antibiotics as part of multiple drug chemotherapy regimens were examined. According to the results of the examination, 12 months after the end of multiple drug chemotherapy, all the patients with the main disease in remission were divided into 2 groups: patients with cardiac remodeling caused by cardiotoxicity (Group 1 = 52) and those with preserved heart function (Group 2 = 124). All patients underwent echocardiographic assessment before chemotherapy, during the treatment regimen with anthracyclines and after the therapy. Genetic material (buccal cells) was collected from all patients for the subsequent typing of alleles of genes NOS3 (rs1799983), EDNRA (rs5335) and NADPH-oxidase (rs4673).Results. Analysis of echocardiographic parameters in patients 12 months after the completion of multiple drug chemotherapy in comparison with those before treatment showed a statistically significant difference between end-systolic and end-diastolic dimensions, as well as a significant reduction in the left ventricular ejection fraction in the group of women who developed cardiotoxicity with anthracycline cardiotoxicity. An association between the development of cardiotoxic lesions with the presence of mutant allele of NOS3 rs1799983 and NADPH-oxidase rs4673 genes has been determined. The presence of the T/T genotype of the NOS3 rs1799983 gene was associated with myocardial damage during multiple drug chemotherapy, along with the T/T genotype of the NADPHoxidase gene rs4673. Importantly, the genotype G/G of the gene NOS3 rs1799983 was more frequently determined in Group 2, suggesting its protective effect against cardiotoxic myocardial damage.Conclusion. The development of the strategy aimed at preventing or reducing the risk of cardiovascular complications in the treatment of cancer is a crucial problem. Genetic typing is an effective measure to predict the increased risk of cardiotoxic effects of anthracyclines.

Prevalence and echocardiographic predictors of atrial fibrillation in patients with heart failure with preserved ejection fraction

Aim. To study the occurrence of atrial fibrillation (AF) in patients with normal ejection fraction heart failure (NEJHF) without AF in anamnesis, and to perform comparative analysis of echocardiographic parameters with the parameters of patients with NEJHF and known AF, as to study independent predictors of AF occurrence in NEJHF. Material and methods. Totally, 182 patients included (105 women) with metabolic syndrome and NEJHF (II-III functional classes by NYHA) at the age 63±12 y. o., with sinus rhythm and no anamnesis of AF (n=118), and with paroxysmal AF (PxAF) in anamnesis (n=28) or persistent (PeAF) in anamnesis (n=36). Results. Among 118 patients with AF in anamnesis, in 49 (41,5%) during 3 years of follow-up, there were cases of PeAF and PxAF. Patients without AF in anamnesis had better relations for left and right ventricles filling comparison (E/e`) under load, index of maximum left atrium volume (LA) (IVLAmax), systolic pressure in pulmonary artery (SPPA) during rest and after exertion, than patients with known episodes of PeAF and PxAF. Patients with PeAF had significantly higher values of the index of post systolic shortening of the left ventricle, rigidity index of LA, IVLAmax, E/e` of RV, interatrial mechanical asynchrony and low values of longitudinal deformation of the LA (LDLA) and velocity parameters of LDLA (VPLDLA). Female sex, systolic arterial pressure, SPPA, IVLAmax, E/e` in load, E/e` of RV, LDLA, longitudinal deformation of the left ventricle and VPLDLA were independent predictors of AF. Conclusion. Increased rigidity, parameters of longitudinal deformation and the volume of LA, as interatrial mechanical asynchrony are strong independent predictors of AF in NEJHF.

Rheumatic Aortic Valve Disease with Mitral Stenosis—A Case Report

Congenitally malformed aortic valves are more susceptible to valve injury due to rheumatic fever, mechanical stress of altered flow patterns, atherosclerotic risk factors and degenerative changes. Rheumatic involvement usually occurs in childhood and it is progressive leading to diffuse thickening and fibrosis at leaflet edges and thus differentiated from other patterns of valve damage. Background of this case report revealed the bicuspid nature of the aortic valve due to rheumatic commissural fusion and analysis of echocardiographic parameters in combined lesions of both aortic and mitral valves with severe LV (left ventricular) dysfunction. Left ventricular (LV) and left atrial (LA) dilations predisposing to the formation of smoke (SEC-spontaneous echo contrast) in LV and LA as a consequence of mitral and aortic valve disease are illustrated by 2D echocardiographic imaging in this 41-year-old male.

Induction of cardiac fibrosis and transforming growth factor-β1 by motorcycle exhaust in rats

Motorcycle exhaust (ME) is a major source of air pollution and a potential health hazard in urban areas where motorcycles are a popular means of transportation. The main objectives of this study were to determine the ability of ME to cause cardiotoxicity in rats and investigate the possible mechanisms of toxicity. Male rats were exposed to 1:10 diluted ME by inhalation 2 h daily and Monday through Friday for 8 weeks. Exposure to ME increased heart weight and decreased cardiac antioxidant enzymes glutathione S-transferase (GST), superoxide dismutase and glutathione peroxidase activities in a concentration- and time-dependent manner. Analysis of echocardiographic parameters indicated that ME increased left ventricle posterior wall thickness, interventricular septum thickness and left ventricle mass. Histopathological examinations of the hearts revealed that ME exposure caused focal cardial degeneration and necrosis, mononuclear cell infiltration, and fibrosis. The results of reverse transcriptase-polymerase chain reaction studies showed that ME decreased GST-M1 and GST-P1 mRNA expression and increased the expression of proinflammatory cytokine interleukin-1β, hypertrophy marker atrial natriuretic peptide, fibrosis markers type I and III collagen, profibrotic cytokine connective tissue growth factor, and hypertrophy and fibrosis mediator transforming growth factor (TGF)-β1 in the heart. The data of Western blot analysis showed that cardiac TGF-β1 protein was induced by ME. These findings demonstrate that subchronic ME exposure caused hypertrophy and fibrosis, and modulated GST and TGF-β1 expression in rat heart possibly by mechanisms involving oxidative stress and inflammation.