Left Ventricular Internal Diameter Research Articles

CARDIOVASCULAR OUTCOMES IMPROVE IN CHILDREN WITH RENOVASCULAR HYPERTENSION FOLLOWING ENDOVASCULAR AND SURGICAL INTERVENTIONS

Objective: Renovascular hypertension (RVH) is a common cause of hypertension in children. It is caused by renal artery stenosis reducing the blood supply to the renal parenchyma and activating the renin-angiotensin-aldosterone axis, often leading to cardiac remodelling. This is a longitudinal observational study that aims to describe the occurrence of hypertensive changes and their severity and also any improvement in cardiac remodelling after successful endovascular and/or surgical intervention in children with RVH. Design and method: All patients with RVH referred to our centre, who had received at least one endovascular intervention, were included. Data was collected by retrospective database review over a 22-year period. We assessed oscillometric blood pressure as well as eight echocardiographic parameters pre- and post-intervention: intraventricular septal diameter (IVSD), posterior wall diameter (PWD), left ventricular internal diastolic diameter (LVIDD), fractional shortening (FS), Relative Wall Thickness (RWT), Left Ventricular Mass (LVM) and Left Ventricular Ejection Fraction (LVEF). Results: 152 patients met inclusion criteria and had on average two endovascular interventions. Six children presented in frank heart failure. 54.4% achieved normal blood pressure (BP) control after intervention. Average z-scores improved in IVSD, PWD and FS; LVMI and RWT also improved. PWD saw the greatest reduction in mean difference in children with an abnormal (z-score reduction of 0.25, p<0.001) and severely abnormal (z-score reduction of 0.23, p<0.001) z-scores between pre- and post-intervention echocardiograms. 45.9% of children had a reduction in prescribed antihypertensive medications. Conclusions: Our study reports improvement in cardiac outcomes after either endovascular or surgical intervention. This is evidenced on BP control and echocardiogram changes in which almost half achieved normalisation in systolic BP readings and reduction in the number of children with abnormal echocardiographic parameters.

FIRST COMPREHENSIVE ECHOCARDIOGRAPHIC ASSESSMENT IN PATIENTS WITH VASCULAR EHLERS-DANLOS SYNDROME WITH OR WITHOUT CELIPROLOL THERAPY AT THE MAXIMUM RECOMMENDED DOSE

Objective: Vascular Ehlers-Danlos syndrome (vEDS) is an inherited connective tissue disorder characterized by arterial fragility. Celiprolol is a beta1-adrenoceptor antagonist with partial beta2 agonist activity that has been shown to reduce rates of vascular events in this setting, though the underlying mechanisms are not yet fully understood. Moreover, few data on echocardiographic assessment are available in patients with vEDS. Design and method: Twenty patients with genetically confirmed diagnosis of vEDS followed at our Institution were divided into two groups (10 patients each) according to whether or not they were on celiprolol therapy at the maximum recommended dose (400 mg daily) for at least 12 months. Both groups were compared to 10 healthy individuals matched for sex, age, body mass index (BMI), and office blood pressure values. Each participant underwent transthoracic echocardiography with tissue Doppler analysis for a comprehensive evaluation of cardiac structure and function. Results: Mean age was 35 years and mean BMI was 21.6 kg/m2. Female sex was prevalent (60%). Left ventricular (LV) internal diameter values tended to be lower in patients with untreated vEDS than in healthy controls, though this difference was not statistically significant (4.33 vs 4.74 cm, respectively; p=0.053). Similar data were observed for LV mass index (56.9 vs 68.6 g/m2; p=0.093), stroke volume (56.6 vs 71.6 mL; p=0.068), and E/A ratio (1.26 vs 1.66; p=0.082), whereas an opposite trend was observed for e’ lateral (13.2 vs 12.2; p=0.096). No statistically significant difference was found between groups in terms of other parameters of LV mass, systolic and diastolic function. A normal LV geometry was found in all the cases. Indices of mechano-energetic efficiency and ventricular-arterial coupling were also similar between groups. No patient presented with aortic root dilation, mitral valve prolapse, valve insufficiency of more than mild degree, or valve stenosis of any degree. Conclusions: Our study suggests that patients with vEDS have normal cardiac mass and geometry, as well as normal systolic and diastolic function. Celiprolol therapy does not seem to significantly influence such aspects. Future studies on larger cohort of patients should confirm these aspects.

Sex Differences in Temporal Regulation of Piezo1 in Resiquimod Accelerated Systemic Lupus

Lupus disproportionally affects women (9:1), particularly women of color, but men with this disease often have more pronounced symptoms than their female counterparts. Individuals with lupus are anywhere from two to fifty times as likely to experience a cardiovascular (CV) event than the rest of the population. Though such complications are widely known, the mechanisms these disease processes are unknown. One well established pathogenesis of many CV diseases stems from an alteration of mechanical forces. The cation channel, Piezo1, is a mechanosensitive channel and is known to play a critical role in CV diseases like heart failure. Therefore, we hypothesized that inducing lupus-associated cardiac pathology in a lupus-prone mouse model would increase the expression of Piezo1. To investigate this, lupus-prone female and male B6.Nba2 mice aged 10-14 weeks were subjected to Resiquimod (R848; a TLR7/8 agonist;100μg/30μl) treatment or acetone vehicle twice a week for four weeks. Echocardiograms were performed every four weeks. Mice were sacrificed and their tissues harvested at 4- and 16-weeks after the start of R848 treatment. Piezo1 levels were subsequently analyzed in the heart by real time quantitative polymerase chain reaction (RTqPCR), immunoblot, and immunofluorescent staining. By echocardiography, female mice treated with R848 showed an increase in left ventricle (LV) wall thickness was seen at four weeks, followed by an increase in internal diameters over the following 12 weeks, culminating in cardiac dysfunction by 16 weeks via significantly decreased ejection fraction (EF; p<0.05) Interestingly, males showed no such cardiac dysfunction at any timepoint. By RTqPCR, female Piezo1 levels were higher overall than their male counterparts (p<0.05). Cardiac Piezo1 gene expression at 4 weeks was shown to be decreased in the R848-treated groups of both sexes. At 16 weeks, this trend was reversed in both male and female mice, showing R848-treatment induced an an upregulation of cardiac Piezo1 compared to each sex’s respective vehicle controls. Interestingly, while Piezo1 protein expression followed the same 4-week trend of downregulation in R848-treated mice regardless of sex, protein expression in the female R848-treated heart continued in a trending increase at the 16-week timepoint, while the male R848 heart showed unchanged. We found that this increase in cardiac Piezo1 in female, R848-treated is significantly correlated with higher left ventricular internal diameters (both LV-EDV (p<0.05) and -ESV (p<0.01)). This data demonstrates a sex difference phenotype in lupus-associated murine cardiac dysfunction, potentially through a Piezo1-mediated pathway. Further investigation is warranted to elucidate the Piezo1-dependent mechanisms involved in lupus-associated cardiovascular disease. Veterans Affairs Biomedical Laboratory Research & Development Career Development Award (CDA-2) 1IK2BX005605-01 to J.P.V.B, Medical University of South Carolina College of Medicine Program Project Grant to and J.P.V.B., and Medical University of South Carolina Core Centers for Clinical Research Project Award P30AR072582 to M.A.C and J.P.V.B. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Pulmonary-vein-to-pulmonary-artery ratio can be utilized to evaluate myxomatous mitral valve disease progression in dogs.

To evaluate the diagnostic value of pulmonary-vein-to-pulmonary-artery ratio (PV:PA) in dogs with myxomatous mitral valve degeneration (MMVD), classified according to the American College of Veterinary Internal Medicine (ACVIM) consensus guidelines. 80 client-owned dogs with either MMVD (n = 65) or no cardiovascular disease (control group; n = 15) between August 5, 2020, and July 19, 2023. This is a retrospective study. Dogs with MMVD were classified according to ACVIM consensus guidelines. Echocardiograms, thoracic radiographs, and other measurements needed in this study were reviewed in all dogs. Spearman correlation was used to determine the correlation between the PV:PA and the following variables: vertebral heart size, vertebral left atrial size, left-atrium-to-aorta ratio, normalized left ventricular internal diameter, and peak transmitral early diastolic velocity. Receiver operating characteristic (ROC) curve analysis was used to evaluate the value of PV:PA in distinguishing between stages B1 and B2 and stages B2 and C. All conventional indices showed correlations with PV:PA. The area under the ROC curve (AUC) for stages B1 and B2 was 0.83, and the cutoff value for differentiating stage B2 was 1.52. The AUC for stages B2 and C was 0.81, and the cutoff value for differentiating stage C was 2.09. PV:PA was significantly different between control and the stage B1 group, stage B1 and B2 group, and stage B2 and C group. PV:PA can be an index that can be used in evaluating MMVD dogs.

Two-dimensional speckle-tracking echocardiography in left ventricular systolic function in patients with systemic lupus erythematosus.

To investigate whether two-dimensional speckle-tracking echocardiography (2DSTE) can be considered a criterion for early left ventricular (LV) systolic impairment in patients with systemic lupus erythematosus (SLE) and to further explore the association with each other. We included 38 patients with SLE and assessed the degree of disease activity according to the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) 2000 scoring criteria, together with 38 healthy controls who were matched by sex and age. Routine LV systolic function evaluation parameters were obtained by echocardiography as well as 2DSTE measurement of LV strain parameters to obtain global longitudinal strain (GLS) values, respectively. (I) On routine LV function parameters such as ejection fractions (EF) and left ventricular end-diastolic internal diameter (LVIDd), the SLE group and the control group did not reflect differences. In contrast, on the LV strain parameter obtained from 2DSTE measurements, the GLS values in all cardiac planes were lower in the SLE group than in the control group and showed statistically significant differences. (II) Correlation analysis showed that there was a correlation between SLEDAI and GLS, especially a meaningful correlation with GLS Avg and GLS A4C, with correlation coefficients of 0.35 and 0.47, respectively. The use of 2DSTE can detect early impaired LV systolic function in SLE patients, and GLS is progressively gaining attention as an indicator of subclinical myocardial injury and LV function in SLE patients. The correlation that exists between GLS and SLEDAI might contribute to a better assessment of cardiac involvement in SLE patients. Key Points • Cardiac involvement has become one of the major factors in the poor prognosis of SLE patients, which directly affects the mortality of SLE patients. Traditional echocardiography is difficult to detect early left ventricular function impairment, thus affecting clinicians' judgment and diagnosis. • 2DSTE can recognize subclinical myocardial injury in SLE patients at an early stage, and its derived strain parameters may be used as an indicator to evaluate myocardial involvement and reflect disease activity in SLE patients.

Percutaneous Coronary Intervention as a Non-Surgical Treatment for Ischemic Mitral Regurgitation in Patients with Multi-Vessel Coronary Artery Disease.

BACKGROUND Multi-vessel coronary artery disease (MVD) represents a severe type of coronary artery disease (CAD). Ischemic mitral regurgitation (IMR) is a common mechanical complication in patients with CAD. This study aimed to retrospectively investigate the efficacy of percutaneous coronary intervention (PCI) on moderate/severe IMR in patients with MVD. MATERIAL AND METHODS Clinical data were collected from 15 patients who underwent successful treatment for MVD combined with moderate/severe IMR through the PCI procedure and achieved complete revascularization between January 2014 and December 2022. Cardiac structural and functional parameters were assessed through echocardiographic evaluations. Color flow recordings of MR jets were obtained through an enlarged view of the 4-chamber cut, and the diagnosis of MR was categorized into mild (<4 cm²), moderate (4-8 cm²), and severe (>8 cm²), based on the MR area. RESULTS The common features of the selected cases were advanced age, low body weight, and renal insufficiency. Cardiac echocardiography revealed an augmentation in the left atrial anteroposterior diameter and left ventricular internal diameter at end-systole after PCI, while the left ventricle internal diameter in diastole, left ventricular ejection fraction, and left ventricular fractional shortening were comparable to preoperative values. All patients had moderate/severe MR preoperatively, and MR improved at 1 month (2.73±0.69) and 12 months (2.26±0.58) after PCI. CONCLUSIONS In cases of MVD accompanied by moderate/severe IMR, undergoing PCI can spare certain elderly patients with low body weight and renal insufficiency from high-risk surgery, alleviating the severity of MR without undergoing mitral valve intervention.

Diagnosis and treatment of feline persistent ductus arteriosus: a retrospective evaluation of 17 cats

The objective of this study was to evaluate the signalement, clinical features, and echocardiographic findings of cats diagnosed with patent ductus arteriosus (PDA) as well as short- and medium-term outcome after successful ligation of the PDA. Over a 10-year period 17 cats were diagnosed with PDA by transthoracic echocardiography. Thirteen cats were surgically treated by thoracotomy and ligation of the PDA. In all cats, a heart murmur was detected. In 88.2% of the cases, this presented as grade 4 out of 6 murmur (15/17 cats). A continuous murmur was more common (10/17 cats; 58.9%) than a systolic murmur (7/17 cats; 41.1%). Echocardiography showed that left ventricular internal diameter end diastole (LVIDd) and left ventricular internal diameter end systole (LVIDs) were significantly above reference values in the majority of cats. Mean diameter of the PDA measured at the widest point of the vessel was 3.4 mm (± 1.08 mm) and mean maximum flow velocity amounted to 5,06 m/sec (2,6m/sec-6,4m/sec). Surgery was successfully performed in all cats treated by surgical ligation and all of these patients were discharged after postoperative inpatient therapy. One cat experienced perioperative bleeding from the PDA, which was stopped efficaciously. This cat exhibited a residual shunt directly postoperatively; this could no longer be visualized in a re-check echocardiography 3 months later. Six cats were followed over a longer period of time. The surgical prognosis in this case study is very good with a postoperative survival rate of 100%. Surgical treatment of PDA is curative in animals not displaying advanced cardiac lesions. The auscultation of a heart murmur can provide initial findings indicative of PDA. Therefore, cardiac auscultation is warranted at every first presentation of a kitten. It must however be taken into consideration that not every cat with PDA necessarily has a continuous murmur but may display a systolic heart murmur. Therefore, it is important give utmost attention to the patients' clinical signs.

Loss of Cardiac PFKFB2 Drives Metabolic, Functional, and Electrophysiological Remodeling in the Heart.

Phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFK-2) is a critical glycolytic regulator responsible for upregulation of glycolysis in response to insulin and adrenergic signaling. PFKFB2, the cardiac isoform of PFK-2, is degraded in the heart in the absence of insulin signaling, contributing to diabetes-induced cardiac metabolic inflexibility. However, previous studies have not examined how the loss of PFKFB2 affects global cardiac metabolism and function. To address this, we have generated a mouse model with a cardiomyocyte-specific knockout of PFKFB2 (cKO). Using 9-month-old cKO and control mice, we characterized the impacts of PFKFB2 on cardiac metabolism, function, and electrophysiology. cKO mice have a shortened life span of 9 months. Metabolically, cKO mice are characterized by increased glycolytic enzyme abundance and pyruvate dehydrogenase activity, as well as decreased mitochondrial abundance and beta oxidation, suggesting a shift toward glucose metabolism. This was supported by a decrease in the ratio of palmitoyl carnitine to pyruvate-dependent mitochondrial respiration in cKO relative to control animals. Metabolomic, proteomic, and Western blot data support the activation of ancillary glucose metabolism, including pentose phosphate and hexosamine biosynthesis pathways. Physiologically, cKO animals exhibited impaired systolic function and left ventricular dilation, represented by reduced fractional shortening and increased left ventricular internal diameter, respectively. This was accompanied by electrophysiological alterations including increased QT interval and other metrics of delayed ventricular conduction. Loss of PFKFB2 results in metabolic remodeling marked by cardiac ancillary pathway activation. This could delineate an underpinning of pathologic changes to mechanical and electrical function in the heart.

Discordance interpretation of left ventricular size between echocardiography and cardiac magnetic resonance in pediatric patients with aortic/mitral regurgitation

PurposeThis study investigated discordance between echocardiography (echo) and cardiac magnetic resonance (CMR) measurements of the left ventricle (LV) in pediatric patients with aortic and/or mitral regurgitation (AR/MR).MethodsRetrospective cohort study of pediatric patients. The cohorts were comprised of patients with AR/MR vs. non-AR/MR. Left ventricular end diastolic volume (LVEDV) by CMR and left ventricular internal diameter diastolic (LVIDd) by echo were obtained from clinical reports then echo images were reviewed to remeasure LVEDV by bullet method. Left ventricular internal diameter systolic (LVIDs) and left ventricular ejection fraction (LVEF) measurements by echo and LVEF by CMR were obtained from clinical reports. Fractional shortening (FS%) was recalculated. Z-scores were calculated using normative data. Correlation between echo and CMR LV measurements was assessed using correlation coefficients. Bland-Altman plots assessed bias between imaging modalities. Receiver operator characteristic (ROC) analysis was performed for detection of LV enlargement and LV dysfunction.ResultsAR/MR patients had greater discrepancy in LV size interpretation by Z-score compared to non-AR/MR patients. This discrepancy persisted when the bullet method short axis measurements were incorporated. There was negative bias in echo-based measurements compared to CMR. The diagnostic performance of echo in identifying moderate LV enlargement was worse for AR/MR pediatrics patients.ConclusionThe discordant interpretation of LV size by echo compared to CMR is worse in pediatric patients with AR/MR when compared to patients without AR/MR even when short axis measurements are incorporated. This finding suggests non-uniform geometrical changes in the LV as it enlarges due to AR/MR.

The athlete's heart: allometric considerations on published papers and relation to cardiovascular variables.

To evaluate the morphology of the "athlete's heart", left ventricular (LV) wall thickness (WT) and end-diastolic internal diameter (LVIDd) at rest were addressed in publications on skiers, rowers, swimmers, cyclists, runners, weightlifters (n = 927), and untrained controls (n = 173) and related to the acute and maximal cardiovascular response to their respective disciplines. Dimensions of the heart at rest and functional variables established during the various sport disciplines were scaled to body weight for comparison among athletes independent of body mass. The two measures of LV were related (r = 0.8; P = 0.04) across athletic disciplines. With allometric scaling to body weight, LVIDd was similar between weightlifters and controls but 7%-15% larger in the other athletic groups, while WT was 9%-24% enlarged in all athletes. The LVIDd was related to stroke volume, oxygen pulse, maximal oxygen uptake, cardiac output, and blood volume (r = ~ 0.9, P < 0.05), while there was no relationship between WT and these variables (P > 0.05). In conclusion, while cardiac enlargement is, in part, essential for the generation of the cardiac output and thus stroke volume needed for competitive endurance exercise, an enlarged WT seems important for the development of the wall tension required for establishing normal arterial pressure in the enlarged LVIDd.

Electroacupuncture pretreatment mediates sympathetic nerves to alleviate myocardial ischemia–reperfusion injury via CRH neurons in the paraventricular nucleus of the hypothalamus

BackgroundMyocardial ischemia–reperfusion can further exacerbate myocardial injury and increase the risk of death. Our previous research found that the paraventricular nucleus (PVN) of the hypothalamus plays a crucial role in the improvement of myocardial ischemia–reperfusion injury (MIRI) by electroacupuncture (EA) pretreatment, but its mechanism of action is still unclear. CRH neurons exhibit periodic concentrated expression in PVN, but further research is needed to determine whether they are involved in the improvement of MIRI by EA pretreatment. Meanwhile, numerous studies have shown that changes in sympathetic nervous system innervation and activity are associated with many heart diseases. This study aims to investigate whether EA pretreatment improves MIRI through sympathetic nervous system mediated by PVNCRH neurons.MethodsIntegrated use of fiber-optic recording, chemical genetics and other methods to detect relevant indicators: ECG signals were acquired through Powerlab standard II leads, and LabChart 8 calculated heart rate, ST-segment offset, and heart rate variability (HRV); Left ventricular ejection fraction (LVEF), left ventricular short-axis shortening (LVFS), left ventricular end-systolic internal diameter (LVIDs) and interventricular septal thickness (IVSs) were measured by echocardiography; Myocardial infarct area (IA) and area at risk (AAR) were calculated by Evans-TTC staining. Pathological changes in cardiomyocytes were observed by HE staining; Changes in PVNCRH neuronal activity were recorded by fiber-optic photometry; Sympathetic nerve discharges were recorded for in vivo electrophysiology; NE and TH protein expression was assayed by Western blot.ResultsOur data indicated that EA pretreatment can effectively alleviate MIRI. Meanwhile, we found that in the MIRI model, the number and activity of CRH neurons co labeled with c-Fos in the PVN area of the rat brain increased, and the frequency of sympathetic nerve discharge increased. EA pretreatment could reverse this change. In addition, the results of chemical genetics indicated that inhibiting PVNCRH neurons has a similar protective effect on MIRI as EA pretreatment, and the activation of PVNCRH neurons can counteract this protective effect.ConclusionEA pretreatment can inhibit PVNCRH neurons and improve MIRI by inhibiting sympathetic nerve, which offers fresh perspectives on the application of acupuncture in the management of cardiovascular disease.

DILATED CARDIOMYOPATHY IN SLENDER-TAILED MEERKATS (SURICATA SURICATTA) UNDER HUMAN CARE.

Meerkats (Suricata suricatta) housed at two accredited zoological institutions in the United States were evaluated via echocardiography, thoracic radiography, and blood biomarkers-taurine and feline N-terminal pro-B-type natriuretic peptide-to determine the prevalence and severity of dilated cardiomyopathy (DCM) in both populations. In total, 24 meerkats were evaluated and 7 were diagnosed with DCM based on the following parameters: left ventricular internal diameter at end diastole > 1.30 cm, left ventricular internal diameter at end systole > 1.10 cm, and a fractional shortening of <18%. Echocardiographic parameters were identified and reported for normal and affected meerkats, whereas thoracic radiographs were not useful for screening for DCM. Meerkats with DCM were treated with pimobendan and/or benazepril and furosemide if indicated. Seven meerkats died during the study period, with the majority exhibiting myocardial fibrosis. Of the blood parameters tested, elevated taurine levels were associated with DCM. Further research is necessary to characterize the etiology of DCM in meerkats.

Analysis of the Effect of Extended Rehabilitation Care at Home on the Psychological Condition and Adherence to Medical Compliance Behavior of Patients with Coronary Heart Disease Combined with Heart Failure

Objective: To analyze the effects of providing extended rehabilitation nursing services at home to patients with coronary heart disease (CHD) combined with heart failure (CHF) on psychological improvement and adherence to medical compliance behavior. Methods: 79 patients with CHD with CHF admitted to Sijia Town Central Health Hospital, Haimen District, Nantong City, Jiangsu Province, between June 2021 and June 2023 were selected and grouped according to the randomized numerical table method. The control group (39 cases) was provided with conventional nursing care and extended rehabilitation nursing care at home was provided to the observation group (40 cases). The psychological status, adherence to medical behaviors, cardiac function, and complications between both groups were compared. Results: The scores of anxieties and depression self-assessment scales (SAS, SDS) of patients in the observation group were lower than those of the control group (t = 2.954, 3.212; P &lt; 0.05); the compliance of patients in the observation group was higher than that of the control group (P &lt; 0.05). The levels of left ventricular ejection fraction, end-systolic and end-diastolic internal diameters (LVEF, LVESD, LVEDD) of patients in the observation group at 58.02 ± 5.34 %, 44.49 ± 5.16 mm, and 49.16 ± 5.76 mm respectively were better than those of the control group after nursing care (t = 3.205, 3.288, 2.633; P &lt; 0.05); the complication rate of the observation group was lower than that of the control group (P &lt; 0.05). Conclusion: Extended rehabilitation nursing at home exhibited a psychological regulation effect on CHD with CHF patients, improved their medical compliance, improved cardiac function, reduced the incidence of complications, and had significant application value.

Rare case of super-response to Cardiac Resynchronization Therapy in Macedonian patient with Dilated Left Ventricular Non-Compaction Cardiomyopathy

Background: Left ventricular non-compaction (LVNC) is rare cardiomyopathy with increased and prominent endomyocardial trabeculations also known as spongy myocardium. It is often found in association with a dilated cardiomyopathy (DCM) and has high incidence of Heart failure (HF). Cardiac resynchronization therapy (CRT) is currently recommended by the available guidelines for selected patients with Heart failure with reduced ejection fraction (HFrEF). Aim: Our case report aims to highlight the therapeutic benefits and superresponse to CRT in a patient with Left ventricular non-compaction cardiomyopathy and HFrEF. Case report: 55-year-old Macedonian male patient with HFrEF, Left bundle branch block (LBBB) remained symptomatic (NYHA III) despite optimal medical treatment (OMT). Echocardiography and CMR findings were in addition to dilated and left ventricular non-compaction cardiomyopathy. Cardiac resynchronization therapy was indicated and 18 months after implantation of CRT-P device we have achieved complete and utter reversibility of systolic myocardial function (EF from 23% to 53%), left ventricular internal diameter was reduced from 90mm to 64mm, left ventricular end systolic volume (LVESV) was reduced from 319ml to 98ml and patient quality of life significantly improved. Conclusion: Cardiac resynchronization therapy is a safe and valuable method of treatment for patients with HFrEF due to dilated left ventricular non-compaction cardiomyopathy.

Relationship between syringomyelia and myxomatous mitral valve disease in Cavalier King Charles spaniels.

Syringomyelia (SM) and myxomatous mitral valve disease (MMVD) are highly prevalent in Cavalier King Charles spaniels (CKCS). Cardiac status in CKCS with and without SM is currently unknown. To investigate the association between SM and MMVD severity in CKCS and CKCS with SM with and without clinical signs of SM. Fifty-five CKCS: 40 with SM (22 symptomatic and 18 asymptomatic) and 15 without SM. A combined retrospective and prospective study. MRI and echocardiography were used to diagnose SM and MMVD, respectively. The association between SM and MMVD severity (left ventricle internal diameter in diastole normalized to bodyweight [LVIDDN] and left atrium to aortic ratio [LA/Ao]) were tested using multivariable linear regression analysis adjusting for sex and age. Overall, no significant difference in LVIDDN and LA/Ao was found between CKCS with or without SM. However, CKCS with symptomatic SM had significantly smaller LVIDDN (1.45 [1.30-1.50]) (median [IQR]) and LA/Ao (1.20 [1.10-1.28]) compared to CKCS with asymptomatic SM (1.60 [1.50-1.90] and 1.40 [1.20-1.75]) as well as CKCS without SM (0.24 [0.03-0.45] and 0.30 [0.05-0.56]) (all P values <.03). An association between MMVD and SM was not confirmed in this cohort of CKCS, indicating that MMVD and SM do not co-segregate. However, CKCS with symptomatic SM had smaller left ventricle and atrial size compared to CKCS with asymptomatic SM and CKCS without SM.

Association between left ventricular remodeling and lipid profiles in obese children: an observational study.

Childhood obesity has become a prominent issue in the society, which can lead to left ventricular remodeling and severe cardiovascular complications in adulthood. It is beneficial to identify the causes of left ventricular remodeling so that targeted measures can be taken to prevent the cardiovascular disease. Therefore, this study aimed to explore the relationship between left ventricular remodeling and changes in blood lipid indexes in obese children. This study was conducted on 40 healthy non-obese children and 140 obese children diagnosed in the pediatric health department of our hospital. Clinical data collected from the two groups were compared. Echocardiography was performed to examine left ventricular configuration and cardiac function. Multiple linear regression analysis was conducted to assess the independent effects of blood lipid levels on echocardiographic parameters. Blood lipid indicators among different left ventricular structural patterns which were classified according to left ventricular mass indexes and relative wall thickness were compared. Obese children exhibited significantly increased height, weight, body mass index (BMI), body fat percentage (BFP), blood pressure, triglycerides, total cholesterol, left ventricular internal diameter (LVIDd), interventricular septum (IVSd), left ventricular posterior wall diastolic thickness (LVPWd), myocardial mass (LVM) and relative wall thickness (RWT), as well as lower high-density lipoprotein cholesterol (HDL-C) and left ventricular ejection fraction (LVEF) compared to the non-obese children (P < 0.05). Multiple linear correlation analysis showed LVM had a significantly positive correlation with BMI (r = 3.21, P = 0.002) and SBP (r = 2.61, P = 0.01); LVMI had a significantly negative correlation with HDL-C (r = -2.45, P = 0.015); RWT had a significantly positive correlation with SBP (r = 2.50, P = 0.013) but a significantly negative correlation with HDL-C (r = -2.35, P = 0.02). Furthermore, there were significant differences in HDL-C values among children with different ventricular configurations (P < 0.05), with the lowest HDL-C value recorded in the concentric hypertrophy group. Obese children will develop left ventricular remodeling. The left ventricular configuration indexes are most significantly associated with serum HDL-C. Lower HDL-C level contributes to severer left ventricular hypertrophy, indicating a concentric hypertrophy pattern.

MSC exosomes attenuate sterile inflammation and necroptosis associated with TAK1-pJNK-NFKB mediated cardiomyopathy in diabetic ApoE KO mice.

Diabetes is a debilitating disease that leads to complications like cardiac dysfunction and heart failure. In this study, we investigated the pathophysiology of diabetes-induced cardiac dysfunction in mice with dyslipidemia. We hypothesize diabetes in ApoE knockout (ApoE-/-) mice induces cardiac dysfunction by increasing inflammation and necroptosis. ApoE-/- mice were divided into experimental groups: Control, Streptozotocin (STZ), STZ + MSC-Exo (mesenchymal stem cell-derived exosomes), and STZ+MEF-Exo (Mouse embryonic fibroblast derived exosomes). At Day 42, we assessed cardiac function, collected blood and heart tissues. Heart tissue samples were analyzed for inflammation, necroptosis, signaling mechanism, hypertrophy and adverse structural remodeling using histology, immunohistochemistry, western blotting, RT-PCR, cytokine array and TF array. STZ treated ApoE-/- mice developed diabetes, with significantly (p<0.05) increased blood glucose and body weight loss. These mice developed cardiac dysfunction with significantly (p<0.05) increased left ventricular internal diameter end diastole and end systole, and decreased ejection fraction, and fractional shortening. We found significant (p<0.05) increased expression of inflammatory cytokines TNF- a, IL-6, IL-1a, IL-33 and decreased IL-10 expression. Diabetic mice also exhibited significantly (p<0.05) increased necroptosis marker expression and infiltration of inflammatory monocytes and macrophages. MSC-Exos treated mice showed recovery of diabetes associated pathologies with significantly reduced blood glucose, recovered body weight, increased IL-10 secretion and M2 polarized macrophages in the heart. These mice showed reduced TAK1-pJNK-NFKB inflammation associated expression and improved cardiac function with significantly reduced cardiac hypertrophy and fibrosis compared to diabetic mice. Treatment with MEF-Exos did not play a significant role in attenuating diabetes-induced cardiomyopathy as these treatment mice presented with cardiac dysfunction and underlying pathologies observed in STZ mice. Thus, we conclude that cardiac dysfunction develops in diabetic ApoE-/- mice, arising from inflammation, necroptosis, and adverse tissue remodeling, which is ameliorated by MSC-Exos, a potential therapeutic for diabetes-induced cardiomyopathy.

Fuyu Decoction ameliorates myocardial fibrosis in rat model of heart failure by regulating Nrf2/GPX4-mediated ferroptosis

This study aims to investigate the effect and mechanism of Fuyu Decoction(FYD) in the treatment of myocardial fibrosis in the rat model of heart failure(HF). Sixty Wistar rats were randomized into a modeling group(n=50) and a sham group(n=10). A post-myocardial infarction HF model was established by ligating the left anterior descending coronary artery in rats. The successfully modeled rats were assigned into model, low-dose(2.5 g·kg~(-1)) FYD(FYD-L), high-dose(5.0 g·kg~(-1)) FYD(FYD-H), and FYD+Nrf2 inhibitor(ML385, 30 mg·kg~(-1)) groups(n=10). FYD was administrated by gavage and ML385 by intraperitoneal injection. The rats in the sham and model groups were administrated with equal amounts of normal saline by gavage. After 8 weeks of intervention, the cardiac function indicators were measured, and the myocardial tissue morphology and collagen deposition were observed. The positive expression of collagens Ⅰ and Ⅲ, apoptosis, and oxidative stress were examined, and the levels of Fe~(2+) and reactive oxygen species(ROS) were determined. The protein levels of nuclear factor erythroid 2-related factor 2(Nrf2), solute carrier family 7 member 11(SLC7A11), glutathione peroxidase 4(GPX4), and acyl-coenzyme A synthase long chain family member 4(ACSL4) in the myocardial tissue were determined. Compared with sham group, the model group showed decreased left ventricular ejection fraction(LVEF) and left ventricular fractional shortening(LVFS), increased left ventricular end internal dimension in systole(LVIDs), left ventricular internal diameter in diastole(LVIDd), and myocardial collagen deposition, positive expression of collagens Ⅰ and Ⅲ, elevated apoptosis rate and malondialdehyde(MDA), Fe~(2+), and ROS levels, lowered superoxide dismutase(SOD) and glutathione peroxidase(GSH) levels, down-regulated protein levels of Nrf2, SLC7A11, and GPX4, and up-regulated protein level of ACSL4. Compared with the model group, the above indicators were restored by FYD. Moreover, ML385 reversed the protective effect of FYD on myocardial fibrosis in HF rats. In conclusion, FYD can inhibit ferroptosis by activating the Nrf2/GPX4 pathway, thereby ameliorating myocardial fibrosis in HF rats.

Jianpi Qinghua Formula Alleviates Diabetic Myocardial Injury Through Inhibiting JunB/c-Fos Expression.

Diabetic cardiomyopathy (DCM) represents a substantial risk factor for heart failure and increased mortality in individuals afflicted with diabetes mellitus (DM). DCM typically manifests as myocardial fibrosis, myocardial hypertrophy, and impaired left ventricular diastolic function. While the clinical utility of the Jianpi Qinghua (JPQH) formula has been established in treating diabetes and insulin resistance, its potential efficacy in alleviating diabetic cardiomyopathy remains uncertain. This study aims to investigate the impact and underlying molecular mechanisms of the JPQH formula (JPQHF) in ameliorating myocardial injury in nonobese diabetic rats, specifically focusing on apoptosis and inflammation. Wistar rats were assigned as the normal control group (CON), while Goto-Kakizaki (GK) rats were randomly divided into three groups: DM, DM treated with the JPQHF, and DM treated with metformin (MET). Following a 4-week treatment regimen, various biochemical markers related to glucose metabolism, cardiac function, cardiac morphology, and myocardial ultrastructure in GK rats were assessed. RNA sequencing was utilized to analyze differential gene expression and identify potential therapeutic targets. In vitro experiments involved high glucose to induce apoptosis and inflammation in H9c2 cells. Cell viability was evaluated using CCK-8 assay, apoptosis was monitored via flow cytometry, and the production of inflammatory cytokines was measured using quantitative real-time PCR (qPCR) and ELISA. Protein expression levels were determined by Western blotting analysis. The investigation also incorporated the use of MAPK inhibitors to further elucidate the mechanism at both the transcriptional and protein levels. The JPQHF group exhibited significant reductions in interventricular septal thickness at end-systole (IVSs) and left ventricular internal diameter at end-systole and end-diastole (LVIDs and LVIDd). JPQHF effectively suppressed high glucose-induced activation of IL-1β and caspase 3 in cardiomyocytes. Furthermore, JPQHF downregulated the expression of myocardial JunB/c-Fos, which was upregulated in both diabetic rats and high glucose-treated H9c2 cells. The JPQH formula holds promise in mitigating diabetic myocardial apoptosis and inflammation in cardiomyocytes by inhibiting JunB/c-Fos expression through suppressing the MAPK (p38 and ERK1/2) pathway.

Inverse Association between Exercising Blood Pressure Response and Left Ventricular Chamber Size and Mass in Women Who Habitually Resistance Train

Exercise is a major modifiable lifestyle factor that leads to temporarily increased systolic blood pressure (SBP), which is thought to influence left ventricular mass normalized to body surface area (LVM/BSA). This relationship has never been studied in women who habitually perform resistance exercise. Purpose: To determine if a direct correlation exists between the SBP response to resistance exercise (change from rest; eSBP) and LVM/BSA in young healthy women who habitually resistance train. Methods: Leg extension resistance exercise was performed while continuously monitoring blood pressure using finger plethysmography. LVM was estimated using echocardiography. Data are shown as mean ± SD. Results: Thirty-one women participated (age 23 ± 3 years, height 164 ± 7 cm, body mass 63.7 ± 10.3 kg). Resting SBP (110 ± 8 mmHg, r = 0.355, p = 0.049) was shown to be directly correlated to LVM/BSA (72.0 ± 28.4 g/m2). Conversely, eSBP (30.8 ± 14.6 ∆mmHg, r = −0.437, p = 0.014) was inversely related to LVM/BSA. eSBP was not correlated to interventricular septum width (0.88 ± 0.12 cm, r = −0.137, p = 0.463) or posterior wall thickness (0.91 ± 0.15 cm, r = −0.084, p = 0.654). eSBP was inversely related to left ventricle internal diameter during diastole (LVIDd) (4.25 ± 0.33 cm, r = −0.411, p = 0.021). Conclusion: Counter to the hypothesis, these data suggest an inverse association between eSBP during resistance exercise and LVM/BSA in healthy young women who resistance train. This relationship is due to a smaller LVIDd with greater eSBP.