Left Ventricular Diastolic Diameter Research Articles

Structural and functional cardiac parameters across occupations: a cross-sectional study in differing work environments

Previous investigations have highlighted notable variations in cardiovascular risk indicators associated with various professional categories. However, only a few studies have examined structural and functional cardiac parameters using echocardiography within distinct occupational groups. Hence, this study endeavored to assess cardiac structural and functional parameters in three additional occupations: firefighters (FFs), police officers (POs), and office workers (OWs). This prospective study encompassed 197 male participants (97 FFs, 54 POs, and 46 OWs) from Germany. All participants underwent 2D and Doppler echocardiography in resting conditions; standard parasternal and apical axis views were employed to evaluate structural (diastolic and systolic) and functional (systolic and diastolic function, and strain) cardiac parameters. All three occupational groups exhibited a tendency towards septal hypertrophy. Notably, OWs exhibited the largest diastolic interventricular septum diameter (IVSd), at 1.33 ± 0.25 cm. IVSd significantly varied between POs and OWs (p = 0.000) and between POs and FFs (p = 0.025). Additionally, during diastole a substantially larger left ventricular posterior wall diameter (LVPWd) was observed in OWs compared to FFs (p = 0.001) and POs (p = 0.013). The left ventricular diastolic cavity diameter (LVIDd) and the left ventricular systolic cavity diameter (LVIDs) were significantly higher in POs than they were in FFs (LVIDd: p = 0.001; LVIDs: p = 0.009), and the LVIDd was notably higher in FFs (p = 0.015) and POs compared to OWs (p = 0.000). FFs exhibited significantly better diastolic function, indicated by higher diastolic peak velocity ratios (MV E/A ratio) and E/E’ ratios, compared to POs (E/A ratio: p = 0.025; E/E’ ratio: p = 0.014). No significant difference in diastolic performance was found between OWs and FFs. Significantly higher E’(lateral) values were noted in POs compared to FFs (p = 0.003) and OWs (p = 0.004). Ejection fraction did not significantly differ among FFs, POs, and OWs (p > 0.6). The left ventricular mass (LV Mass) was notably higher in POs than it was in FFs (p = 0.039) and OWs (p = 0.033). Strain parameter differences were notably improved in two- (p = 0.006) and four-chamber (p = 0.018) views for FFs compared to POs. Concentric remodeling was the predominant change observed in all three occupational groups. Significant differences in the presence of various forms of hypertrophy were observed in FFs, POs, and OWs (exact Fisher test p-values: FFs vs. OWs = 0.021, POs vs. OWs = 0.002). OWs demonstrated notably higher rates of concentric remodeling than FFs did (71.77% vs. 47.9%). This study underscores disparities in both functional and structural parameters in diverse occupational groups. Larger prospective studies are warranted to investigate and delineate differences in structural and functional cardiac parameters across occupational groups, and to discern their associated effects and risks on the cardiovascular health of these distinct professional cohorts.

Application of intensive management of risk awareness combined with cardiac rehabilitation nursing in elderly patients with acute myocardial infarction and heart failure.

The aim of this study is to assess the impact of intensive risk awareness management along with cardiac rehabilitation nursing in elderly patients with acute myocardial infarction and heart failure. We selected 101 elderly patients with acute myocardial infarction and heart aging treated from January 2022 to March 2023. They were divided into control and observation groups based on hospitalization numbers. The control group (n = 50) received routine nursing, while the observation group (n = 51) received intensive risk awareness management and cardiac rehabilitation nursing. We compared medication possession ratio (MPR), cardiac function, self-care ability scale scores, quality-of-life, incidents, and satisfaction between the 2 groups. Before intervention, there was no significant difference in MPR values between the 2 groups (P > .05). After intervention, MPR values increased in both groups, with a greater increase in the observation group (P < .05). Cardiac function showed no significant difference before intervention (P > .05), but after intervention, the observation group had lower left ventricular end-systolic and diastolic diameters and higher left ventricular ejection fraction compared to the control group (P < .05). Self-care skills, health knowledge, self-responsibility, and self-concept scores improved in both groups after intervention, with higher scores in the observation group (P < .05). The observation group had higher scores in various quality-of-life domains (P < .05). The total incidence of adverse events was lower in the observation group (5.88%) compared to the control group (20.00%) (P < .05). Patient satisfaction was significantly higher in the observation group (96.08%) than in the control group (84.00%) (P < .05). Intensive risk awareness management combined with cardiac rehabilitation nursing in elderly patients with acute myocardial infarction and heart aging can enhance medication compliance, improve quality-of-life, enhance self-care abilities, boost cardiac function, reduce incidents, and increase patient satisfaction.

Cardiac screening in pediatric patients with neurofibromatosis type 1: similarities with Noonan syndrome?

The aims of this study were to assess: (1) similarities in the prevalence and types of ECG and conventional echocardiographic findings described in NS in asymptomatic patients with NF1, and (2) the presence of discrete myocardial dysfunction in NF1 patients using myocardial strain imaging. Fifty-eight patients with NF1 (ages 0-18 years), and thirty-one age-matched healthy controls underwent cardiac assessment including blood pressure measurements, a 12-lead ECG, and detailed echocardiography. Quantification of cardiac chamber size, mass and function were measured using conventional echocardiography. Myocardial strain parameters were assessed using 2-Dimensional (2D) Speckle tracking echocardiography. Asymptomatic patients with NF1 had normal electrocardiograms, none with the typical ECG patterns described in NS. However, patients with NF1 showed significantly decreased calculated Z scores of the left ventricular internal diameter in diastole and systole, reduced left ventricular mass index and a higher incidence of cardiac abnormal findings, mainly of the mitral valve, in contrast to the frequently described types of cardiac abnormalities in NS. Peak and end systolic global circumferential strain were the only significantly reduced speckle tracking derived myocardial strain parameter. Children with NF1 demonstrated more dissimilarities than similarities in the prevalence and types of ECG and conventional echocardiographic findings described in NS. The role of the abnormal myocardial strain parameter needs to be explored.

The interaction of choline and one-carbon / folate metabolism derangements on the cardiac remodeling process with or without diabetes

Proper nutrition helps protect from illness and disease. Choline (Ch), an essential molecule of substantial importance for the optimal development and function of several biological systems, plays a crucial role in the pathway of one-carbon metabolism. On the other hand, Ch-deprivation (CD) has been linked with abnormal fat metabolism, insulin resistance, and myocardial dysfunction. The Ch-deficiency setting is an established experimental model of non-alco¬holic steatohepatitis that resembles the human non-alcoholic fatty liver disease (NAFLD); a disease with constantly increasing incidence and prevalence. NAFLD, commonly associated with metabolic comorbidities such as obesity and type 2 diabetes mellitus, consists a high risk for cardiovascular disease. Experimental data of dietary CD through the administration of a Ch-deficient diet to rodents have revealed myocardial monocyte infiltration along with cardiac interstitial oedema and fibrosis, as well as a deleterious effect on cardiac valves that could lead to impaired heart mechanical properties which resemble to a restrictive pattern of cardiomyopathy characterised mainly by diastolic dysfunction. In a Ch-deprived diabetic experimental model, the diastolic heart failure has been characterized by a concentric hypertrophied myocardium, a left ventricular cavity with a thinner wall, and an increased left ventricular diastolic diameter, in addition to a left atrial dilatation that could also exert functional derangement and provoke arrhythmogenesis, thereby jeopardising cardiac output.

Effect of Butorphanol-Medetomidine and Butorphanol-Dexmedetomidine on Echocardiographic Parameters during Propofol Anaesthesia in Dogs.

This study compared the effects of butorphanol-medetomidine and butorphanol-dexmedetomidine combinations on echocardiographic parameters during propofol anaesthesia in dogs. The dogs were randomly divided into two groups. In the butorphanol-medetomidine (BM) group, butorphanol (0.2 mg/kg) and medetomidine (15 μg/kg) were intravenously administered; in the butorphanol-dexmedetomidine (BD) group, butorphanol (0.2 mg/kg) and dexmedetomidine (7.5 μg/kg) was used. Anaesthesia was induced with propofol and maintained with a constant-rate infusion of propofol (0.2 mg/kg/min). The echocardiographic parameters were assessed in conscious dogs (T0). Echocardiography was conducted again at 10 min post premedication (T1), followed by assessments at 30 (T2), 60 (T3), and 90 (T4) mins. The dogs were subjected to diagnostic procedures (radiography, computed tomography) under anaesthesia. A significant reduction in heart rate and cardiac output was noted in both groups at T1. There was no significant difference in the stroke volume between the BM and BD groups. The application of butorphanol-dexmedetomidine caused a significant increase in the left ventricular internal diameter in diastole and the diameter of the left atrium compared to that caused by butorphanol-medetomidine. This study documented that butorphanol-medetomidine and butorphanol-dexmedetomidine combinations caused similar reductions in heart rate and cardiac output in both groups. 'New´ valvular regurgitation occurred following their administration.

The impact of intravenous medetomidine and vatinoxan on echocardiographic evaluation of dogs with stage B1 mitral valve disease

Introduction / objectiveThe purpose of this study was to investigate the echocardiographic effects of intravenous medetomidine and vatinoxan in dogs with stage B1 mitral valve disease. We hypothesised medetomidine-vatinoxan would reduce the need for manual restraint during echocardiography without producing detrimental cardiovascular effects or echocardiographic changes. AnimalsTwelve client owned dogs with stage B1 mitral valve disease. MethodsA transthoracic echocardiographic examination was performed before and after sedation with intravenous medetomidine (10 μg/kg) and vatinoxan (200 μg/kg). Vital parameters were also recorded, and the level of sedation was assessed subjectively. The data were analysed with Student’s t-tests with an alpha-level of <0.05. ResultsEnd-systolic volume and left ventricular systolic diameter increased (from 0.89 ± 0.19 mL/kg to 1.13 ± 0.29 mL/kg and 0.96 ± 0.12 cm to 1.10 ± 0.10 cm, respectively) and ejection fraction (from 66.33 ± 4.0% to 56.23 ± 9.54%) and fractional shortening (from 36.13 ± 5.42% to 27.24 ± 5.6%) decreased significantly after sedation. End diastolic volume, left ventricular diastolic diameter, and left atrial size remained statistically unchanged, while aortic (from 1.34 ± 0.2 m/s to 0.99 ± 0.14 m/s) and pulmonic (from 0.94 ± 0.16 m/s to 0.66 ± 0.15 m/s) velocities decreased significantly. No dogs had a mean arterial pressure below 65 mmHg. Sedation enabled echocardiographic examination without manual restraint. No adverse effects were observed with the dose studied. ConclusionsEchocardiographic parameters were not completely comparable with the baseline values, which should be taken into consideration when evaluating dogs sedated with intravenous medetomidine-vatinoxan.

IMPROVEMENT OF RENAL HAEMODYNAMICS AND ECHOCARDIOGRAPHIC PARAMETERS IN PHARMACOLOGICAL CONTROLLED HYPERTENSIVES

Objective: A study was carried out to evaluate the influence of blood pressure lowering treatment with combined doses of olmesartan plus amplodipina compared with those of either drug at a single dose level. Design and method: By double-blind, three-way crossover study (balanced Latin square design) in 102 subjects (mean age 51.9 +/- 7.42 years) with essential hypertension we used Olmesartan 40 mg plus Amplodine 5 mg compared with those of either drug at a single and higher dose level (40 or 10 mg daily, respectively). Left ventricular mass and function were evaluated by M-B mode echocardiography, renal function by glomerular filtration rate (GFR) and by serum and 24-h urinary Na+ and K+ during wash-out period and after 24 weeks of treatment. Results: The supine blood pressure for subjects given placebo was 171/103 mmHg. After 24 weeks of treatment, systolic and diastolic supine blood pressure were significantly lower with 40 mg iolmesartan plus 5 mg amplodipine (134/84 mmHg) than with 10 mg amplodipine (137/84 mmHg) or with 40 mg olmesartan (144/85 mmHg). Left ventricular posterior wall and septal thickness were significantly and similarly reduced in all groups. Left ventricular systolic and diastolic end diameters were not significantly changed. Left ventricular mass (LVM) was significantly reduced in Olmesartan plus Amplodipine group and Olmesartan group. GFR was not significantly altered. The 24-h urinary Na+ significantly increased with olmesartan, more so than amplodipine. The combination was tolerated better than either monotherapy. We observed no clinically significant changes in laboratory variables including blood lipoproteins. Conclusions: The combination of olmesartan plus amplodipina reduced blood pressure more effectively and was better tolerated than other drug alone. All three groups showed similar changes in echocardiographic indices and no change in renal function.

Plasma levels of Sirtuin 7 are decreased in patients with essential hypertension

BackgroundSirtuin 7 (SIRT7), as a nicotinamide adenine dinucleotide-dependent protein/histone deacetylase, has been implicated in the pathogenesis of cardiovascular diseases. However, whether SIRT7 is related to hypertension remains largely unclear. Thus, this study aims to explore the effects and correlation between SIRT7 and hypertension. MethodsA total of 72 patients with essential hypertension and 82 controls with non-hypertension were recruited at Beijing Tongren Hospital Affiliated with Capital Medical University from July 2022 to June 2023. Plasma SIRT7 expression was measured using enzyme-linked immunosorbent assay analysis. Clinical baseline characteristics, laboratory measurements, echocardiographic data, and medical therapy were collected. ResultsPlasma levels of SIRT7 were lower in hypertensive patients compared with non-hypertensive patients [0.97 (0.58–1.30) vs. 1.24 (0.99–1.46) ng/mL, P < 0.001, respectively]. Furthermore, compared with the low SIRT7 group, there were lower levels of systolic blood pressure, hyperlipidemia, and the ultrasonic electrocardiogram parameters left ventricular end-diastolic diameter and left atrial in diastole in the high SIRT7 group (P < 0.05, respectively). More importantly, multivariate logistic regression analyses indicated that plasma SIRT7 was a predictor of hypertension [OR: 0.06, 95 % CI (0.02–0.19), P < 0.001]. Receiver operating characteristics curve analysis revealed that the optimal cutoff value for plasma SIRT7 levels in detecting hypertension was determined as 0.85 ng/mL with a sensitivity of 73.6 % and a specificity of 89.0 %. The area under the curve for SIRT7 was 0.821 (95 % CI, 0.751–0.878; P < 0.001). ConclusionPlasma levels of SIRT7 are decreased in patients with essential hypertension, implying its potential as a biomarker for diagnosing essential hypertension..

A transcriptomic analysis of correlation between mitochondrial function and energy metabolism remodeling in mice with myocardial fibrosis following myocardial infarction

To investigate the changes of mitochondrial respiratory function during myocardial fibrosis in mice with myocardial infarction (MI) and its correlation with the increase of glycolytic flux. Forty C57BL/6N mice were randomized into two equal groups to receive sham operation or ligation of the left anterior descending coronary artery to induce acute MI. At 28 days after the operation, 5 mice from each group were euthanized and left ventricular tissue samples were collected for transcriptomic sequencing. FPKM method was used to calculate gene expression levels to identify the differentially expressed genes (DEGs) in MI mice, which were analyzed using GO and KEGG databases to determine the pathways affecting the disease process. Heat maps were drawn to show the differential expressions of the pathways and the related genes in the enrichment analysis. In primary cultures of neonatal mouse cardiac fibroblasts (CFs), the changes in mitochondrial respiration and glycolysis levels in response to treatment with the pro-fibrotic agonist TGF-β1 were analyzed using Seahorse experiment. The mouse models of MI showed significantly increased diastolic and systolic left ventricular diameter (P < 0.05) and decreased left ventricular ejection fraction (P < 0.0001). A total of 124 up-regulated and 106 down-regulated DEGs were identified in the myocardial tissues of MI mice, and GO and KEGG enrichment analysis showed that these DEGs were significantly enriched in fatty acid metabolism, organelles and other metabolic pathways and in the mitochondria. Heat maps revealed fatty acid beta oxidation, mitochondrial dysfunction and increased glycolysis levels in MI mice. In the primary culture of CFs, treatment with TGF-β1 significantly reduced the basal and maximum respiratory levels and increased the basal and maximum glycolysis levels (P < 0.0001). During myocardial fibrosis, energy metabolism remodeling occurs in the CFs, manifested by lowered mitochondrial function and increased energy generation through glycolysis.

Cardiac autonomic dysfunction and structural remodeling: the potential mechanism to mediate the relationship between obstructive sleep apnea and cardiac arrhythmias.

Cardiac arrhythmias are very common in patients with obstructive sleep apnea (OSA), especially atrial fibrillation (AF) and nonsustained ventricular tachycardia (NVST). Cardiac autonomic dysfunction and structural remodeling caused by OSA provide the milieu for cardiac arrhythmia development. This study aimed to determine whether OSA is associated with various cardiac arrhythmias and investigate potential pathophysiologic pathways between them. The analysis covered 600 patients with clinical suspicion of OSA hospitalized in Renmin Hospital of Wuhan University between January 2020 and May 2023. After undergoing sleep apnea monitor, all subjects received laboratory tests, Holter electrocardiography, and Echocardiography. Compared with those without OSA and adjusting for potential confounders, subjects with moderate OSA had three times the odds of AF (odds ratio [OR] 3.055; 95% confidence interval [CI], 1.002-9.316; p = 0.048). Subjects with severe OSA had three times the odds of AF (OR 3.881; 95% CI, 1.306-11.534; p = 0.015) and NSVT (OR 3.690; 95% CI, 0.809-16.036; p = 0.046). There were significant linear trends for the association between OSA severity with AF and NVST (p < 0.05). And this association was mediated by cardiac structural changes including left atrial diameter, left ventricular diastolic diameter, right atrial diameter and right ventricular diameter. In addition, the ratio of low-frequency and high-frequency individually mediated the association between severe OSA and NVST. This study demonstrated that severe OSA was independently associated with AF and NSVT, and this association was mediated by autonomic nervous system changes and cardiac structural remodeling.

Assessment of left and right ventricular systolic function in dogs with multicentric lymphoma

ObjectiveMyocardial dysfunction in cardio-oncology is generally thought to be related to the cardiotoxicity of chemotherapy treatment. However, it is known that some tumors have direct effects on myocardial function. These effects have already been studied in man, but there are no publications of these of the effects in dogs. Novel advanced echocardiographic techniques may allow early detection of myocardial dysfunction when compared to conventional echocardiographic techniques. This study aims to assess myocardial systolic function in dogs with multicentric lymphoma prior to initiation of chemotherapy. AnimalsFifteen dogs with multicentric lymphoma and nineteen healthy dogs. MethodsCase-control study. Dogs with multicentric lymphoma and healthy control dogs underwent physical examination, electrocardiography, systolic blood pressure measurement, standard and speckle tracking echocardiography to assess biventricular systolic function. ResultsThere were no differences between groups in terms of ejection fraction, fractional shortening, left ventricular systolic and diastolic diameter, tricuspid annular plane systolic excursion, mitral annular plane systolic excursion and fractional area change of the right ventricle (RV). However, there was a reduction in the values of global circumferential strain (p = 0.0003), RV strain (p = 0.01) and RV tissue motion annular displacement (p < 0.05) in the dogs with lymphoma when compared to the control group. ConclusionsSpeckle tracking techniques appear to demonstrate early systolic dysfunction, primarily affecting the RV, in dogs with lymphoma prior to chemotherapy treatment.

Association between echocardiographic indexes and urinary Neutrophil Gelatinase-Associated Lipocalin (uNGAL) in dogs with myxomatous mitral valve disease

Neutrophil gelatinase-associated lipocalin (NGAL) is a biomarker of tubular damage, and its elevation has been described in human and canine cardiorenal syndrome.The aim was to evaluate the association between echocardiographic indexes and urine NGAL (uNGAL) and uNGAL normalized to urine creatinine (uNGALC) in dogs with MMVD.This is a multicentric prospective cross-sectional study. A total of 77 dogs with MMVD at different ACVIM stages were included. All dogs underwent echocardiography, serum chemistry, and urinalysis. Echocardiographic data analyzed were shortening fraction (SF), left ventricular diastolic (LVIDDn) and systolic (LVIDSn) diameters normalized for body weight, left atrium to aortic root ratio (LA/Ao), maximal (LAVMax) and minimal (LAVMin) left atrial volumes, LA stroke volume (LASV), early diastolic mitral peak velocity (EVmax), EVmax to tissue Doppler E' wave (E/E'), aortic (VTIAo) and mitralic (VTIMit) velocity time integrals and their ratio (VTIMit/VTIAo), and tricuspid regurgitation velocity (TRVmax).In the univariate analysis LASV, TRVmax, LAVMax, LVIDDn, and VTIMit/VTIAo were independent predictors of increased uNGAL and uNGALC; however, only LASV [(OR: 1.96, 95% CI: 1.16 to 3.31) P = 0.01 for NGAL, and (OR: 2.79, 95% CI: 1.50 to 5.17) P < 0.001 for NGALC] and TRVmax [(OR: 1.73, 95% CI: 1.20–2.51) P = 0.002 for NGAL, and (OR: 1.50, 95% CI: 10.07–2.10) P = 0.015 for NGALC] remained statistically significant in the multivariable analysis.Based on our results, LASV and TRVmax are associated with increased uNGAL and uNGALC. These parameters might detect dogs with MMVD at higher risk of developing kidney damage.

Long-term prognosis and prognostic factors after primary prophylactic implantable cardioverter-defibrillator therapy

BackgroundLittle is known regarding which patients with ischemic cardiomyopathy (ICM) should be considered for prophylactic therapies, such as an implantable cardioverter-defibrillator (ICD), in the primary percutaneous intervention era. The aim of this study was to investigate the influence of non-sustained ventricular tachycardia (NSVT) on major adverse cardiac events (MACE) in heart failure with reduced ejection fraction (HFrEF) patients. MethodsWe retrospectively analyzed patients of ICM and non-ICM who underwent ICD implantation at our institute from October 2006 to August 2020. MACE were defined as composite outcome of cardiovascular death, heart failure hospitalization, and appropriate ICD therapies. ResultsA total of 167 patients were enrolled [male, 138 (83 %); age, 62.1 ± 11.7 years; left ventricular ejection fraction, 23.5 ± 6.1 %; left ventricular diastolic diameter, 67.4 ± 9.0 mm; atrial fibrillation, 47 (28 %); NSVT, 124 (74 %); use of class III antiarrhythmic drugs, 55 (33 %); ischemic cardiomyopathy, 56 (34 %); cardiac resynchronization therapy, 73 (44 %)]. The median follow-up duration was 61 months. MACE occurred with 71 patients (43 %). When comparing baseline characteristics of the patients, left ventricular ejection fraction (p = 0.02) and atrial fibrillation (p = 0.04) were significantly associated with MACE. The multivariable Cox analysis for the target variable MACE identified atrial fibrillation (hazard ratio 2.00; 95 % confidence index 1.18–3.37; p = 0.01) as an independent predictor for MACE. ConclusionsPrior NSVT before ICD implantation was not an independent predictor of future MACE in patients with HFrEF with primary prophylactic ICD. In contrast, atrial fibrillation was associated with worse prognosis. To predict the prognosis of patients with primary prophylactic ICD, these factors should be assessed as comprehensive risk stratification factors for MACE.

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.

Songorine ameliorates LPS-induced sepsis cardiomyopathy by Wnt/β-catenin signaling pathway-mediated mitochondrial biosynthesis.

Septic cardiomyopathy (SCM) is manifested by impairment of cardiac contractile function with myocardial mitochondrial dysregulation. Natural product, songorine (SGR), a diterpenoid alkaloid derived from the lateral root of Aconitum carmichaeli, has been reported for the treatment of heart failure. Here, the protective role of SGR in heart injury of SCM was investigated and its underlying action of mechanism was explored. Firstly, the mouse and cardiomyocytes (H9C2 cell) SCM model induced by LPS were established to evaluate the therapeutic effect of SGR. The in vivo results exhibited that SGR rescued the survival rate of SCM mice, restored the loss of ejection fraction (EF) and fractional shortening (FS), and reduced left ventricular systolic diameter and left ventricular diastole diameter (LVIDs, LVIDd) by echocardiography. SGR improved the mitochondrial biosynthesis and myocardial fiber structure and arranged them neatly by transmission electron microscope (TEM). Further, SGR inhibited inflammatory targets myeloperoxidase (MPO) and tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), and plasminogen activator inhibitor-1 (PAI-1). And SGR activated the mitochondrial biosynthesis-related peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), β-catenin, and matrix metallopeptidase 2 (MMP2) proteins. Meanwhile, the in vitro results showed that SGR promoted the increased the myocardial H9C2 cell viability, and mitochondrial biosynthesis and structure. SGR also blocked the inflammatory factors and reversed PGC-1α, β-catenin, and MMP2 in vitro, while SGR alleviated the myocardial cell apoptosis via flow cytometry. The findings indicate that SGR mitigates sepsis-caused myocardial damage by Wnt/β-catenin signaling pathway-mediated mitochondrial biosynthesis. SGR may be a promising candidate for treatment of SCM.

Impact of maternal age and body mass index on the structure and function of the heart in newborns: a Copenhagen Baby Heart Study

BackgroundMaternal obesity and advanced age have been associated with an increased risk of structural congenital heart defects in the offspring. Whether these factors may also cause abnormalities in infant cardiac dimension and function is unknown. This study investigates whether maternal body mass index (BMI) and maternal age are associated with changes in left ventricular (LV) dimensions and function in the newborn.MethodsInfants enrolled in the Copenhagen Baby Heart Study (CBHS), who were born at term, and contributed with a transthoracic echocardiography (TTE) within 60 days of birth were included. The exposure variables were prepregnancy maternal BMI (kg/m2) < 18.5; 18.5–24.9 (reference); 25–29.9; 30–34.9 and ≥ 35 and maternal age (years) < 25; 25–29; 30–34 (reference); 35–39 and ≥ 40. Outcomes were LV parameters ascertained by 2D-echocardiography. Associations between each maternal factor and infant LV parameters were analysed with either a linear model adjusted for the child’s weight and length at birth, gestational age, sex, age at TTE, and maternal smoking, or a linear mixed model, further adjusted for random effects of analyst and month of analysis. Analyses investigating impact of maternal BMI were adjusted for maternal age, and vice versa.ResultsThe study cohort included 24,294 infants. Compared with infants in the BMI reference group, infants born to women with a BMI ≥ 25 kg/m2 generally had smaller measures of LV internal diameters in end-diastole, reaching statistical significance for BMI 30–34.9 kg/m2 [-0.11 ± 0.04 mm, p = 0.01]. All groups of infants born to women with a BMI ≥ 25 kg/m2 had significantly smaller LV internal diameters in end-systole: BMI 25–29.9 kg/m2 [-0.04 ± 0.02 mm, p = 0.04], BMI 30–34.9 kg/m2 [-0.12 ± 0.03 mm, p = 0.001] and BMI ≥ 35 kg/m2 [-0.11 ± 0.05 mm, p = 0.03].Compared with infants in the age reference group, infants born to women ≥ 40 years had significantly smaller LV internal diameters in end-diastole [-0.15 ± 0.04 mm, p = 0.001] and end-systole [-0.09 ± 0.04 mm, p = 0.009].ConclusionsSystematic population-based echocardiography of infants showed that a maternal prepregnancy BMI ≥ 25 kg/m2 and maternal age ≥ 40 years were associated with smaller systolic and diastolic LV diameters. The long-term effects are unknown.Clinical trial registrationApril 2016, Copenhagen Baby Heart, NCT02753348.

Correlation between the insertion-deletion variant of the angiotensin-converting enzyme gene and various classes of heart failure.

The angiotensin-converting enzyme (ACE) genetic variation for insertion/deletion (I/D) is located at the 16th intron of the ACE gene. A number of studies investigated the homozygous deletion genotype of ACE and its association with cardiovascular diseases. However, ACE's genetic variation and its association with heart failure (HF) is yet to be confirmed. We examined the possibility of the association between the ACE I/D gene variant with the severity of HF. The ACE genotypes were determined by polymerase chain reactions using samples derived from 150 patients with HF and 90 healthy subjects which were age and gender-matched. These patients included those of all four of the New York Heart Association (NYHA) classes. Echocardiography was performed on all HF patients and ejection fraction (EF), left ventricular systolic and diastolic diameters were measured. The HF patients were redistributed to systolic where EF is equal and less than 45% and non-systolic HF where EF is more than 45%. We demonstrate a statistically significant difference in DD genotype in NYHA class IV in comparison to the control group. The values of odds ratio (OR) (95%CI) of the DD genotype (DD vs ID and II) were 3.37 (1.01-11.19) (p value = 0.039) and the OR (95%CI) of the D allele (D vs I) was 2.55 (0.98-6.65) (p value = 0.049). Higher frequencies of D allele compared to I allele is linked to severity of HF. DD variant of the ACE gene is associated with NYHA class IV heart failure. This could have a profound impact on risk stratification and prognosis of HF in the management of this condition.

Left ventricular strain and myocardial work in short-term peritoneal dialysis patients

Background Initiation of dialysis encompasses new cardiovascular challenges on patients with end-stage renal disease (ESRD). This study used two-dimensional speckle-tracking echocardiography (2D-STE) to investigate the change of left ventricular (LV) myocardial function undergoing peritoneal dialysis (PD) within 1–3 months. Methods A total of 56 patients with ESRD and 27 healthy controls were enrolled in this prospective study. Mean duration of PD was 44.41 ± 16.44 days. We evaluated LV myocardial function of patients with ESRD in baseline and within 1–3 months after PD by 2D-STE with global longitudinal strains (GLS) and myocardial work (MW). Based on the level of serum phosphate before PD, patients were divided into two groups: the group with normal serum phosphate or hyperphosphatemia. Results Compared with healthy controls, patients with ESRD had impaired GLS (p < .001) and increased global work index (GWI) (p = .034), global constructive work (GCW) (p < .001), global wasted work (GWW) (p < .001), and lower global work efficiency (GWE) (p = .002). After PD therapy, GWI (p = .001), GCW (p < .001), and GWW (p = .023) decreased and closed to healthy subjects (p > .05) and no significant improvement was observed in GLS (p = .387). GLS of basal segments worsened in the hyperphosphatemia group (p = .005) and GWW reduced remarkably in the group with normal serum phosphate after PD treatment (p = .008). The change of left ventricular internal diameter in diastole (LVIDd) was the only parameter influenced GWI in post-dialysis patients (β = 0.324, p = .013). Conclusions Short-term PD treatment improved LV MW in ESRD patients. They benefited more when receiving treatment before the increase of serum phosphorus.

Long-acting CRF2 peptide agonist improves cardiac function in a rat heart failure model

Abstract Introduction Corticotropin-releasing factor receptor type 2 (CRF2) is a G protein-coupled receptor largely expressed in the cardiorenal system. Upon CRF2 activation, endogenous ligands such as urocortin-2 (UCN-2) or urocortin-3 (UCN-3) have been reported to increase cardiac function, decrease vascular resistance and improve natriuresis and diuresis in heart failure (HF) patients and in various experimental heart failure settings. However UCN-2 or -3 suffer from a very short half-life which markedly limit further clinical investigations in HF patients. For this purpose, a very long acting CRF2 peptide agonist has been developed. Objectives The aim of this study is to determine the acute effect on cardiac hemodynamic of a long acting CRF2 peptide agonist, COR-1167, in a rat model of chronic heart failure. Methods In 10-week-old Wistar rats, a total occlusion of the left anterior descending coronary artery was performed to induce myocardial infarction. Twelve weeks after myocardial infarction, rats had developed heart failure and received COR-1167 at the dose of 0.3 µg/kg or 1 µg/kg, or placebo, administered SC. Left ventricular dimensions and function were then assessed by echocardiography and left ventricular pressure-volume analysis. Results Three months after left coronary artery ligation rats displayed the classical features of heart failure as illustrated by an increase in left ventricular diastolic diameter and reduced ejection fraction, and decreases in LV end-systolic pressure, dP/dtmax and LV end-systolic pressure volume relationship. Major LV diastolic dysfunction developed, as shown by the increases in LV end-diastolic pressure, and LV end-diastolic pressure volume relationship and the decrease in dP/dtmin. Echocardiography and left ventricular pressure-volume analysis showed that COR-1167 at 0.3 and 1 µg/kg SC improved in a dose-dependent manner cardiac contractility and relaxation as assessed by LVESPVR and LVEDPVR, respectively. In addition, stroke volume and cardiac output were significantly ameliorated by COR-1167 at 1.0 µg/kg SC, with no change in heart rate. Conclusion Single acute administration of COR-1167 improved cardiac function in a rat model of heart failure with reduced ejection fraction. Altogether these results confirm that CRF2 agonism is an attractive therapeutic target for the treatment of heart failure.

Mortality and predictors of death in women and men with congestive heart failure due to ischemic and nonischemic cardiomyopathy

Abstract Background Heart failure (HF) is one of the leading causes of death from cardiovascular disease. Studies have shown that women have better survival than men, despite the higher number of hospitalizations among women. However, little is known about differences in mortality and predictors of death in women and men with heart failure due to ischemic (iCMP) and nonischemic (niCMP) cardiomyopathy. Purpose To analyze the mortality and predictors of death in women and men with iCMP and niCMP cardiomyopathy. Methods From February 2017 to September 2020, we analyzed mortality and predictors of death in women and men with CHF by iCMP and niCMP. Baseline data included clinical features and echocardiographic findings. Statistical analyses were performed using the Kaplan-Meier (K-M) method and Cox proportional hazards methods to analyze mortality rates in women and men. We used the Score Chi-Square of Cox regression to search for death predictors for women and men. Results We studied 7,487 patients, mean age of 64.3 ± 14.2 years, 4,417 (59%) males. Women with iCMP and niCMP had, respectively, higher mean age (p&amp;lt;0.0001), higher mean left ventricular ejection fraction (LVEF) (p&amp;lt;0.001), and smaller left ventricular diastolic diameter (LVDD) (p&amp;lt; 0.001). The mean dose of carvedilol was similar in both genders for iCMP and niCMP. Over a 3-year follow-up period, 420 (15.7%) men and 325 (14.7%) women with niCMP died (p=NS), and in iCMP, 519 (29.8%) men and 211 men died. (24.5%) women (p=0.004). Higher mortality was observed in women with iCMP compared to men with iCMP (p&amp;lt;0.0001). The cumulative incidence of death was higher in men (K-M: log-rank p&amp;lt;0.0001) with iCMP, but similar for niCMP (Figure). Cox regression for death adjusted for age, sex, previous myocardial infarction (MI), diabetes, previous stroke, chronic kidney disease (CKD), atrial fibrillation (AF), HF phenotype (systolic, diastolic, or mildly reduced ejection fraction), and LVEF showed that CKD, AF, diabetes, stroke, LVEF, and age, in descending order of Score Chi-Square, were the main predictors of death for niCMP and CKD, stroke, diabetes, AF, LVEF, age, and MI for iCMP. Conclusions Women had a better prognosis than men in iCMP, but similar mortality in niCMP. Gender was not an independent variable of death. Secondary prevention of cardiovascular events from the main predictors of death can significantly reduce the death rate in women and men with CHF by iCMP and niCMP.