Search

Context: Plantar intrinsic foot muscle strength training is difficult to master to a degree sufficient to elicit muscle hypertrophy in most individuals. It is possible that combining neuromuscular electrostimulation (NMES) and blood flow restriction (BFR) can elicit plantar intrinsic foot muscle hypertrophy regardless of the individual's technique. This study aimed to determine the effects of NMES training with BFR on acute muscle swelling in the abductor hallucis. Design: Randomized, controlled, single-blind trial design. Methods: Forty-eight participants were randomly allocated to the NMES + BFR, NMES, or Sham NMES + BFR groups. All participants received abductor hallucis NMES for 15 minutes. Participants in the NMES + BFR and Sham NMES + BFR groups received NMES with BFR. The intensity of NMES was the sensory threshold in the Sham NMES + BFR group. The cross-sectional area of the abductor hallucis was measured pretraining and posttraining using ultrasonography by a single investigator blinded to the participants' allocations. Results: After 15 minutes of training, the cross-sectional area of the abductor hallucis was significantly increased in the NMES + BFR (P<.001) and the Sham NMES + BFR (P = .004) groups. Moreover, the rate of increase was significantly higher in the NMES + BFR group than in the NMES or the Sham NMES + BFR groups (P<.001 and P = . 001, respectively). Conclusions: Since it is possible that the amount of muscle swelling immediately after training correlates with muscle hypertrophy when training is continued, the results of this study suggest that NMES training with BFR is a training method that can be expected to produce plantar intrinsic foot muscle hypertrophy. Further studies are needed to confirm the long-term effects of NMES training with BFR. [ABSTRACT FROM AUTHOR]

BACKGROUND: N6-methyladenosine (m6A) is a hot research topic in the mechanism of pathological cardiac remodeling and plays an important role in the development of cardiovascular diseases. OBJECTIVE: To summarize the possible mechanism by which m6A modification in non-coding RNAs regulates the main processes of pathological cardiac remodeling, such as pathological cardiac hypertrophy, cardiomyocyte death, myocardial fibrosis and vascular remodeling. METHODS: “m6A, non-coding RNA, pathological cardiac hypertrophy, cardiomyocyte apoptosis, cardiomyocyte pyroptosis, cardiomyocyte ferroptosis, myocardial fibrosis, vascular remodeling” were used as search terms in Chinese and English. Relevant literature from CNKI, PubMed and Web of Science databases published from January 1974 to April 2023 was retrieved, and finally 86 eligible articles were reviewed. RESULTS AND CONCLUSION: m6A modification is a highly dynamic and reversible modification. Pathological cardiac remodeling mainly involves pathological cardiac hypertrophy, cardiomyocyte apoptosis, cardiomyocyte pyroptosis, cardiomyocyte ferroptosis, myocardial fibrosis and vascular remodeling. m6A-related enzymes can regulate pathological cardiac remodeling processes through various non-coding RNAs and different signaling pathways, which can be used as a new potential intervention for cardiovascular diseases. In pathological cardiac remodeling, research on the regulatory relationship between m6A modification and non-coding RNAs is still in its infancy. With the development of epigenetics, m6A modification in non-coding RNAs is expected to have a new development in the regulation of pathological cardiac remodeling. [ABSTRACT FROM AUTHOR]

• The study found a higher prevalence of cardiac remodeling in the HDP (Hypertensive Disorders of Pregnancy) group compared to the NP (Non-Pregnant) group. • Eccentric hypertrophy was the most common type of cardiac remodeling in both groups, followed by concentric remodeling, and then concentric hypertrophy, which was specific to the HDP group. • There was a notable difference in left atrium diameter for both groups, favoring the HDP group, and this was accompanied by diastolic dysfunction. • The aortic root exhibited significant remodeling when comparing the two groups, with the remodeling favoring the HDP group. • The findings suggest that echocardiography should be considered for the assessment and treatment of women identified with HDP. • Long-term studies focusing on assessing the risk of developing aortic dissection in women with a history of HDP should be considered, particularly due to the remodeled aortic root. Hypertensive disorders of pregnancy (HDP) are among the leading causes of maternal morbidity and mortality. The primary objective of this study was to ascertain whether maternal cardiac remodeling is more prevalent in HDP than normotensive pregnancy and if significant change in aortic root size is involved. The secondary objective was to determine the types of cardiac remodeling often associated with HDP. A systematic search was conducted across four electronic databases, including Medline, PubMed, Cochrane and EMBASE. The reference lists of selected articles were also searched to ensure no relevant studies were missed. The Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines were followed in this systematic review. Out of 5,278 articles identified by the search terms, 9 were eligible for inclusion in the meta -analysis. The investigation unveiled a greater prevalence of maternal cardiac remodeling in HDP than normotensive pregnancies. The commonest type of maternal cardiac remodeling in both HDP and normotensive pregnancies was eccentric left ventricular hypertrophy, followed by concentric left ventricular remodeling which was more specific to HDP. Notably, left atrial diameter was significantly increased in HDP than normotensive pregnancies, suggesting higher prevalence of diastolic dysfunction. Additionally, the aortic root dimension was significantly increased in HDP than normotensive pregnancies. This study underscores the importance of monitoring cardiac health in pregnancy, particularly in those with hypertensive disorders, in order to mitigate potential complications and improve maternal outcomes. Finally, the risk of aortic dissection that may occur as a long-term effect of aortic root enlargement in women with history of HDP ought to be investigated in future studies. [ABSTRACT FROM AUTHOR]

There is a lack of effective therapeutic drugs for pulmonary arterial hypertension. Previous studies have demonstrated the positive cardiovascular system protective effects of the new peptide ACTY116. However, its stability in ordinary aqueous solution injections is poor and its half‐life in the body is short, which has hindered the development of preparations. This study aimed to prepare in situ forming implants (ISFIs) of the peptide ACTY116 and investigate its impact on pulmonary arterial hypertension. We prepared ISFIs using NMP/TA as a solvent and PLGA as a polymer. These ISFIs exhibited low viscosity, low toxicity and sustained release properties. In a mouse model of pulmonary hypertension induced by SU5416/hypoxia, both ISFIs and ACTY116 peptides effectively reduced pulmonary hypertension, cardiac hypertrophy and pulmonary blood vessel wall thickness. In conclusion, this study highlights the potential of ACTY116 as a treatment for pulmonary arterial hypertension and suggests that incorporating it into an in‐situ gel implant could be a promising option. [ABSTRACT FROM AUTHOR]

Neuroblastoma is a common pediatric tumor arising from the post-ganglionic sympathetic nervous system and is associated with hypertension in 25% of cases. We describe an unusual case of labile, multi-drug resistant hypertension associated with chemotherapy administration for neuroblastoma and provide potential management strategies in this scenario. We report the case of a 4-year-old female with a history of headaches who presented with hypertensive emergency and evidence of end-organ damage, including posterior reversible encephalopathy syndrome, acute cerebral infarct, concentric left ventricular hypertrophy, and growth failure secondary to a large, abdominal catecholamine-secreting neuroblastoma, which compressed the kidney vasculature and inferior vena cava. She was classified as intermediate risk according to Children's Oncology Group criteria and underwent chemotherapy, complicated by labile hypertension, followed by surgical resection. Vigilance in monitoring and treatment of hypertension is recommended during chemotherapy for neuroblastoma due to the potential catecholamine release in the setting of tumor lysis. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular death is the main cause of death in patients with end-stage kidney disease (ESKD). Left ventricular hypertrophy (LVH) and left atrial diameter (LAD) enlargement are frequent cardiac alterations in patients with ESKD and are major risk factors for cardiovascular events. However, it remains unclear whether there is an association between combined LAD or LVH and all-cause or cardiovascular mortality in this population. Methods: A single-centre, retrospective cohort study including 576 haemodialysis (HD) patients was conducted. Patients were evaluated by cardiac ultrasound, and the study cohort was divided into four groups according to LAD and LVH status: low LAD and non-LVH; low LAD and LVH; high LAD and non-LVH; and high LAD and LVH. We used Kaplan–Meier analysis and Cox proportional hazard regression to analyse all-cause and cardiovascular mortality after multivariate adjustment. Results: LAD was associated with an increased risk of all-cause mortality (HR 2.371, 1.602–3.509; p < 0.001). No significant differences were found between LVH and the risk of all-cause mortality. Patients with high LAD and LVH had significantly greater all-cause and cardiovascular mortality than did those with low LAD and non-LVH after adjustments for numerous potential confounders (HR 3.080, 1.608–5.899; p = 0.001) (HR 4.059, 1.753–9.397; p = 0.001). Conclusion: Among maintenance haemodialysis (MHD) patients, LAD was more strongly associated with mortality than was LVH. A high LAD and LVH are associated with a greater risk of mortality. Our results emphasize that the occurrence of LAD and LVH in combination provides information that may be helpful in stratifying the risk of MHD patients. [ABSTRACT FROM AUTHOR]

The myocardium is a highly oxidative tissue in which mitochondria are essential to supply the energy required to maintain pump function. When pathological hypertrophy develops, energy consumption augments and jeopardizes mitochondrial capacity. We explored the cardiac consequences of chronic swimming training, focusing on the mitochondrial network, in spontaneously hypertensive rats (SHR). Male adult SHR were randomized to sedentary or trained (T: 8-week swimming protocol). Blood pressure and echocardiograms were recorded, and hearts were removed at the end of the training period to perform molecular, imaging, or isolated mitochondria studies. Swimming improved cardiac midventricular shortening and decreased the pathological hypertrophic marker atrial natriuretic peptide. Oxidative stress was reduced, and even more interesting, mitochondrial spatial distribution, dynamics, function, and ATP were significantly improved in the myocardium of T rats. In the signaling pathway triggered by training, we detected an increase in the phosphorylation level of both AKT and glycogen synthase kinase-3 β, key downstream targets of insulin-like growth factor 1 signaling that are crucially involved in mitochondria biogenesis and integrity. Aerobic exercise training emerges as an effective approach to improve pathological cardiac hypertrophy and bioenergetics in hypertension-induced cardiac hypertrophy. [ABSTRACT FROM AUTHOR]

Cardiac hypertrophy (CH) is an adaptive response to maintain cardiac function; however, persistent stress responses lead to contractile dysfunction and heart failure. Although inflammation is involved in these processes, the mechanisms that control cardiac inflammation and hypertrophy still need to be clarified. The NLRP3 inflammasome is a cytosolic multiprotein complex that mediates IL-1β production. The priming step of NLRP3 is essential for increasing the expression of its components and occurs following NF-κB activation. Hyperthyroidism triggers CH, which can progress to maladaptive CH and even heart failure. We have shown in a previous study that thyroid hormone (TH)-induced CH is linked to the upregulation of S100A8, leading to NF-κB activation. Therefore, we aimed to investigate whether the NLRP3 inflammasome is involved in TH-induced CH and its potential role in CH pathophysiology. Hyperthyroidism was induced in NLRP3 knockout (NLRP3-KO), Caspase-1-KO and Wild Type (WT) male mice of the C57Bl/6J strain, aged 8–12 weeks, by triiodothyronine (7 μg/100 g BW, i.p.) administered daily for 14 days. Morphological and cardiac functional analysis besides molecular assays showed, for the first time, that TH-induced CH is accompanied by reduced NLRP3 expression in the heart and that it occurs independently of the NLRP3 inflammasome and caspase 1-related pathways. However, NLRP3 is important for the maintenance of basal cardiac function since NLRP3-KO mice had impaired diastolic function and reduced heart rate, ejection fraction, and fractional shortening compared with WT mice. [ABSTRACT FROM AUTHOR]

Introduction: Leukotrienes play a significant role in the pathogenesis of adenoid hypertrophy (A.H.). Therefore, we aimed to analyse the role of montelukast, a leukotriene receptor antagonist, alone or in combination with mometasone, a potent local intranasal steroid, for the treatment of A.H. Methods: Participants were children with A.H. were treated with montelukast alone or montelukast and mometasone furoate. The main outcome measures were effect of montelukast on clinical symptoms of A.H. A literature review was conducted using online search engines, Cochrane Library, PubMed, Web of Science and Scopus, for randomized clinical trials assessing children with A.H. treated with montelukast alone or montelukast and mometasone furoate. Seven randomized clinical trials (RCTs) were included with 742 children. Results: Our study reveals that montelukast alone or in combination with intranasal mometasone furoate significantly improves clinical symptoms of adenoid hypertrophy such as snoring, sleeping disturbance, mouth breathing and A/N ratio. Montelukast was superior to placebo in decreasing snoring (SMD = −1.00, 95% CI [−1.52, −0.49]), sleep discomfort (SMD = −1.26, 95% CI [−1.60, −0.93]), A/N ratio (MD = −0.11, 95% CI [−0.14, −0.09]) and mouth breathing (SMD = −1.36, 95% CI [−1.70, −1.02]). No difference was detected between montelukast and mometasone versus mometasone alone in snoring (SMD = −0.21, 95%CI [−0.69, 0.27]); however, the combination group was superior to the mometasone alone in mouth breathing (SMD = −0.46, 95% CI [−0.73, −0.19]). Conclusions: The limitation of studies included a small sample size, with an overall low to medium quality. Thus, further larger, higher‐quality RCTs are recommended to provide more substantial evidence. [ABSTRACT FROM AUTHOR]

Background- Primary Hyperparathyroidism (PHPT) has been associated with increased cardiovascular morbidity and early death. Data on the extent and clinical significance of cardiovascular abnormalities in primary hyperparathyroidism (PHPT) are conflicting. The main objective of this study was to evaluate the cardiac function in patients with PHPT without other known risk factors and to analyze the effect of parathyroidectomy. Methodology- In a Prospective Observational Cohort design, sixteen patients with Primary Hyperparathyroidism underwent Two-dimensional echocardiography, Electrocardiography, serum N-terminal pro-brain natriuretic peptide (NT-proBNP, a myocardial damage marker), before and 3 months after successful parathyroidectomy. Result- We observed significant improvement in Left ventricular ejection fraction (p = 0.010) in patients undergoing parathyroid surgery after 3 months postoperatively. There is significant reduction in LVMI (p=0.044) & posterior wall thickness (p=0.007), which are indicators of left ventricular hypertrophy after 3 months of surgery. Conclusion- Patients with PHPT who are symptomatic exhibit significant cardiovascular dysfunction, which improves three months following successful parathyroidectomy. As a part of screening, we should consider routine cardiovascular evaluation in all symptomatic patients of PHPT. Symptomatic PHPT patients should undergo early curative surgery for the reversal of the cardiovascular dysfunction and in asymptomatic PHPT patients also early surgery is recommended for the prevention of end organ damage. [ABSTRACT FROM AUTHOR]

Objective(s): Right ventricular hypertrophy (RVH) often results in failure of the right ventricle or even the left ventricle. Rosmarinic acid (RA), a natural polyphenol, is commonly found in Boraginaceae species and some species of ferns and hornworts. This study looked at how RA affects oxidative stress and left ventricular hemodynamic functions as well as RVH in monocrotaline (MCT) induced RVH model rats. Materials and Methods: To cause RVH, MCT (60 mg/kg) was intraperitoneally (IP) injected. Rats were given saline or RA (10, 15, and 30 mg/kg, gavage, over 21 days). In anesthetized rats, the lead II electrocardiogram was recorded. The hemodynamic functions of the isolated heart were measured using the Langendorff apparatus (at constant pressure). Investigations were made into the right ventricular hypertrophy index (RVHI), the activities of superoxide dismutase, catalase, glutathione, and Wnt and β-catenin gene expressions in the left ventricle. H&E staining was used. Results: A significant decline in electrocardiogram parameters and anti-oxidant enzyme activities, an increase in QTc (Q-T corrected) intervals, MDA (Malondialdehyde), RVHI, and Wnt/β-catenin gene expression, and also significant changes in the hemodynamic parameters were demonstrated in the MCT group. RA improved the above-mentioned factors. Conclusion: According to the findings, RA may act as a cardioprotective agent against cardiovascular complications brought on by RVH due to its capacity to boost the activity of cardiac anti-oxidant enzymes and decrease the expression of genes involved in vascular calcification. [ABSTRACT FROM AUTHOR]

Pulmonary hypertension (PH) and cardiac dysfunction are established comorbidities of congenital diaphragmatic hernia (CDH). However, there is very little data focusing on arterial hypertension in CDH. This study aims to investigate the incidence of arterial hypertension in neonates with CDH at hospital discharge. Archived clinical data of 167 CDH infants who received surgical repair of the diaphragmatic defect and survived for > 60 days were retrospectively analyzed. Blood pressure (BP) values were averaged for the last 7 days before discharge and compared to standard BP values for sex, age, and height provided by the AHA in 2004. BP values reaching or extending the 95th percentile were defined as arterial hypertension. The use of antihypertensive medication was analyzed at discharge and during hospitalization. Arterial hypertension at discharge was observed in 19 of 167 infants (11.3%) of which 12 (63%) were not receiving antihypertensive medication. Eighty patients (47.9%) received antihypertensive medication at any point during hospitalization and 28.9% of 152 survivors (n = 44) received antihypertensive medication at discharge, although in 45.5% (n = 20) of patients receiving antihypertensive medication, the indication for antihypertensive medication was myocardial hypertrophy or frequency control. BP was significantly higher in ECMO compared to non-ECMO patients, despite a similar incidence of arterial hypertension in both groups (13.8% vs. 10.1%, p = 0.473). Non-isolated CDH, formula feeding, and minimal creatinine in the first week of life were significantly associated with arterial hypertension on univariate analysis. Following multivariate analysis, only minimal creatinine remained independently associated with arterial hypertension. Conclusion: This study demonstrates a moderately high incidence of arterial hypertension in CDH infants at discharge and an independent association of creatinine values with arterial hypertension. Physicians should be aware of this risk and include regular BP measurements and test of renal function in CDH care and follow-up. What is Known: • Due to decreasing mortality, morbidity is increasing in surviving CDH patients. • Pulmonary hypertension and cardiac dysfunction are well-known cardiovascular comorbidities of CDH. What is New: • There is a moderately high incidence of arterial hypertension in CDH infants at discharge even in a population with frequent treatment with antihypertensive medication. • A more complicated hospital course (ECMO, higher degree of PH, larger defect size) was associated with a higher risk for arterial hypertension. [ABSTRACT FROM AUTHOR]

Salt‐sensitive hypertension is common among individuals with essential hypertension, and the prevalence of left ventricular hypertrophy (LVH) has increased. However, data from early identification of the risk of developing LVH in young adults with salt‐sensitive hypertension are lacking. Thus, the present study aimed to design a nomogram for predicting the risk of developing LVH in young adults with salt‐sensitive hypertension. A retrospective analysis of 580 patients with salt‐sensitive hypertension was conducted. The training set consisted of 70% (n = 406) of the patients, while the validation set consisted of the remaining 30% (n = 174). Based on multivariate analysis of the training set, predictors for LVH were extracted to develop a nomogram. Discrimination curves, calibration curves, and clinical utility were employed to assess the predictive performance of the nomogram. The final simplified nomogram model included age, sex, office systolic blood pressure, duration of hypertension, abdominal obesity, triglyceride‐glucose index, and estimated glomerular filtration rate (eGFR). In the training set, the model demonstrated moderate discrimination, as indicated by an area under the receiver operating characteristic (ROC) curve of 0.863 (95% confidence interval: 0.831–0.894). The calibration curve exhibited good agreement between the predicted and actual probabilities of LVH in the training set. Additionally, the validation set further confirmed the reliability of the prediction nomogram. In conclusions, the simplified nomogram, which consists of seven routine clinical variables, has shown good performance and clinical utility in identifying young adults with salt‐sensitive hypertension who are at high risk of LVH at an early stage. [ABSTRACT FROM AUTHOR]

Background: Left ventricular enlargement (LVE) is a common manifestation of cardiac remodeling that is closely associated with cardiac dysfunction, heart failure (HF), and arrhythmias. This study aimed to propose a machine learning (ML)-based strategy to identify LVE in HF patients by means of pulse wave signals. Method: We constructed two high-quality pulse wave datasets comprising a non-LVE group and an LVE group based on the 264 HF patients. Fourier series calculations were employed to determine if significant frequency differences existed between the two datasets, thereby ensuring their validity. Then, the ML-based identification was undertaken by means of classification and regression models: a weighted random forest model was employed for binary classification of the datasets, and a densely connected convolutional network was utilized to directly estimate the left ventricular diastolic diameter index (LVDdI) through regression. Finally, the accuracy of the two models was validated by comparing their results with clinical measurements, using accuracy and the area under the receiver operating characteristic curve (AUC-ROC) to assess their capability for identifying LVE patients. Results: The classification model exhibited superior performance with an accuracy of 0.91 and an AUC-ROC of 0.93. The regression model achieved an accuracy of 0.88 and an AUC-ROC of 0.89, indicating that both models can quickly and accurately identify LVE in HF patients. Conclusion: The proposed ML methods are verified to achieve effective classification and regression with good performance for identifying LVE in HF patients based on pulse wave signals. This study thus demonstrates the feasibility and potential of the ML-based strategy for clinical practice while offering an effective and robust tool for diagnosing and intervening ventricular remodeling. [ABSTRACT FROM AUTHOR]

Objectives Methods Results Interpretation Neurogenic muscle hypertrophy (NMH) is a rare condition characterized by focal muscle hypertrophy caused by chronic partial nervous injury. Given its infrequency, underlying mechanisms remain poorly understood. Inspired by two clinical cases, we conducted a systematic review to gain insights into the different aspects of NMH.We systematically searched online databases up until May 30, 2023, for reports of muscle hypertrophy attributed to acquired neurogenic factors. We conducted an exploratory analysis to identify commonly associated features. We also report two representative clinical cases.Our search identified 63 reports, describing 93 NMH cases, to which we added our two cases. NMH predominantly affects patients with compressive radiculopathy (68.4%), negligible muscular weakness (93.3%), and a chronic increase in muscle bulk. A striking finding in most neurophysiological studies (60.0%) is profuse spontaneous discharges, often hindering the analysis of voluntary traces. Some patients exhibited features consistent with more significant muscle damage, including higher creatine phosphokinase levels, muscle pain, and inflammatory muscle infiltration. These patients are sometimes referred to in literature as “focal myositis.” Treatment encompassed corticosteroid, Botulinum Toxin A, decompressive surgery, antiepileptic medications, and nerve blocks, demonstrating varying degrees of efficacy. Botulinum Toxin A yielded the most favorable response in terms of reducing spontaneous discharges.This systematic review aims to provide a clear description and categorization of this uncommon presentation of an often‐overlooked neurological disorder. Though questions remain about the underlying mechanism, evidence suggests that aberrant fiber overstimulation along with increased workload that promotes focal damage may result in muscle hypertrophy. This may serve as a guide for therapeutic interventions. [ABSTRACT FROM AUTHOR]

Cognitive reserve is the ability to actively cope with brain deterioration and delay cognitive decline in neurodegenerative diseases. It operates by optimizing performance through differential recruitment of brain networks or alternative cognitive strategies. We investigated cognitive reserve using Huntington's disease (HD) as a genetic model of neurodegeneration to compare premanifest HD, manifest HD, and controls. Contrary to manifest HD, premanifest HD behave as controls despite neurodegeneration. By decomposing the cognitive processes underlying decision making, drift diffusion models revealed a response profile that differs progressively from controls to premanifest and manifest HD. Here, we show that cognitive reserve in premanifest HD is supported by an increased rate of evidence accumulation compensating for the abnormal increase in the amount of evidence needed to make a decision. This higher rate is associated with left superior parietal and hippocampal hypertrophy, and exhibits a bell shape over the course of disease progression, characteristic of compensation. A study of cognitive reserve in neurodegenerative disease combining drift diffusion models with MRI highlights a reorganization of decision-making processes correlated to left parietal and hippocampal hypertrophy. [ABSTRACT FROM AUTHOR]

Cardiac hypertrophy is an adaptive response to stressors such as high cardiac workload, which might lead to abnormal cardiac function and heart failure. Previous studies have indicated that macrophage migration inhibitory factor (MIF) might play a protective role in cardiac hypertrophy. Here, we aimed to illustrate the mechanism of MIF in protecting against pressure overload‐induced cardiac hypertrophy. Transverse aortic constriction (TAC) mouse model was established and we found that overexpression of MIF protected against pressure overload‐induced cardiac hypotrophy in TAC treated mice, as evidenced by significantly decreased the heart weight. In addition, transthoracic echocardiography showed that overexpression of MIF restored ejection fraction in TAC‐treated mice. While TAC treatment resulted in a much larger cardiomyocyte size in mice, MIF overexpression notably decreased the cardiomyocyte size. Next, we demonstrated that MIF overexpression promoted the expression of miR‐29b‐3p which further downregulated the expression of its downstream target HMG box protein 1 (HBP1). Overexpression of HBP1 reversed the effect of MIF in alleviating Ang‐II induced oxidative stress in cardiomyocytes. In conclusion, our findings suggest that MIF could attenuate pressure overload‐induced cardiac hypertrophy through regulating the miR‐29b‐3p/HBP1 axis. [ABSTRACT FROM AUTHOR]

Brown adipose tissue (BAT) is correlated to cardiovascular health in rodents and humans, but the physiological role of BAT in the initial cardiac remodeling at the onset of stress is unknown. Activation of BAT via 48 h cold (16°C) in mice following transverse aortic constriction (TAC) reduced cardiac gene expression for LCFA uptake and oxidation in male mice and accelerated the onset of cardiac metabolic remodeling, with an early isoform shift of carnitine palmitoyltransferase 1 (CPT1) toward increased CPT1a, reduced entry of long chain fatty acid (LCFA) into oxidative metabolism (0.59 ± 0.02 vs. 0.72 ± 0.02 in RT TAC hearts, p <.05) and increased carbohydrate oxidation with altered glucose transporter content. BAT activation with TAC reduced early hypertrophic expression of β‐MHC by 61% versus RT‐TAC and reduced pro‐fibrotic TGF‐β1 and COL3α1 expression. While cardiac natriuretic peptide expression was yet to increase at only 3 days TAC, Nppa and Nppb expression were elevated in Cold TAC versus RT TAC hearts 2.7‐ and 2.4‐fold, respectively. Eliminating BAT thermogenic activation with UCP1 KO mice eliminated differences between Cold TAC and RT TAC hearts, confirming effects of BAT activation rather than autonomous cardiac responses to cold. Female responses to BAT activation were blunted, with limited UCP1 changes with cold, partly due to already activated BAT in females at RT compared to thermoneutrality. These data reveal a previously unknown physiological mechanism of UCP1‐dependent BAT activation in attenuating early cardiac hypertrophic and profibrotic signaling and accelerating remodeled metabolic activity in the heart at the onset of cardiac stress. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI) remains a major threat to human health due to the limited energy supply, disordered cell metabolism, massive cardiomyocyte death, and restricted regeneration. Although currently available therapies may relieve myocardial damage, restoring the dysregulated energy metabolism to normal levels has not yet been achieved. MOTS‐c has recently been identified as a regulator of biological metabolism to combat aging; however, its role in reprogramming cardiac metabolism remains to be elucidated. Here, MOTS‐c is chemically conjugated to self‐assembling Q11 peptide to fabricate an injectable hydrogel (MQgel) aimed to improve mitochondria function and cardiomyocyte metabolism post‐MI. It is observed that MQgel effectively protects mitochondria from oxidative damage and normalized cardiomyocyte metabolism, including glucose uptake, glycolysis, and the tricarboxylic acid (TCA) cycle, thereby inhibiting cardiomyocyte death and enhancing cardiomyocyte activity. In a rat MI model, intramyocardial injection of MQgel successfully minimizes the infarct area and fibrosis, promotes angiogenesis, suppresses myocardial hypertrophy, and improves cardiomyocyte survival and metabolic enzyme activity, all of which collaboratively attenuate the maladaptive cardiac remodeling and boost cardiac function and tissue repair. The findings suggest that the self‐assembled mitochondria metabolism‐regulatory peptide hydrogel effectively treats MI, and cellular bioenergy modulation provides a new therapeutic approach for tissue repair after injury. [ABSTRACT FROM AUTHOR]

The article focuses on a 12-year-old with juvenile absence epilepsy discovered to have elevated blood pressure during a sports physical, prompting further evaluation. Topics include the patient's clinical presentation, including asymptomatic hypertension, and diagnostic findings such as abnormal electrocardiogram (ECG) and echocardiogram results indicating left ventricular hypertrophy.

The specific pathophysiological pathways through which diabetes exacerbates myocardial ischemia/reperfusion (I/R) injury remain unclear; however, dysregulation of immune and inflammatory cells, potentially driven by abnormalities in their number and function due to diabetes, may play a significant role. In the present investigation, we simulated myocardial I/R injury by inducing ischemia through ligation of the left anterior descending coronary artery in mice for 40 min, followed by reperfusion for 24 h. Previous studies have indicated that protein kinase Cβ (PKCβ) is upregulated under hyperglycemic conditions and is implicated in the development of various diabetic complications. The Y4 RNA fragment is identified as the predominant small RNA component present in the extracellular vesicles of cardio sphere-derived cells (CDCs), exhibiting notable anti-inflammatory properties in the contexts of myocardial infarction and cardiac hypertrophy. Our investigation revealed that the administration of Y4 RNA into the ventricular cavity of db/db mice following myocardial I/R injury markedly enhanced cardiac function. Furthermore, Y4 RNA was observed to facilitate M2 macrophage polarization and interleukin-10 secretion through the suppression of PKCβ activation. The mechanism by which Y4 RNA affects PKCβ by regulating macrophage activation within the inflammatory environment involves the inhibition of ERK1/2 phosphorylation In our study, the role of PKCβ in regulating macrophage polarization during myocardial I/R injury was investigated through the use of PKCβ knockout mice. Our findings indicate that PKCβ plays a crucial role in modulating the inflammatory response associated with macrophage activation in db/db mice experiencing myocardial I/R, with a notable exacerbation of this response observed upon significant upregulation of PKCβ expression. In vitro studies further elucidated the protective mechanism by which Y4 RNA modulates the PKCβ/ERK1/2 signaling pathway to induce M2 macrophage activation. Overall, our findings suggest that Y4 RNA plays an anti-inflammatory role in diabetic I/R injury, suggesting a novel therapeutic approach for managing myocardial I/R injury in diabetic individuals. [ABSTRACT FROM AUTHOR]

Background: The atherogenic index of plasma (AIP) is a simple and reliable marker of insulin resistance and is closely associated with various cardiovascular diseases (CVDs). However, the relationships between AIP and left ventricular (LV) geometric indicators have not been adequately assessed. This study was carried out to investigate the association between AIP and LV geometric abnormalities in obstructive sleep apnea (OSA) patients. Methods: This retrospective cross-sectional study included a total of 618 OSA patients (57.3 ± 12.4 years, 73.1% males, BMI 28.1 ± 4.2 kg/m2) who underwent echocardiography. Patients with OSA were diagnosed with clinical symptoms and an apnea-hypopnea index ≥ 5.0. LV hypertrophy (LVH) was defined as left ventricular mass index (LVMIh2.7) ≥ 50.0 g/m2.7 for men and 47.0 g/m2.7 for women. AIP was calculated as log10 (TG/HDL-C). Results: Compared with the non-LVH group, AIP was significantly higher in the LVH group (0.19 ± 0.29 vs 0.24 ± 0.28, P = 0.024) and the concentric LVH group (0.18 ± 0.29, 0.19 ± 0.30, 0.20 ± 0.26 and 0.29 ± 0.29 in the control, concentric remodeling, eccentric hypertrophy and concentric hypertrophy groups, respectively, P = 0.021). Meanwhile, in the group of patients with the highest AIP tertile, the levels of LVMIh2.7 (42.8 ± 10.5, 43.2 ± 9.3 and 46.1 ± 12.1 in the T1, T2 and T3 groups, respectively, P = 0.003), and the prevalence of LVH (25.2%, 24.0% and 34.6% in the T1, T2 and T3 groups, respectively, P = 0.032) and concentric LVH (10.7%, 9.8% and 20.2% in the T1, T2 and T3 groups, respectively, P = 0.053) were higher compared with those in the other groups. Positive correlations between AIP and LV geometric indicators including the LVMIh2.7, LVMIBSA, LV mass (LVM), diastolic left ventricular inner diameter (LVIDd), diastolic left ventricular posterior wall thickness (PWTd) and diastolic interventricular septal thickness (IVSTd), were revealed according to correlation analysis (P < 0.05). Furthermore, AIP was independently associated with LVMIh2.7 according to multivariate linear regression model (β = 0.125, P = 0.001). Notably, AIP remained independently associated with an elevated risk of LVH [odds ratio (OR) = 1.317 per 1 standard deviation (SD) increment, 95% confidence interval (CI): 1.058 - 1.639, P = 0.014) and concentric LVH (OR = 1.545 per 1 SD increment, 95% CI: 1.173 - 2.035, P = 0.002) after fully adjusting for all confounding risk factors by multivariate logistic regression analyses. Conclusions: AIP was independently associated with an increased risk of LVH and concentric LVH in OSA patients. Therefore, AIP, as a practical and cost-effective test, might be useful in monitoring hypertrophic remodeling of the heart and improving CVDs risk stratification in clinical management of OSA. [ABSTRACT FROM AUTHOR]

Cardiac hypertrophy can be appreciated microscopically by assessing for myocyte hypertrophy. Features of myocyte hypertrophy include increased myocyte diameter, together with increase in nuclear hyperchromicity, size and irregularity, and an increase in binucleated myocytes. There is limited literature to demonstrate whether these features are uniform within the myocardium in the post mortem setting. This study compared the myocyte diameter, myocyte nuclear length, and proportion binucleated myocytes between the free wall of the left ventricle and interventricular septum in 21 post mortem cases. It showed regional variation in myocyte hypertrophy parameters between the free walls of the left ventricle and intraventricular septum. Over 75% of cases showed significant differences in myocyte nuclear length and myocyte diameter (ANOVA one-way, p < 0.05), whereas binucleated myocyte nuclei did not show any significant difference. The result of this study has implication in sampling and assessing myocyte hypertrophy. Further studies are recommended to explore the reasons why this variation occurred and whether it is clinically significant. [ABSTRACT FROM AUTHOR]

Type 2 diabetes predisposes patients to heart disease, which is the primary cause of death across the globe. Type 2 diabetes often accompanies obesity and is defined by insulin resistance and abnormal glucose handling. Insulin resistance impairs glucose uptake and results in hyperglycemia, which damages tissues such as kidneys, liver, and heart. 2-oxoglutarate (2-OG)- and iron-dependent oxygenases (2-OGDOs), a family of enzymes regulating various aspects of cellular physiology, have been studied for their role in obesity and diet-induced insulin resistance. However, nothing is known of the 2-OGDO family member 2-oxoglutarate and iron-dependent prolyl hydroxylase domain containing protein 1 (OGFOD1) in this setting. OGFOD1 deletion leads to protection in cardiac ischemia-reperfusion injury and cardiac hypertrophy, which are two cardiac events that can lead to heart failure. Considering the remarkable correlation between heart disease and diabetes, the cardioprotection observed in OGFOD1-knockout mice led us to challenge these knockouts with high-fat diet. Wildtype mice fed a high-fat diet developed diet-induced obesity, insulin resistance, and glucose intolerance, but OGFOD1 knockout mice fed this same diet were resistant to diet-induced obesity and insulin resistance. These results support OGFOD1 down-regulation as a strategy for preventing obesity and insulin handling defects. [ABSTRACT FROM AUTHOR]

Background: Abnormal remodeling of distal pulmonary arteries in patients with pulmonary arterial hypertension (PAH) leads to progressively increased pulmonary vascular resistance, followed by right ventricular hypertrophy and failure. Despite considerable advancements in PAH treatment prognosis remains poor. We aim to evaluate the potential for using the cytokine resistin as a genetic and biological marker for disease severity and survival in a large cohort of patients with PAH. Methods: Biospecimens, clinical, and genetic data for 1121 adults with PAH, including 808 with idiopathic PAH (IPAH) and 313 with scleroderma-associated PAH (SSc-PAH), were obtained from a national repository. Serum resistin levels were measured by ELISA, and associations between resistin levels, clinical variables, and single nucleotide polymorphism genotypes were examined with multivariable regression models. Machine-learning (ML) algorithms were applied to develop and compare risk models for mortality prediction. Results: Resistin levels were significantly higher in all PAH samples and PAH subtype (IPAH and SSc-PAH) samples than in controls (P <.0001) and had significant discriminative abilities (AUCs of 0.84, 0.82, and 0.91, respectively; P <.001). High resistin levels (above 4.54 ng/mL) in PAH patients were associated with older age (P =.001), shorter 6-min walk distance (P =.001), and reduced cardiac performance (cardiac index, P =.016). Interestingly, mutant carriers of either rs3219175 or rs3745367 had higher resistin levels (adjusted P =.0001). High resistin levels in PAH patients were also associated with increased risk of death (hazard ratio: 2.6; 95% CI: 1.27–5.33; P <.0087). Comparisons of ML–derived survival models confirmed satisfactory prognostic value of the random forest model (AUC = 0.70, 95% CI: 0.62–0.79) for PAH. Conclusions: This work establishes the importance of resistin in the pathobiology of human PAH. In line with its function in rodent models, serum resistin represents a novel biomarker for PAH prognostication and may indicate a new therapeutic avenue. ML-derived survival models highlighted the importance of including resistin levels to improve performance. Future studies are needed to develop multi-marker assays that improve noninvasive risk stratification. [ABSTRACT FROM AUTHOR]

Background: There is increasing interest in elucidating the relationship between adenoid hypertrophy (AH) and allergic rhinitis (AR). However, the impact of aeroallergen sensitization patterns on children with AH and AR remains unclear. Methods: Patients aged 2–8 years (recruited from January 2019 to December 2022) with nasal symptoms were assessed for allergies, adenoid size, and respiratory viral infection history. The serum total immunoglobulin E (IgE) and specific IgE levels were measured, and flexible nasal endoscopy was performed. The relationship between AH, aeroallergen sensitization patterns, and lymphocyte subpopulations in adenoid samples was analyzed using flow cytometry. Results: In total, 5281 children were enrolled (56.5% with AR; and 48.6% with AH). AH was more prevalent in children with AR. Compared to nonsensitized individuals, those polysensitized to molds had a higher prevalence of AH (adjusted OR 1.61, 95% CI 1.32–1.96) and a greater occurrence of two or more respiratory viral infections, particularly in adenoidectomy patients. The percentages and corrected absolute counts of regulatory T (Treg) cells, activated Tregs, class‐switched memory B cells (CSMBs), natural killer (NK) T cells, and NK cell subpopulations were reduced in the adenoid tissues of children with both AH and AR (AH‐AR) compared to AH‐nAR children. Polysensitization in AH‐AR children correlated with lower CSMB percentages. Conclusion: Polysensitivity to molds is associated with an increased risk of AH in children with AR. Fewer B cells, NK cells, and Treg cells with an effector/memory phenotype were detected in the adenoids of AR children, and these lower percentages of immune cells, particularly CSMBs, were closely linked to aeroallergen sensitization models and respiratory viral infection. [ABSTRACT FROM AUTHOR]

Objective: The aim of this study was to investigate whether urinary glycosaminoglycans (GAG) levels reflect clinical status in men with lower urinary tract symptoms and if they could be used as a marker in management of overactive bladder (OAB). Methods: A total of 34 patients were recruited who were admitted with LUTS and diagnosed as having clinically bladder outlet obstruction (BOO) due to prostate enlargement. These newly diagnosed, never treated patients underwent routine investigation, consisting of history, physical examination, PSA, ultrasound, uroflowmetry, assessment of symptoms scored by both International Prostate Symptom Score (IPSS) and Marmara- Overactive Bladder Questionnaire (M-OBQ). The patients were divided into two groups as those with an initial M-OBQ score < 12 (group 1) and ≥ 13 (group 2). Alfa blocker was initiated in eligible patients. Further evaluations included prostate volume measurement, pre- and post-treatment urinary GAG levels, IPSS and M-QAOB values and maximum urine flow rate (Qmax). Results: Before treatment, urinary GAG level was 21.5 mg/gCr (6.1-45.5) in Group 1, and 23.35 mg/gCr (15.6-32.6) in Group 2 (p =0.845). After the treatment, the GAG level in Group 1 and Group 2 were found to be 19.8 mg/gCr (7.4-70.5) and 18 (7.6- 41.7), respectively (p = 0.511). No difference in GAG levels was found in subgroup analysis for patients with or without OAB. Conclusions: In recent years, there have been many studies investigating the relationship between LUTS and urinary markers. However, in our prospective study, no relationship was found between pre- and post- treatment urinary GAG levels in patients with LUTS with or without OAB. [ABSTRACT FROM AUTHOR]

Background: Stimulation of ventricular hypertrophy and heart rate are two major cardiac effects of thyroid hormone (TH). The aim of this study was to determine in vivo which TH receptor (TR)—α or β—and which mode of TR action—canonical gene expression or DNA-binding independent noncanonical action—mediate these effects. Methods: We compared global TRα and TRβ knockout mice (TRαKO; TRβKO) with wild-type (WT) mice to determine the TR isoform responsible for T3 effects. The relevance of TR DNA binding was studied in mice with a mutation in the DNA-binding domain that selectively abrogates DNA binding and canonical TR action (TRαGS; TRβGS). Hearts were studied with echocardiography at baseline and after 7 weeks of T3 treatment. Gene expression was measured with real-time polymerase chain reaction. Heart rate was recorded with radiotelemetry transmitters for 7 weeks in untreated, hypothyroid, and T3-treated mice. Results: T3 induced ventricular hypertrophy in WT and TRβKO mice, but not in TRαKO mice. Hypertrophy was also induced in TRαGS mice. Thus, hypertrophy is mostly mediated by noncanonical TRα action. Similarly, repression of Mhy7 occurred in WT and TRαGS mice. Basal heart rate was largely dependent on canonical TRα action. But responsiveness to hypothyroidism and T3 treatment as well as expression of pacemaker gene Hcn2 were still preserved in TRαKO mice, demonstrating that TRβ could compensate for absence of TRα. Conclusions: T3-induced cardiac hypertrophy could be attributed to noncanonical TRα action, whereas heart rate regulation was mediated by canonical TRα action. TRβ could substitute for canonical but not noncanonical TRα action. [ABSTRACT FROM AUTHOR]

Background: Thyroid hormones regulate cardiac functions mainly through direct actions in the heart and by binding to the thyroid hormone receptor (TR) isoforms α1 and β. While the role of the most abundantly expressed isoform, TRα1, is widely studied and well characterized, the role of TRβ in regulating heart functions is still poorly understood, primarily due to the accompanying elevation of circulating thyroid hormone in TRβ knockout mice (TRβ-KO). However, their hyperthyroidism is ameliorated at thermoneutrality, which allows studying the role of TRβ without this confounding factor. Methods: Here, we noninvasively monitored heart rate in TRβ-KO mice over several days using radiotelemetry at different housing temperatures (22°C and 30°C) and upon 3,3′,5-triiodothyronine (T3) administration in comparison to wild-type animals. Results: TRβ-KO mice displayed normal average heart rate at both 22°C and 30°C with only minor changes in heart rate frequency distribution, which was confirmed by independent electrocardiogram recordings in freely-moving conscious mice. Parasympathetic nerve activity was, however, impaired in TRβ-KO mice at 22°C, and only partly rescued at 30°C. As expected, oral treatment with pharmacological doses of T3 at 30°C led to tachycardia in wild-types, accompanied by broader heart rate frequency distribution and increased heart weight. The TRβ-KO mice, in contrast, showed blunted tachycardia, as well as resistance to changes in heart rate frequency distribution and heart weight. At the molecular level, these observations were paralleled by a blunted cardiac mRNA induction of several important genes, including the pacemaker channels Hcn2 and Hcn4, as well as Kcna7. Conclusions: The phenotyping of TRβ-KO mice conducted at thermoneutrality allows novel insights on the role of TRβ in cardiac functions in the absence of the usual confounding hyperthyroidism. Even though TRβ is expressed at lower levels than TRα1 in the heart, our findings demonstrate an important role for this isoform in the cardiac response to thyroid hormones. [ABSTRACT FROM AUTHOR]

The efficacy of convolutional neural network (CNN)-enhanced electrocardiography (ECG) in detecting hypertrophic cardiomyopathy (HCM) and dilated HCM (dHCM) remains uncertain in real-world applications. This retrospective study analyzed data from 19,170 patients (including 140 HCM or dHCM) in the Shinken Database (2010–2017). We evaluated the sensitivity, positive predictive rate (PPR), and F1 score of CNN-enhanced ECG in a "basic diagnosis" model (total disease label) and a "comprehensive diagnosis" model (including disease subtypes). Using all-lead ECG in the "basic diagnosis" model, we observed a sensitivity of 76%, PPR of 2.9%, and F1 score of 0.056. These metrics improved in cases with a diagnostic probability of ≥ 0.9 and left ventricular hypertrophy (LVH) on ECG: 100% sensitivity, 8.6% PPR, and 0.158 F1 score. The "comprehensive diagnosis" model further enhanced these figures to 100%, 13.0%, and 0.230, respectively. Performance was broadly consistent across CNN models using different lead configurations, particularly when including leads viewing the lateral walls. While the precision of CNN models in detecting HCM or dHCM in real-world settings is initially low, it improves by targeting specific patient groups and integrating disease subtype models. The use of ECGs with fewer leads, especially those involving the lateral walls, appears comparably effective. [ABSTRACT FROM AUTHOR]

• Maternal copper deficiency induced growth retardation in offspring. • Maternal copper deficiency caused cardiac dysfunction and liver injury in offspring. • Autophagy is activated by copper deficiency in offspring. Maternal nutritional deficiencies during pregnancy result in birth defects and elevate the risk of cardiovascular diseases and metabolic diseases. Accumulating evidence suggests that deficiency of copper, a fundamental trace element involved in several pivotal physiological processes, promotes the onset of multiple diseases, notably heart and liver diseases. Yet, exploration into the effects of maternal copper deficiency (CuD) on offspring is still limited. In this study, we hypothesized that maternal CuD induced cardiomyopathy and liver injury in offspring through the activation of autophagy. We established a maternal CuD mouse model by feeding pregnant C57BL/6 mice with a CuD diet until the end of the experiment. Echocardiography, histological analysis, western blotting, and quantitative polymerase chain reaction were performed on offspring at postnatal day 14. We found that maternal CuD caused growth retardation and early postnatal death in the offspring. Furthermore, our results revealed that CuD induced cardiac systolic dysfunction, cardiac hypertrophy, hepatic steatosis, and liver injury. Moreover, higher expression of LC3 and lower expression of p62 were observed in the heart tissues and liver tissues of CuD mice compared with the control group, indicating that CuD induced autophagy activation. In conclusion, maternal CuD caused severely deleterious effects on the heart and liver of the offspring via activating autophagy. To explore the effect of dietary maternal CuD on offspring, we established an animal model by feeding pregnant mice with a CuD diet. We found that CuD caused cardiac systolic dysfunction and liver injury. Moreover, we presented the increased LC3 and decreased p62 in CuD mouse heart tissues and liver tissues. These results indicate that CuD causes systolic dysfunction and hepatic steatosis in offspring, which is associated with activation of autophagy. Abbreviations: CuA, copper adequate; CuD, copper deficiency. [Display omitted] [ABSTRACT FROM AUTHOR]

Proper protein degradation is required for cellular protein homeostasis and organ function. Particularly, in post-mitotic cells, such as cardiomyocytes, unbalanced proteolysis due to inflammatory stimuli and oxidative stress contributes to organ dysfunction. To ensure appropriate protein turnover, eukaryotic cells exert two main degradation systems, the ubiquitin-proteasome-system and the autophagy-lysosome-pathway. It has been shown that proteasome activity affects the development of cardiac dysfunction differently, depending on the type of heart failure. Studies analyzing the inducible subtype of the proteasome, the immunoproteasome (i20S), demonstrated that the i20S plays a double role in diseased hearts. While i20S subunits are increased in cardiac hypertrophy, atrial fibrillation and partly in myocarditis, the opposite applies to diabetic cardiomyopathy and ischemia/reperfusion injury. In addition, the i20S appears to play a role in autophagy modulation depending on heart failure phenotype. This review summarizes the current literature on the i20S in different heart failure phenotypes, emphasizing the two faces of i20S in injured hearts. A selection of established i20S inhibitors is introduced and signaling pathways linking the i20S to autophagy are highlighted. Mapping the interplay of the i20S and autophagy in different types of heart failure offers potential approaches for developing treatment strategies against heart failure. [Display omitted] • Impaired immunoproteasome (i20S) activity differently affects heart failure types. • i20S is increased in cardiac hypertrophy, atrial fibrillation and in myocarditis. • i20S is decreased in diabetic cardiomyopathy and ischemia/reperfusion injury. • i20S can directly impact autophagy via Atg5 degradation and Akt/mTOR activation. • Lack of i20S increases mitochondrial fission and decreases AMPK activity. [ABSTRACT FROM AUTHOR]

Background: In patients with hypertrophic cardiomyopathy (HCM), impaired augmentation of stroke volume and diastolic dysfunction contribute to exercise intolerance. Systolic–diastolic (S‐D) coupling characterizes how systolic contraction of the left ventricle (LV) primes efficient elastic recoil during early diastole. Impaired S‐D coupling may contribute to the impaired cardiac response to exercise in patients with HCM. Methods: Patients with HCM (n = 25, age = 47 ± 9 years) and healthy adults (n = 115, age = 49 ± 10 years) underwent a cardiopulmonary exercise testing (CPET) and echocardiogram. S‐D coupling was defined as the ratio of LV longitudinal excursion of the mitral annulus during early diastole (EDexc) and systole (Sexc) and compared between groups. Peak oxygen uptake (peak V̇O2) (Douglas bags), cardiac index (C2H2 rebreathe), and stroke volume index (SVi) were assessed during CPET. Linear regression was performed between S‐D coupling and peak V̇O2, peak cardiac index, and peak SVi. Results: S‐D coupling was lower in HCM (Controls: 0.63 ± 0.08, HCM: 0.56 ± 0.10, p < 0.001). Peak V̇O2 and stroke volume reserve were lower in patients with HCM (Peak VO2 Controls: 28.5 ± 5.5, HCM: 23.7 ± 7.2 mL/kg/min, p < 0.001, SV reserve: Controls 39 ± 16, HCM 30 ± 18 mL, p = 0.008). In patients with HCM, S‐D coupling was associated with peak V̇O2 (r = 0.47, p = 0.018), peak cardiac index (r = 0.60, p = 0.002), and peak SVi (r = 0.63, p < 0.001). Conclusion: Systolic–diastolic coupling was impaired in patients with HCM and was associated with fitness and the cardiac response to exercise. Inefficient S‐D coupling may link insufficient stroke volume generation, diastolic dysfunction, and exercise intolerance in HCM. [ABSTRACT FROM AUTHOR]

BACKGROUND: In the last decades, emerging evidence has shown that muscle growth is not homogeneous along a muscle head. This phenomenon is known as regional muscle hypertrophy and has led to several questions regarding the implications it may have for health and sports performance. OBJECTIVE: The aim of this study was to determine whether regional hypertrophy can be predicted by surface electromyography (sEMG). METHODS: 36 participants performed two arm exercises (preacher curls and inclined curls) in a random order to muscle failure at 70% of the 1 RM of the bicep curl exercise. As every participant performed a different number of repetitions, Peak sEMG and the integral of the sEMG of the last 3 repetitions was analyzed an compared to previously performed maximal voluntary isometric contractions (MVIC). RESULTS: The independent sample t -tests showed no significant differences neither in the peak nor in the integral of the sEMG between exercises for any given region. CONCLUSIONS: sEMG cannot be used to predict regional hypertrophy. [ABSTRACT FROM AUTHOR]

Objective: To assess the role of laryngo-tracheo-bronchoscopy in children with obstructive sleep apnoea by identifying airway abnormalities at surgery, that occur separately or in addition to adenotonsillar hypertrophy, and examining the correlation with respiratory parameters. Methods: A retrospective study was conducted of children with obstructive sleep apnoea who underwent laryngo-tracheo-bronchoscopy intra-operatively, performed by a single ENT surgeon from February 2016 to July 2019. Pre- and post-operative minimum oxygen saturation, apnoea-hypopnoea index, and oxygen desaturation index were recorded. Results: Sixty-five children were identified; 34 were aged less than three years and 31 were aged three years or more. 77 per cent and 13 per cent respectively had an airway abnormality; the t -test showed a significantly higher mean oxygen desaturation index and lower mean minimum oxygen saturation pre-operatively compared to children without an airway abnormality. Conclusion: An update of the surgical pathway for children aged less than three years with obstructive sleep apnoea is required to include laryngo-tracheo-bronchoscopy intra-operatively. A t -test analysis of the pre-operative respiratory parameters suggests that airway abnormalities contribute to obstructive sleep apnoea severity. [ABSTRACT FROM AUTHOR]

Background: Klippel‐Trenaunay‐Weber syndrome (KTWS) is a rare disease with a wide range of manifestations. KTWS is characterized by a clinical triad of varicosities of the extremities, cutaneous vascular malformations, and hypertrophy of soft tissues and long bones. The diagnosis is made clinically supplemented with magnetic resonance imaging and computed tomography. Aim: Hereby we aim to highlight the significance of the possible life‐threatening first‐time presentations associated with the GI system in previously undiagnosed KTWS patients. Patient: We report the case of a 47‐year‐old male with KTWS, who presented with various symptoms such as rectorrhagia since childhood, digestive problems and abnormal lateral vascular malformations of the left buttock which extended all the way to the leg, vascular malformations of the left fourth and fifth toes as well as soft tissue swelling of the left foot. There was no evidence of other clinical presentations. The patient was hospitalized with severe rectorrhagia and a hemoglobin level of 3/9. Physical examination revealed a blood pressure of 85/55 and pulse rate of 115. Ruptured aneurysm of the superior mesenteric artery was found on angiography and subsequently treated with embolization. Dermatologic evaluation showed pitting edema of the left leg and foot and multiple vascular lesions. Thus a diagnosis of KTWS was established. Pulsed dye laser therapy and compression bandage was performed for the patient. The patient's follow‐up was done 3 months after discharge for which the patient was again consulted by a dermatologist and gastroenterologist. Lymphedema of the left leg had improved to a great extend so treatment with compression bandage was continued. Colonoscopy was repeated for the patient to evaluate and control possible active sources of bleeding, due to potential life‐threating complications. Results: According to previous findings, there have been few case reports of KTWS presenting with gastrointestinal manifestations, fewer of which have covered acute life‐threatening bleedings associated with this system. [ABSTRACT FROM AUTHOR]

Multiple intramuscular variables have been proposed to explain the high variability in resistance training induced muscle hypertrophy across humans. This study investigated if muscular androgen receptor (AR), estrogen receptor α (ERα) and β (ERβ) content and fiber capillarization are associated with fiber and whole‐muscle hypertrophy after chronic resistance training. Male (n = 11) and female (n = 10) resistance training novices (22.1 ± 2.2 years) trained their knee extensors 3×/week for 10 weeks. Vastus lateralis biopsies were taken at baseline and post the training period to determine changes in fiber type specific cross‐sectional area (CSA) and fiber capillarization by immunohistochemistry and, intramuscular AR, ERα and ERβ content by Western blotting. Vastus lateralis volume was quantified by MRI‐based 3D segmentation. Vastus lateralis muscle volume significantly increased over the training period (+7.22%; range: −1.82 to +18.8%, p < 0.0001) but no changes occurred in all fiber (+1.64%; range: −21 to +34%, p = 0.869), type I fiber (+1.33%; range: −24 to +41%, p = 0.952) and type II fiber CSA (+2.19%; range: −23 to +29%, p = 0.838). However, wide inter‐individual ranges were found. Resistance training increased the protein expression of ERα but not ERβ and AR, and the increase in ERα content was positively related to changes in fiber CSA. Only for the type II fibers, the baseline capillary‐to‐fiber‐perimeter index was positively related to type II fiber hypertrophy but not to whole muscle responsiveness. In conclusion, an upregulation of ERα content and an adequate initial fiber capillarization may be contributing factors implicated in muscle fiber hypertrophy responsiveness after chronic resistance training. [ABSTRACT FROM AUTHOR]

Simple Summary: The contrast-enhanced ultrasound (CEUS) allows the evaluation of the vascularization of an organ, using contrast agents composed of gas microbubbles, such as sulfur hexafluoride. Prostate perfusion is increased in dogs with benign prostatic hyperplasia (BPH), due to the stimulation of dihydrotestosterone (DHT). In the present study, CEUS is applied for monitoring dogs with BPH, receiving osaterone acetate (OSA). Fifteen intact adult dogs are referred for BPH. A CPSE assay and B-mode ultrasound confirm the diagnosis. CEUS is performed before OSA treatment (D0) and highlights the rapid diffusion times of the contrast agent (length of the wash-in and wash-out phases). Prostatic cysts and parenchymal alteration are also detected. After treatment (D1), the CPSE and prostate volume are significantly reduced, while CEUS detects a significant increase in wash-in and wash-out times and a reduction in parenchymal abnormalities. These findings confirm the decrease in prostatic perfusion after OSA treatment and, although preliminary, are promising for the broader use of CEUS for the diagnosis and monitoring of dogs with BPH. The prostate is the only sexual gland of the male dog, and dihydrotestosterone (DHT) regulates its growth. In intact dogs, constant DHT stimulation results in benign prostatic hyperplasia (BPH) that can be treated with osaterone acetate (OSA). This study describes the effects of OSA treatment, detected by contrast-enhanced ultrasonography (CEUS), highlighting prostatic vascularization with a contrast agent composed of gas microbubbles. Fifteen dogs (2–8 years) of different sizes and breeds (4–30 kg) diagnosed with BPH are involved in the study. Before treatment (D0), CPSE is measured (294.05 ± 115.97 ng/mL), and a B-mode ultrasound is performed (Vratio = 2.80 ± 1.85), confirming BPH. CEUS highlights the length of the wash-in (11.93 ± 2.08 s) and wash-out (42.20 ± 6.99 s) phases of the contrast agent in the prostate and the presence of cysts and parenchymal alteration. Dogs are treated with OSA (0.5 mg/kg for 7 days) and reassessed after 21 days (D1): CPSE and prostate volume are significantly (p < 0.001) reduced. The length of the wash-in (14.73 ± 2.54 s) and wash-out (51.13 ± 6.03 s) phases are significantly (p < 0.001) increased. The results confirm the effectiveness of the treatment, particularly the reduction in prostatic perfusion, confirmed by the increase in diffusion times of the contrast. Although preliminary, these findings are promising for the use of CEUS in monitoring dogs with BPH. [ABSTRACT FROM AUTHOR]

Simple Summary: Historically, there have been very few reports of elevated thyroid hormone (hyperthyroidism) due to thyroid dysfunction in equid species (horses, mules, donkeys, zebras). Hyperthyroidism is a relatively common problem in cats and humans. Increased appetite, weight loss and muscle wasting, elevated heart rate and elevated blood pressure are common clinical signs in these species. In the few case reports of hyperthyroid horses, they often present with weight loss and increased appetite, but there have not been any documented cardiac changes (elevated heart rate, heart murmur, elevated blood pressure) in these patients. The mule investigated in this case report presented with a persistently elevated heart rate and systolic murmur. Cardiac imaging revealed structural changes consistent with those seen in other hyperthyroid mammals. This case report documents the diagnosis, treatment and management and provides long-term follow up of endocrine and cardiac disease in a mule with primary hyperthyroidism. Primary hyperthyroidism is a rarely diagnosed endocrinopathy in equids and there have been no previous reports of structural and functional cardiac changes associated with hyperthyroidism in these species. This case report investigates a 20-year-old mule gelding that presented for a three-month history of thin body condition despite polyphagia, with a heart murmur and elevated free and total thyroid hormone concentrations. On presentation, physical exam revealed a body condition score of two out of nine, persistent tachycardia, pansystolic heart murmur and firm bilateral ventral proximal cervical masses. Bloodwork confirmed markedly elevated free T4, total T4 and T3 concentrations. Echocardiogram demonstrated left ventricular concentric hypertrophy with increased ventricular and atrial systolic function. Bilateral thyroidectomy was performed under standing sedation without complications. Histopathology demonstrated adenocarcinoma of the left thyroid gland and multiple adenomas with osseous metaplasia within the right thyroid. The mule was supplemented with levothyroxine sodium two weeks post-op after a thyroid panel demonstrated undetectable concentrations. Polyphagia resolved following surgery and the mule began gaining weight. Echocardiographic changes improved but did not resolve at two years post-operative. Continued bi-annual follow up and monitoring of thyroid levels was recommended. This case represents the first documentation of hemodynamically relevant cardiac remodeling in an equid associated with primary hyperthyroidism. [ABSTRACT FROM AUTHOR]

Increased mitochondrial reactive oxygen species (ROS) formation is important for the development of right ventricular (RV) hypertrophy (RVH) and failure (RVF) during pulmonary hypertension (PH). ROS molecules are produced in different compartments within the cell, with mitochondria known to produce the strongest ROS signal. Among ROS-forming mitochondrial proteins, outer-mitochondrial-membrane-located monoamine oxidases (MAOs, type A or B) are capable of degrading neurotransmitters, thereby producing large amounts of ROS. In mice, MAO-B is the dominant isoform, which is present in almost all cell types within the heart. We analyzed the effect of an inducible cardiomyocyte-specific knockout of MAO-B (cmMAO-B KO) for the development of RVH and RVF in mice. Right ventricular hypertrophy was induced by pulmonary artery banding (PAB). RV dimensions and function were measured through echocardiography. ROS production (dihydroethidium staining), protein kinase activity (PamStation device), and systemic hemodynamics (in vivo catheterization) were assessed. A significant decrease in ROS formation was measured in cmMAO-B KO mice during PAB compared to Cre-negative littermates, which was associated with reduced activity of protein kinases involved in hypertrophic growth. In contrast to littermates in which the RV was dilated and hypertrophied following PAB, RV dimensions were unaffected in response to PAB in cmMAO-B KO mice, and no decline in RV systolic function otherwise seen in littermates during PAB was measured in cmMAO-B KO mice. In conclusion, cmMAO-B KO mice are protected against RV dilatation, hypertrophy, and dysfunction following RV pressure overload compared to littermates. These results support the hypothesis that cmMAO-B is a key player in causing RV hypertrophy and failure during PH. [ABSTRACT FROM AUTHOR]

The association between vitamin D deficiency and cardiovascular disease remains a controversial issue. This study aimed to further elucidate the role of vitamin D signaling in the development of left ventricular (LV) hypertrophy and dysfunction. To ablate the vitamin D receptor (VDR) specifically in cardiomyocytes, VDRfl/fl mice were crossed with Mlcv2-Cre mice. To induce LV hypertrophy experimentally by increasing cardiac afterload, transverse aortic constriction (TAC) was employed. Sham or TAC surgery was performed in 4-month-old, male, wild-type, VDRfl/fl, Mlcv2-Cre, and cardiomyocyte-specific VDR knockout (VDRCM-KO) mice. As expected, TAC induced profound LV hypertrophy and dysfunction, evidenced by echocardiography, aortic and cardiac catheterization, cardiac histology, and LV expression profiling 4 weeks post-surgery. Sham-operated mice showed no differences between genotypes. However, TAC VDRCM-KO mice, while having comparable cardiomyocyte size and LV fibrosis to TAC VDRfl/fl controls, exhibited reduced fractional shortening and ejection fraction as measured by echocardiography. Spatial transcriptomics of heart cryosections revealed more pronounced pro-inflammatory and pro-fibrotic gene regulatory networks in the stressed cardiac tissue niches of TAC VDRCM-KO compared to VDRfl/fl mice. Hence, our study supports the notion that vitamin D signaling in cardiomyocytes plays a protective role in the stressed heart. [ABSTRACT FROM AUTHOR]

Aim: To evaluate changes in allograft kidney length in renal transplant recipients and the relationship with estimated glomerular filtration rate (eGFR). Methods: This single‐centre retrospective study of renal transplant recipients was conducted at Flinders Medical Centre (FMC) from January 2007 to June 2020. Donor and recipient details, renal allograft length from transplant ultrasounds at 0, 1, 3, 6 and 12 months were collected. The association between compensatory renal hypertrophy (CRH) and eGFR and its magnitude was analysed using multivariate multilevel mixed‐effects linear regression models. Results: A total of 183 renal transplant recipients were studied. 100 of 175 recipients (62.9%) demonstrated an increase in renal length defined as any increase in maximal longitudinal diameter on serial ultrasounds. Twenty‐three recipients (13.1%) had no change in transplant length and 42 recipients (24%) had a decrease in length. The mean increase in kidney length over the first 12 months was 0.57 cm. Ninety of 156 (57.7%) recipients with a renal ultrasound within a month post‐transplant demonstrated a mean increase kidney length of 0.3 cm. Multivariate analysis demonstrated that eGFR increased by 2.5 mL/min/1.73 m2 (95% CI 0.72– 4.4; p =.006) with every 1 cm increase in kidney length. Absolute changes in kidney length did not demonstrate any statistically significant correlation with eGFR in both complete case and multiple imputation analysis. Conclusion: An increase in transplant kidney length is common in renal transplant recipients and is associated with enhanced eGFR. However, further studies need to be performed to study the association of absolute change in kidney length and eGFR. Summary at a glance: Compensatory renal hypertrophy has been well described in patients post‐nephrectomy and in the remaining kidney of living kidney donors. This study demonstrates that increase in renal transplant length in keeping with compensatory renal hypertrophy occurs in renal allografts. [ABSTRACT FROM AUTHOR]

The benefits of Blood Flow Restriction Therapy (BFRT) have gained attention in recent times. This review aimed to evaluate the immediate (up to 24 hours), intermediate (up to 6 weeks), and long term (6–10 weeks) effects of BFRT plus exercises (EX) compared to EX only on athletic performance (sprint and jump performance), muscle strength, and hypertrophy in athletes and physically active population. A literature search was conducted to select randomized controlled trials across four electronic databases from inception till April 2021. The search yielded twenty-seven studies in total. Based on eligibility criteria, twenty-one studies were analyzed. No differences were found between both groups for immediate (standardized mean difference [SMD] −0.02, 95% confidence interval [CI] −0.31, 0.27) and long-term effects (SMD −0.30, 95%CI −0.90, 0.30) on sprint performance. For jump performance, no significant effect was observed immediately (SMD −0.02 (95% CI −1.06, 1.02) and long term (SMD −0.40 (95% CI −1.46, 0.67). Similarly, muscle torque at intermediate (SMD 0.90 (95% CI −1.01, 2.81) and long term (SMD −0.54 (95% CI −1.19, 0.12), muscle strength at intermediate (SMD 1.12 (95% CI 0.20, 2.04), and long term (SMD −0.07 (95% CI −0.56, 0.42) also showed non-significant effects. Muscle hypertrophy at intermediate (SMD 0.16 (95% CI −0.31, 0.63) and long term (SMD −0.20 (95% CI −0.90, 0.50) were not statistically significant. There was no significant difference observed in BFRT plus EX group compared to the EX-group on athletic performance, muscle strength, and muscle hypertrophy. [ABSTRACT FROM AUTHOR]

The heart has the ability to detect and respond to changes in mechanical load through a process called mechanotransduction. In this study, we focused on investigating the role of the cardiac-specific N2B element within the spring region of titin, which has been proposed to function as a mechanosensor. To assess its significance, we conducted experiments using N2B knockout (KO) mice and wildtype (WT) mice, subjecting them to three different conditions: 1) cardiac pressure overload induced by transverse aortic constriction (TAC), 2) volume overload caused by aortocaval fistula (ACF), and 3) exercise-induced hypertrophy through swimming. Under conditions of pressure overload (TAC), both genotypes exhibited similar hypertrophic responses. In contrast, WT mice displayed robust left ventricular hypertrophy after one week of volume overload (ACF), while the KO mice failed to undergo hypertrophy and experienced a high mortality rate. Similarly, swim exercise-induced hypertrophy was significantly reduced in the KO mice. RNA-Seq analysis revealed an abnormal β-adrenergic response to volume overload in the KO mice, as well as a diminished response to isoproterenol-induced hypertrophy. Because it is known that the N2B element interacts with the four-and-a-half LIM domains 1 and 2 (FHL1 and FHL2) proteins, both of which have been associated with mechanotransduction, we evaluated these proteins. Interestingly, while volume-overload resulted in FHL1 protein expression levels that were comparable between KO and WT mice, FHL2 protein levels were reduced by over 90% in the KO mice compared to WT. This suggests that in response to volume overload, FHL2 might act as a signaling mediator between the N2B element and downstream signaling pathways. Overall, our study highlights the importance of the N2B element in mechanosensing during volume overload, both in physiological and pathological settings. [Display omitted] • We investigated the role of the N2B element within titin, as a mechanosensor. • Under pressure overload, N2B KO mice exhibited normal hypertrophic responses. • Volume overload resulted in attenuated hypertrophy and a high initial mortality rate. • An abnormal β-adrenergic response to volume overload existed in the N2B KO mice. • The N2B element of titin is important in mechanosensing during volume overload. [ABSTRACT FROM AUTHOR]

BACKGROUND Despite the widespread use of botulinum toxin (BTX) injection for the treatment of masseter muscle hypertrophy (MMH), there is no standard treatment option. OBJECTIVE We report the efficacy and safety for BTX in MMH over a period of 48 weeks. METHODS In double-blinded, placebo-controlled phase 3 trials, 180 patients (randomized 1:1) received treatment with placebo (normal saline) or prabotulinumtoxinA (48 units). Masseter muscle thickness (at maximal clenching and resting positions), 3D imaging analysis, and masseter muscle hypertrophy scale grades were analyzed at each time point. After the 24-week CORE study, all patients who met the same criteria of the CORE study at week 24 (n 5 114) received only prabotulinumtoxinA, regardless of previous treatment, for an additional 24 weeks (48 weeks in total) for the open-label extension study. RESULTS The largest differences in mean and percent changes from baseline in masseter muscle thickness were observed at 12 weeks, and there were significant differences between the 2 groups at all time points (all p, .001). The effect was independent of the number of injections. No serious adverse event was observed. CONCLUSION PrabotulinumtoxinA could effectively ameliorate MMH without major complications. [ABSTRACT FROM AUTHOR]

Introduction: Cardiovascular diseases are a major cause of death among patients with Diabetic Kidney Disease (DKD). Left Ventricular Hypertrophy (LVH) is a threatening prognostic sign and an independent risk factor for cardiovascular mortality and morbidity. A number of epidemiological studies have proven that LVH is common in patients with DKD. Aim: To estimate the Serum Uric Acid (SUA) levels in DKD patients and its association with LVH and estimated Glomerular Filtration Rate (eGFR). Materials and Methods: The current study was a cross-sectional study conducted at KR Hospital, Mysuru, a teritary care hospital, in Mysuru, Karnataka, India, during the period from 1st January 2020 to 31st December 2020. which included 53 patients with DKD. The demographic data, relevant investigations like Renal Function Test (RFT), SUA levels, complete haemogram, Fasting Blood Sugar (FBS), Postprandial Blood Sugar (PPBS), glycosylated haemoglobin, Liver Function Tests (LFT), urine routine, Urine Albumin Creatinine Ratio (UACR), electrocardiogram, 2D echo were done. The results were tabulated, and the patients were classified into those with high and low SUA levels. They were also evaluated for the presence of additional risk factors like hypertension and Ischaemic Heart Disease (IHD). Data obtained was analysed statistically using Statistical Packages of Social Sciences (SPSS) version 21.0 software. Mean, Standard Deviation (SD), Chi-square test, and Fischer's-exact tests were used where appropriate, with a p-value <0.05 considered statistically significant. Patients were classified into two groups, one with SUA more than 6.5 and the other with less than 6.5, as normouricaemia and hyperuricaemia, respectively. Results: The majority of the cases were in the age group of 51-60 years, accounting for 43.4%. Out of 53 patients, males constituted 60.4% and females 30.6%, with a male-to-female ratio of 1.52:1. Total 33 patients (62.3%) were hypertensive, 32 patients (60.4%) had LVH, and 15 patients (28.3%) had IHD. Among 38 patients with SUA levels >6.5 mg/dL, the mean UACR value was higher (1807.9 mg/gm), the mean eGFR value was 32.4 mL/min/1.73 m2, and the mean Left Ventricular Mass index (LVMI) was 117.1 g/m2, which was statistically significant. Conclusion: In patients with DKD, higher SUA levels were associated with significantly higher values of UACR, lower eGFR values, higher LVMI values, and an increased risk for LVH, hypertension, and IHD. However, there was no significant association between higher uric acid levels and HbA1c. [ABSTRACT FROM AUTHOR]

Pediatric ECG standards have been defined without echocardiographic confirmation of normal anatomy. The Pediatric Heart Network Normal Echocardiogram Z-score Project provides a racially diverse group of healthy children with normal echocardiograms. We hypothesized that ECG and echocardiographic measures of left ventricular (LV) dimensions are sufficiently correlated in healthy children to imply a clinically meaningful relationship. This was a secondary analysis of a previously described cohort including 2170 digital ECGs. The relationship between 6 ECG measures associated with LV size were analyzed with LV Mass (LVMass-z) and left ventricular end-diastolic volume (LVEDV-z) along with 11 additional parameters. Pearson or Spearman correlations were calculated for the 78 ECG-echocardiographic pairs with regression analyses assessing the variance in ECG measures explained by variation in LV dimensions and demographic variables. ECG/echocardiographic measurement correlations were significant and concordant in 41/78 (53%), though many were significant and discordant (13/78). Of the 6 ECG parameters, 5 correlated in the clinically predicted direction for LV Mass-z and LVEDV-z. Even when statistically significant, correlations were weak (0.05–0.24). R2 was higher for demographic variables than for echocardiographic measures or body surface area in all pairs, but remained weak (R2 ≤ 0.17). In a large cohort of healthy children, there was a positive association between echocardiographic measures of LV size and ECG measures of LVH. These correlations were weak and dependent on factors other than echocardiographic or patient derived variables. Thus, our data support deemphasizing the use of solitary, traditional measurement-based ECG markers traditionally thought to be characteristic of LVH as standalone indications for further cardiac evaluation of LVH in children and adolescents. [ABSTRACT FROM AUTHOR]

Objectives: Current research suggests static stretch-induced maximal strength increases and muscle hypertrophy with potential to substitute resistance-training routines. However, most studies investigated the plantar flexors. This study explored the effects of a static stretching program on maximal strength, hypertrophy and flexibility of the pectoralis major and compared the effects with those of traditional resistance training. Methods: Eighty-one (81) active participants were allocated to either a static stretching, strength-training or control group. Pectoralis stretching was applied 15 min/day, 4 days per week for 8 weeks, while resistance training trained 3 days per week, 5 × 12 repetitions. Results: There was an increase in all parameters (strength: p < 0.001, ƞ2 = 0.313, muscle thickness: p < 0.001, ƞ2 = 0.157–0.264, flexibility: p < 0.001, ƞ2 = 0.316) and a time*group interaction (strength: p = 0.001, ƞ2 = 0.154, muscle thickness: p = 0.008–0.001, ƞ2 = 0.117–0.173, flexibility: p < 0.001, ƞ2 = 0.267). Post-hoc testing showed no difference between both intervention groups regarding maximal strength and muscle thickness (p = 0.905–0.983, d = 0.036–0.087), while flexibility increased in the stretching group (p = 0.001, d = 0.789). Conclusion: Stretching showed increases in maximal strength and hypertrophy, which were comparable with commonly used resistance training. Based on current literature, the influence of mechanical tension as the underlying mechanism is discussed. Furthermore, as equipment and comparatively long stretching durations are requested to induce meaningful strength increases in recreationally active participants, practical application seems limited to special circumstances. [ABSTRACT FROM AUTHOR]

Hyperthyroidism is a condition where the thyroid gland produces high levels of thyroid hormone. Heart diseases are one of the main complications of hyperthyroidism. Several studies have shown that losartan (LOS) and diminazene aceturate (DIZE) possess cardioprotection effects against cardiac hypertrophy, ischemic heart disease, and heart failure. The research aimed to investigate the cardioprotection of LOS, DIZE, and their combination in the case of levothyroxine (LT4)-induced cardiomyopathy in rats. Hyperthyroidism was induced by LT4 in drinking water (12 mg/L) for 28 days. LOS (10 mg/kg, orally) and/or DIZE (15 mg/kg, subcutaneously) were administrated in rats with hyperthyroidism for 28 days. Decreased serum creatine kinase myoglobin and lactate dehydrogenase levels and cardiac hypertrophy by DIZE and combination therapy in hyperthyroidism rats have been reported. Cardiac hemodynamic findings showed that DIZE and its combination with LOS decreased the LT4-mediated left ventricular developed pressure (LVDP), rate pressure product (RPP), and RPP recovery percentage. Elevated cardiac oxidative stress and inflammation were confirmed by decreasing cardiac superoxide dismutase (SOD) activity and increasing the total oxidative stress and tumor necrosis factor-alpha (TNF-α) levels. SOD activity and TNF-α level were reversed by LOS and DIZE administration, respectively. Generally, DIZE and combination therapy with LOS improved cardiac dysfunction caused by hyperthyroidism in rats, whereas LOS alone has not been able to effectively respond to this dysfunction. [ABSTRACT FROM AUTHOR]