Articles tagged with Cardiac Hypertrophy
A major international study has identified ways to detect patients with hypertrophic cardiomyopathy at serious risk of sudden death, heart failure or other dangerous outcomes. The findings will help save lives by improving the ability to determine who is at greatest risk and spare low-risk patients from unneeded heart implants.
High-intensity interval training shows strongest vascular benefits in cardiovascular patients. HIIE consistently improves flow-mediated dilation and vasodilation, with combined high-intensity programs showing the largest estimated effects on endothelial function.
Researchers identify circulating extracellular vesicles produced in diseased kidneys as the culprit behind toxicity in the heart. The discovery could lead to the development of a blood test to identify patients at high risk for serious heart problems and novel treatments to prevent and treat heart failure.
A study found that longer accumulations of steps in one go have a greater health benefit than short bouts spread out across the day. Walking continuously for 10-15 minutes per day was associated with lower risk of cardiovascular events and mortality.
A study published in Annals of Translational Medicine found that intense light therapy can lower troponin levels and increase ANGPTL4 protein, protecting heart tissue. The treatment may reduce the risk of myocardial injuries after non-cardiac surgery, which affects 20% of patients and increases one-year mortality rates.
A new Leicester study found that women with type 2 diabetes are nearly twice as likely as men to have hidden heart damage, according to researchers. The study used advanced MRI scans and data from four studies conducted at the NIHR Leicester Biomedical Research Centre.
Scientists are working on a genetic cure for the world's most common inherited heart disease, hypertrophic cardiomyopathy (HCM), with a new gene editing tool. The team aims to correct mutations that cause the disease, which affects 14 million people worldwide.
Research led by Amsterdam UMC reveals the hearts of female elite athletes have different characteristics compared to their male counterparts. Female athletes exhibit dilation of the heart chambers, whereas males show thickening in combination with a dilation of the heart muscle. This finding can aid doctors in identifying possible hear...
A study published in the European Heart Journal found that male bodybuilders have a high risk of sudden cardiac death, with professional bodybuilders facing a more than fivefold increase in risk. The study highlights the need for greater awareness, preventive strategies and policy changes within the bodybuilding community.
A centralized notification pathway increased hypertension treatment in individuals with left ventricular hypertrophy. This study highlights the potential of leveraging underutilized cardiovascular data to enhance healthcare delivery.
Researchers at the University of Virginia Health System have developed a computational tool called LogiRx that can predict how drugs will affect biological processes in the body. The tool has demonstrated its potential by identifying a promising candidate to prevent heart failure, a leading cause of death worldwide.
A new study reveals that the protein CRTC plays a crucial role in maintaining a healthy heart by ensuring it is neither too thick nor too thin. The research also shows that overexpression of CRTC causes cardiac hypertrophy, leading to adverse cardiovascular events.
A new study by UCL researchers suggests that a vest mapping the heart's electrical activity could help identify people at high risk of sudden cardiac death. The electrocardiographic imaging (ECGI) vest combines signals with MRI images to generate 3D models, potentially predicting risk factors for life-threatening heart rhythms.
A new study found that arterial stiffness is a novel cause of premature heart damage among adolescents, leading to increased blood pressure and insulin resistance. The study discovered that adolescents with high arterial stiffness had a 23-27% increased risk of structural heart damage.
A study published in Science reveals that ganglia in the neck region are responsible for disrupting melatonin production and causing sleep disturbances in people with heart conditions. Researchers found that macrophages accumulate in the ganglion, leading to inflammation and scarring, which can be treated with drugs.
Researchers at TUM have developed a method to create mini-hearts in Petri dishes using stem cells. The resulting organoids mimic the earliest stages of human heart development and can be used to investigate congenital heart defects, potentially leading to new treatment methods.
Researchers discovered a mechanism involving ribosomes that enables the heart to toggle between a regular maintenance mode and an energy-boost mode. This finding provides clues for developing medicines targeting specific ribosomes to treat cardiovascular disease.
A study by CNIC scientists has identified a key role for the MKK3/6–p38γ/δ signaling pathway in cardiac hypertrophy. Inhibition of p38α promotes an unexpected activation of the other branch of the pathway, consisting of the proteins MKK3, p38γ, and p38δ. This activation induces another key pathway in cardiac hypertrophy, the mTOR pathway.
Scientists have identified a key mechanism causing the heart's muscle to thicken, leading to irregular rhythms and heart failure. A new peptide treatment could prevent or stop further thickening, offering hope for patients with cardiac hypertrophy.
Researchers at Lewis Katz School of Medicine at Temple University discover a molecular pathway driving maladaptive processes in heart failure, revealing the importance of GRK5's catalytic activity and nuclear presence. The study opens doors to new therapeutic strategies for treating this devastating condition.
Researchers at CNIC have identified a new mechanism involved in the regulation of cardiac hypertrophy, which may spur the development of new tools for its treatment. The SRSF4-GAS5-glucocorticoid receptor axis plays a crucial role in regulating ventricular function and preventing excessive heart muscle growth.
A recent study found that etelcalcetide slowed FGF23 levels and left ventricular mass growth by 6-8% in dialysis patients. The treatment could potentially reduce sudden cardiac death risk in this population with high cardiovascular risk.
A study published in Circulation reveals that FoxO1 plays a crucial role in regulating abnormal heart growth, a condition characterized by cardiac hypertrophy. The research suggests that targeting FoxO1 could lead to the development of novel therapies for cardiac hypertrophy.
Researchers at UNC School of Medicine discovered that Lin28a is needed for the development of pathological hypertrophy, a process where the adult heart enlarges in response to cardiac stress. This discovery could lead to more potent therapeutics for heart disease treatment.
Scientists identified a calcineurin variant CnAβ1 that reduces cardiac hypertrophy and improves heart function by preserving mitochondrial ATP production. This study may lead to new treatment strategies for conditions like aortic stenosis.
Cardiac diseases cause pathological growth leading to heart failure. Researchers found epigenetic marks responsible for this growth are lost in disease, allowing cells to switch back to fetal form and leading to irregular rhythms. This finding points to a new strategy for epigenetic therapy.
Researchers at Beth Israel Deaconess Medical Center have identified a developmental cause of adult-onset cardiac hypertrophy, a leading cause of heart failure. The study reveals that genetic mutations affecting the Ras/MAPK cell signaling pathway can lead to the development of cardiac hypertrophy in adults.
A study by Charité researchers has identified a specific protein and its splice variant as crucial in the development of cardiac hypertrophy. Initial activation of this protein leads to an increase in production of proteins associated with early cardiac development, causing the abnormal thickening of heart muscle.
Duke researchers discovered a gene called Raf that acts as a switch to turn on Yorkie, making fly hearts grow bigger. The study sheds light on the genetic circuitry of signals governing growth and may help understand how human hearts respond to disease.
Researchers have found that a drug already approved to treat multiple sclerosis may also slow and potentially reverse cardiac hypertrophy, a disorder that often leads to heart failure. By mimicking certain lipids in the body, FTY-720 significantly reduces heart mass and improves overall cardiac function.
A lab study found that Gilenya, an MS treatment, reverses ventricular hypertrophy's symptoms and prevents fatal arrhythmias. Researchers discovered Pak1's role in heart disease and developed a potential new therapy.
Researchers aim to determine how vitamin D affects cardiac structure and function, vascular function, and left ventricular hypertrophy in blacks with hypertension. The study could identify vitamin D as a safe and effective therapy to stop or reverse cardiac ravages caused by high blood pressure.
Researchers identify MKK4 enzyme as a potential therapeutic target for treating cardiac arrhythmias caused by cardiac hypertrophy, leading to sudden cardiac death in young athletes. The study reveals how the enzyme prevents arrhythmias by modifying connexin protein, ensuring synchronized heart contractions.
Researchers at the University of Rochester Medical Center have identified a potential molecular mechanism to prevent cardiac hypertrophy, the precursor to heart failure. The study reveals that inhibiting histone deacetylase 5 and activating the PKA enzyme can stop unwanted enlargement of the heart.
Researchers at Cincinnati Children's Hospital Medical Center identified the protein CIB1 as a prime candidate for regulating cardiac hypertrophy. Over-expression of CIB1 triggers biochemical processes leading to cardiac enlargement and dysfunction.
A study of 500 patients found that EKG readings can yield false positive diagnoses for left ventricular hypertrophy with a rate of 77-82%, while false negatives occur at a rate of 6-7%. This can lead to unnecessary additional screenings.
A new study reveals that Sirt3 helps protect the mouse heart by blocking cardiac hypertrophic response through Foxo3a-dependent antioxidant defense mechanisms. Mice lacking Sirt3 developed enlarged hearts, while those overexpressing Sirt3 were protected from cardiac hypertrophy under similar conditions.
Young adults who have been incarcerated are more likely to develop high blood pressure and left ventricular hypertrophy. They also face barriers to accessing regular medical care.
A new genetic test has identified mutations in 10 genes as a possible cause of cardiac hypertrophy in children. The test found that nearly 50% of children without family histories had mutations in these genes, shedding light on the underlying causes of the condition.
Researchers developed a new mouse model to predict the loss of orally taken drugs due to metabolism by CYP3A, a key enzyme involved in first-pass metabolism. The study found that mice lacking functional CYP3A proteins accumulated docetaxol at higher levels, demonstrating the enzyme's role in intestinal metabolism.
A $2 million federal grant will help the OHSU Cardiac Arrhythmia Center pinpoint those at greatest risk of sudden cardiac arrest due to left ventricular hypertrophy. The study aims to improve identification and prediction methods, potentially averting disaster before it happens.
Researchers found a link between obesity and left ventricular hypertrophy (LVH), a thickening of the heart muscle, in obese patients with a BMI of 30 or greater. The study analyzed 17,261 heart ultrasounds and identified narrowing of the aortic valve as a strong predictor of LVH.
Researchers at the University of Leeds have discovered a mechanism to prevent cardiac hypertrophy by increasing the levels of REST protein, halting the progression of the fatal heart condition. This finding offers a new approach to treating the cause of heart hypertrophy rather than its symptoms.
Researchers at Vanderbilt University found that treatment with TGF-beta inhibitors may help prevent cancer metastasis in patients. Additionally, a study from the University of Michigan discovered that a negative feedback pathway involving leptin receptor signaling may contribute to leptin resistance in obese individuals.
Researchers link young adults with hypertension or prehypertension to an increased risk of heart enlargement. The study found that those with hypertension had a three times higher prevalence of left ventricular hypertrophy compared to those with normal blood pressure.
Penn researchers suggest novel genetic causes for cardiac hypertrophy and new therapeutic agents against it. They also demonstrate that anti-HDAC drugs can block the development of hypertrophy in animal models.
A post-hoc analysis of the LIFE study found a close to 50% risk reduction in sudden death among losartan-treated diabetic patients compared to those treated with atenolol. Lars Lindholm comments that the results are exploratory and require confirmation.
A post-hoc analysis of the LIFE study found that losartan significantly reduced sudden cardiac death in diabetic patients with hypertension and left ventricular hypertrophy compared to atenolol. The results showed a nearly 50% risk reduction in sudden death for losartan-treated patients.
Researchers found that estrogen production protects females from cardiac hypertrophy, but not males. By blocking estrogen receptors, female mice developed cardiac enlargement similar to males.
The study reveals that female mice develop cardiac hypertrophy when estrogen is blocked, mimicking human conditions. The discovery could lead to a better understanding of the molecular signals causing heart enlargement and potential ways to prevent or reverse it.
Recent research highlights the significance of sodium-calcium exchange in various physiological processes, including vision, secretion, and cardiac contractility. The study also explores its potential applications in cancer therapy and heart function.
Researchers discovered a molecular pathway that leads to heart enlargement and found a way to block it using immunosuppressant drugs. The study used mice whose progression from cardiac hypertrophy mirrored humans', finding that activated calcineurin is sufficient to induce cardiac hypertrophy.