New findings from Cleveland Clinic researchers show for the first time that the gut microbiome impacts stroke severity and functional impairment following stroke. The results, published in Cell Host & Microbe, lay the groundwork for potential new interventions to help treat or prevent stroke.
The research was led by Weifei Zhu, Ph.D., and Stanley Hazen, M.D., Ph.D., of Cleveland Clinic's Lerner Research Institute. The study builds on more than a decade of research spearheaded by Dr. Hazen and his team related to the gut microbiome's role in cardiovascular health and disease, including the adverse effects of TMAO (trimethylamine N-oxide)—a byproduct produced when gut bacteria digest certain nutrients abundant in red meat and other animal products.
Last edited by weatheriscool on Tue Apr 11, 2023 4:23 am, edited 1 time in total.
Wearable ultrasound patch could warn of cardiovascular problems
By Ben Coxworth
July 23, 2021
It goes without saying that the earlier someone can be warned of an impending heart attack or stroke, the better. A new skin patch could provide such warnings, by sending ultrasound pulses into the wearer's body.
Building upon a previously developed device, the patch was created at the University of California-San Diego by a team led by Prof. Sheng Xu. Worn on the neck or chest, it consists of a thin sheet of flexible, stretchable polymer, inside of which is a 12 by 12 grid of millimeter-sized ultrasound transducers. The patch is currently hard-wired to a computer and power source, but plans call for it to ultimately be self-contained and wireless.
In one operational mode, all of the transducers can be set to transmit ultrasound wave pulses at the same time. This produces an ultrasound beam that focuses directly down onto one area of the body, up to 14 cm (5.5 in) beneath the skin.
In the other mode, the transducers transmit their waves out of sync with one another, but still rapidly enough that they form one cohesive beam. In this case, however, that beam can be pointed in different angles, as opposed to just straight down from the patch. This means that different areas could be scanned without having to stick the patch right above each one.
Johns Hopkins University scientists have developed a new tool for predicting which patients suffering from a complex inflammatory heart disease are at risk of sudden cardiac arrest. Published in Science Advances, their method is the first to combine models of patients' hearts built from multiple images with the power of machine learning.
"This robust new personalized technology outperformed clinical metrics in forecasting future arrhythmia and could transform the management of cardiac sarcoidosis patients," said senior author Natalia Trayanova, a Johns Hopkins professor of biomedical engineering and co-director of the Alliance for Cardiovascular Diagnostic and Treatment Innovation (ADVANCE).
Doctors don't currently have precise methods for assessing which patients with cardiac sarcoidosis, a condition causing inflammation and scarring that can trigger irregular heartbeats, are likely to have a fatal arrhythmia, meaning that some patients don't survive, while others undergo uncecessary, invasive interventions. A recent meta-analysis cited in the study found that roughly only one third of CS patients receive adequate treatment.
High blood pressure is the world's leading killer but poor rates of blood pressure control remain common. A new strategy where patients are started on a pill containing four medicines, each at a quarter of their usual doses, has been shown to be much more effective in getting blood pressure under control, compared to the common practice of monotherapy, where treatment commences with just one drug.
This first large-scale, randomized controlled clinical trial of starting this novel combination blood pressure medication brought blood pressure under control in 80 percent of participants in 12 weeks, compared to 60 percent in the control group who nonetheless had access to the best patient care.
Traditionally doctors have started with one drug and then follow up to consider adding or changing treatment—but this strategy is often not successful in practice and blood pressure control rates have remained stubbornly low for decades.
A combination therapy of aspirin, statins and at least two blood pressure medications given in fixed doses can slash the risk of fatal cardiovascular disease (CVD) by more than half, says an international study led by Hamilton researchers.
The fixed-dose combination (FDC) therapies were examined both with and without aspirin versus control groups in a combined analysis of more than 18,000 patients without prior CVD from three large clinical trials. FDCs including aspirin cut the risk of heart attacks by 53 percent, stroke by 51 percent, and deaths from cardiovascular causes by 49 percent.
The results were welcomed by international leaders in cardiovascular research.
Approximately 19 million people worldwide die of CVD and twice as many experience heart attacks or strokes every year.
About 80 percent of cardiovascular events occur in individuals without a prior history of such illness, meaning effective preventative strategies including medications in people without CVD is essential, if the majority of heart attacks, strokes and related deaths in the world are to be prevented, the authors of the study state.
An antioxidant drug reverses atherosclerosis and could be used to prevent heart attacks and strokes due to clots, according to research funded by the British Heart Foundation (BHF) and published today in JAHA: Journal of the American Heart Association.
Atherosclerosis is the build-up of fatty deposits in the arteries. When a type of fat called LDL cholesterol becomes oxidized and builds up to form plaques in the artery walls, inflammation and damage increase which can cause the plaques to rupture and cause blood to clot.
These clots can block vital arteries that allow blood to flow to the heart, causing a heart attack, or to the brain causing a stroke.
Previously, researchers at the University of Reading discovered that LDL cholesterol can be oxidized in acidic small 'bags' called lysosomes in immune cells within the artery wall.
Now, Professor David Leake and his team have found that the antioxidant drug, cysteamine, has the power to switch off, and even reverse, this damaging process.
A team of researchers affiliated with several institutions in Germany and one in Canada has found that it is possible to reprogram heart muscle to repair damaged tissue. In their paper published in the journal Science, the group describes their approach to repairing damaged hearts in mice and how well it worked when tested.
There are two main kinds of heart attack. The first occurs when something prevents the heart from beating. The second occurs when blood flow is restricted to parts of the heart, preventing the muscle in that area from beating. The first kind is generally fatal unless the heart can be restarted very quickly. The second is generally less serious, but can leave permanent, debilitating scarring. In this new effort, the researchers have found a way to prevent such scarring—at least in mice.
The work built on prior research that showed that in the case of a baby experiencing heart damage in utero, the heart can repair itself because the cardiomyocyte cells are in a state that allows rejuvenation. This is not the case after birth or later in life, as the cardiomyocytes have no ability to regenerate. After several years of effort, the researchers discovered a way to get adult cardiomyocytes to revert back to fetal-like cardiomyocytes by reprogramming them using the Yamanaka factors c-Myc, Klf4, Sox2 and Oct4. Their research showed that such factors express for cell renewal. The reprogramming also featured an on/off switch using the antibiotic doxycycline.
To track cardiovascular health, doctors measure blood pressure, cholesterol levels and blood sugar, among a number of other cardiovascular disease risk factors. Such measures can help predict whether a person is at risk of heart attack or stroke. But there is no blood test that can accurately assess the degree to which a person's arteries may be narrowing or at risk of blockage.
Now, researchers at Washington University School of Medicine in St. Louis have shown that high levels of a specific protein circulating in the blood accurately detect a severe type of peripheral artery disease that narrows the arteries in the legs and can raise the risk of heart attack and stroke. The protein, called circulating fatty acid synthase (cFAS), is an enzyme that manufactures saturated fatty acids. Until recently, fatty acid synthase was thought to be found only inside cells. The new study suggests that fatty acid synthase also circulates in the bloodstream and may have an important role in the plaque formation characteristic of cardiovascular disease.
The study appears online in the journal Scientific Reports.
Implantable medical devices including cardiac pacemakers and brain pacemakers are increasingly prevalent, although replacing their batteries surgically is a drawback for long-term functionality and patient health. Current devices are also large and rigid, with potential discomfort to the patient post-implantation. To address this problem, Peng Jin and a research team in mechanics and electronics in Beijing China, developed a thin, battery-free and flexible implantable system for wireless recharging and communication via ultrasound. The results automatically determined abnormal heartbeats and responded by simulating the heart electrically to demonstrate the potential of the device for emerging treatments.
Medical devices for power transfer
Implantable electronic equipment (IEE) is vital in the medical field to perform drug delivery and physiological parameter monitoring as cardiac and brain pacemakers. Implantable glucose sensors can also provide accurate, real-time glucose monitoring to assist diabetic individuals. The applications of IEE are, however, held back by shortcomings of the batteries used. A possible solution is the adoption of an implantable fuel system using endogenous substances such as glucose to create electricity via an electrochemical reaction. The power transfer method can be delivered wirelessly through tissue. To accomplish an optimal setup exceeding conventional methods of wireless power transfer and communication, Jin et al. developed an implantable acoustic energy transfer and communication device (AECD). The flexible electronic technology-based device was soft, comfortable and well-adapted to the human biological structure, as a stretchable ultrasonic device for ultrasonic energy transfer and efficient communication.
Cardiovascular procedures like bypass grafting and vessel stenting are some of the most common surgeries performed in the United States, but about half of them will require additional corrective measures, according to Craig Duvall, Cornelius Vanderbilt Chair and undergraduate director of biomedical engineering. The need for follow-up procedures is often due to intimal hyperplasia, a condition where blood vessels become re-blocked by abnormal growth or migration of smooth muscle cells in the wall of the blood vessel. A team of researchers led by Duvall has developed a nanomedicine to combat this condition.
A primary cause of IH is the response to injury by the vascular smooth muscle cells that reside in the wall of the surgically manipulated blood vessel. The physical manipulation of the vascular tissue by surgeons during lifesaving procedures injures the smooth muscle cells and causes them to undergo abnormally high rates of cell division. Duvall and his colleagues in bioengineering, molecular and cellular biology and the School of Medicine found that MK2i-NP, a long-lasting inhibitor of smooth muscle cell stress response, is an effective therapeutic for IH.
Predicting when atherosclerotic changes in the arteries in a stable state will progress to acute cardiovascular disease has remained unresolved. The authors of the paper currently published in Nature Communications, led by first author Prof. Ulrich Flögel, MD, Institute of Molecular Cardiology, Faculty of Medicine, Heinrich Heine University, Düsseldorf, Germany, present an imaging technique—the targeted and multicolor nanotracer platform technology—that visualizes the hazard patterns in the development of progressive coronary disease in a mouse model.
Hazard pattern using the example of a mouse heart (top in cross-section) with a massively worn out and thus in its performance strongly impaired right heart as consequential damage to be seen in the follow-up examination (bottom right compared to bottom left).
The cascade of these vascular diseases ranges from inflammation of the vessel, thrombosis with subsequent detachment of minute particles of the vascular plaque, to vascular occlusion resulting in permanent damage due to, for example, myocardial infarction.
To show the hazard patterns, three molecules (ligands)—are coupled to different types of perfluorocarbon nanoemulsion. They are specifically directed respectively to sites of inflammation, acute and chronic thrombi. There, they embed themselves and become visible and distinguishable through the use of a specific MRI imaging technique (19F-MRI).
It's clear that taking out the trash is an essential process in maintaining a clean and tidy home. But did you know that your body has a similar process for waste removal in which damaged cells are "thrown out"? A research team in Japan has recently shed new light on the dynamics of this process—termed efferocytosis—following ischemic stroke.
In a new study published this month in Science Immunology, researchers from the University of Tsukuba use a mouse model to identify the role of a key cell receptor, CD300a, in the process of efferocytosis after stroke.
During ischemic stroke, blockage of a blood vessel supplying the brain leads to disrupted blood flow, which can trigger cell death. Dying cells in turn trigger inflammatory responses that may worsen damage in the brain and lead to neurological impairment. Therefore, the elimination of dying cells through efferocytosis is a key part of minimizing the effects of ischemic stroke. However, the process of efferocytosis is not fully understood. The group led by researchers from the University of Tsukuba sought to further clarify the role of efferocytosis in ischemic stroke, particularly in the super-acute phase, which occurs within hours of the initial onset of stroke.
Patients with mitral and tricuspid valve regurgitation, a condition sometimes called "leaky heart valves," appeared to do better after two years if they had a tricuspid valve repair at the time of mitral valve surgery, according to a study supported by the National Heart, Lung, and Blood Institute (NHLBI), a part of the National Institutes of Health. The primary findings were released at the American Heart Association's Scientific Sessions and published in the New England Journal of Medicine.
Researchers found patients who had the mitral valve surgery with the tricuspid annuloplasty were less likely to die, need a tricuspid valve reoperation, or have tricuspid regurgitation advance to a severe stage during a two-year period after treatment, compared to those who had the mitral valve surgery alone. However, patients who had both procedures were more likely to need a permanent pacemaker.
The surgical protocol aims to prevent regurgitation, which occurs when flaps on the heart valves don't close properly and blood flows backward into the heart. This can make it harder for blood to move efficiently throughout the body. In severe cases, regurgitation can increase the risk for an irregular heart rhythm, stroke, or heart failure.
The risk of developing cardiovascular disease is strongly associated with the "bad" LDL cholesterol. A large study by scientists at Karolinska Institutet now shows that two proteins that transport cholesterol particles in the blood provide early and reliable risk information. The researchers now advocate introducing new guidelines for detecting cardiac risk and say the results may pave the way for early treatment, which could help lower morbidity and fatality rates.
Cardiovascular disease is the most common cause of death globally and includes a wide range of conditions, such as stroke and myocardial infarction with atherosclerosis in different organs of the body. In many cases the disease can be prevented and arrested with lifestyle changes and lipid-lowering treatments using statins and other methods.
The data generally used to assess elevated cardiac risk are reference values for the "bad" LDL cholesterol. In some medical conditions, other types of fat particles are also measured along with apolipoproteins, which transport cholesterol in the blood. International guidelines for cardiovascular disease recommend using the apolipoprotein apoB, which transports the "bad" cholesterol, as an alternative risk marker for people with type 2 diabetes, overweight (high BMI) and very high levels of blood lipids.
Engineers at the University of California San Diego have developed a powerful new tool that monitors the electrical activity inside heart cells, using tiny "pop-up" sensors that poke into cells without damaging them. The device directly measures the movement and speed of electrical signals traveling within a single heart cell—a first—as well as between multiple heart cells. It is also the first to measure these signals inside the cells of 3D tissues.
The device, published Dec. 23 in the journal Nature Nanotechnology, could enable scientists to gain more detailed insights into heart disorders and diseases such as arrhythmia (abnormal heart rhythm), heart attack and cardiac fibrosis (stiffening or thickening of heart tissue).
"Studying how an electrical signal propagates between different cells is important to understand the mechanism of cell function and disease," said first author Yue Gu, who recently received his Ph.D. in materials science and engineering at UC San Diego. "Irregularities in this signal can be a sign of arrhythmia, for example. If the signal cannot propagate correctly from one part of the heart to another, then some part of the heart cannot receive the signal so it cannot contract."
A Cleveland Clinic-led study has revealed new insights into how a diet rich in red meat increases risk for cardiovascular disease. The findings were published in Nature Microbiology and build on more than a decade of research by lead author Stanley Hazen, MD, Ph.D..
In a previous series of landmark studies, Dr. Hazen found that a byproduct that forms when gut bacteria digest certain nutrients abundant in red meat and other animal products—called TMAO (trimethylamine N-oxide)—increases the risk of heart disease and stroke.
The latest findings offer a more comprehensive understanding of the two-step process by which gut microbes convert the nutrient carnitine into TMAO, an atherosclerosis- and blood clot-promoting molecule, following the ingestion of a red meat-rich diet.
"These new studies identify the gut microbial gene cluster responsible for the second step of the process that links a red meat-rich diet to elevated cardiac disease risks," said Dr. Hazen, who directs the Cleveland Clinic Center for Microbiome & Human Health. "This discovery helps point us towards new therapeutic targets to prevent or reduce diet-associated cardiovascular disease risk."
Membrane-associated proteins play a vital role in a variety of cellular processes, yet little is known about the membrane-association mechanism. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is one such protein with an important role in cardiovascular health, but its mechanism of action on the phospholipid membrane was unknown. To address this, researchers at University of California San Diego School of Medicine used state-of-the-art experimental and computational tools to show exactly how the enzyme interacts with the membrane and extracts its specific substrates.
The findings are publishing Jan. 3, 2022 in the online issue of Proceedings of the National Academy of Sciences.
Lp-PLA2 works on lipoproteins in the bloodstream, including common forms like low- and high-density lipoprotein (LDL and HDL). These lipoprotein particles are made up of a spherical layer of phospholipids surrounding a drop of fat and cholesterol esters. Over time, the phospholipids in this outer layer become oxidized, attracting free radicals and further oxidation, which contributes to plaque buildup and cardiovascular disease.
Not too long ago, the idea of taking—for instance—a skin cell and transforming it into a muscle cell was unthinkable. About 10 years ago, however, revolutionary research showed that it is indeed possible to reprogram differentiated adult cells into other types fully capable of conducting new functions.
Cell reprogramming is a main interest of the lab of Dr. Todd Rosengart, chair and professor of the Michael E. DeBakey Department of Surgery at Baylor College of Medicine, whose research focuses on finding innovative therapeutic approaches for heart failure.
"Heart failure remains the leading cause of death from heart disease," said Rosengart, DeBakey-Bard Chair in Surgery and professor of molecular and cellular biology at Baylor. "Nearly 5 million Americans can be expected to develop advanced congestive heart failure, and heart transplant or mechanical circulatory support implantation currently are the only options for patients with end-stage heart disease. However, these options are limited. We need to improve how to treat this devastating condition."
After a heart attack, the parts of the heart muscle that die do not regenerate into new heart tissue; instead, they are replaced by a scar that does not help the heart to beat. "The idea behind cell reprogramming is to coach the heart to heal itself by inducing the scar tissue, which is made mostly of fibroblasts, to change into functional heart muscle," said Rosengart, professor of heart and vascular disease at the Texas Heart Institute.
Researchers have succeeded at reprogramming fibroblasts from small animals to become heart muscle, with dramatic improvements in heart function. The challenge has been to apply this technology to human cells—human fibroblasts are more resistant to reprogramming. In this study, Rosengart and his colleagues explored a novel strategy to enhance the reprogramming efficiency of human fibroblasts.
Scientists have developed an artificial intelligence (AI) system that can analyze eye scans taken during a routine visit to an optician or eye clinic and identify patients at a high risk of a heart attack.
Doctors have recognized that changes to the tiny blood vessels in the retina are indicators of broader vascular disease, including problems with the heart.
In the research, led by the University of Leeds, deep learning techniques were used to train the AI system to automatically read retinal scans and identify those people who, over the following year, were likely to have a heart attack.
Deep learning is a complex series of algorithms that enable computers to identify patterns in data and to make predictions.
Writing in the journal Nature Machine Intelligence, the researchers report that the AI system had an accuracy of between 70% and 80% and could be used as a second referral mechanism for in-depth cardiovascular investigation.
The use of deep learning in the analysis of retinal scans could revolutionize the way patients are regularly screened for signs of heart disease.
(EurekAlert) CHICAGO (January 30, 2022) — Patients with mitral valve disease who live in disadvantaged communities are more likely to experience complications and are at higher risk for death after surgery than those with higher socioeconomic status (SES), according to research presented at the 58th Annual Meeting of The Society of Thoracic Surgeons.
“We collaboratively undertook this work with The Society of Thoracic Surgeons to better understand the impact of socioeconomic status on mitral valve surgery in the US,” said Amit Iyengar, MD, MSE, from the University of Pennsylvania in Philadelphia. “The STS Adult Cardiac Surgery Database was linked with a very robust composite metric that evaluates average SES based on census block tract groups, and showed it relates to mortality and rate of achieving a successful repair, independent of all other demographic or hospital and surgeon-level characteristics we had available.”
Using data from the STS Adult Cardiac Surgery Database, Dr. Iyengar and colleagues identified 46,831 adult patients who underwent—for the first time—isolated mitral valve repair or replacement for degenerative mitral disease from 2012 to 2018. Socioeconomic status was calculated using the 2018 Area Deprivation Index (ADI), a geographically-derived measure used to assess average income, education, employment, and housing quality for a given region. For this research, the group queried the ADI at a single city block level or rural equivalent.
“We confirmed the effect of ADI by looking at it more closely in smaller bootstrapped subsets,” said Dr. Iyengar. “We did this thoughtfully, trying to shed some light on the mechanisms by which socioeconomic status would affect outcomes.”
The researchers determined that low SES patients—who more commonly received health care under government payor programs such as Medicare and Medicaid (63% vs. 49%)—had more urgent/emergent surgery (21% vs. 13%), with minimally-invasive approaches used less often (24% vs. 39%).
