Category: Cardiovascular Disease

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Study Finds Positive Effects with Anaesthetic Drug after Cardiac Arrest

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If a patient is successfully resuscitated after a cardiac arrest and circulation resumes, they are not out of the woods yet. A number of factors can influence whether and how they survive the trauma in the subsequent phase. But a multicentre study of 571 patients has shown that the administration of the anaesthetic midazolam has a positive effect.

In cases where the patient required anaesthesia after successful resuscitation, midazolam improved the chances of optimal oxygen saturation and CO2 levels in the blood. The risk of a renewed drop in blood pressure or a renewed circulatory arrest didn’t increase. “This specific group of patients who have been successfully resuscitated should definitely be included in the guidelines for pre-hospital anaesthesia. Midazolam has proven to have a particularly positive effect in this group,” concludes Dr Gerrit Jansen, lead author of the study, which was published in the journal Deutsches Ärzteblatt International.

In the event of a cardiac arrest, rapid intervention is essential: If first aiders carry out resuscitation measures in good time, the patient’s circulation can be restarted in the best-case scenario. “However, it’s often the case that the patient hasn’t yet regained consciousness,” explains Gerrit Jansen. In this phase, there are various factors that can affect the chances of survival and subsequent permanent limitations due to the circulatory arrest.

“Some patients display protective reflexes after resuscitation, such as coughing or defensive movements, which make the emergency responders’ work more difficult. They often have to perform extended airway management, for example by intubating the patient in the same way as during surgery. This frequently requires sedation or anaesthesia,” explains Jansen. Until now, there has been concern that anaesthetic drugs could have a negative impact on the circulatory system, which has only just been restored. According to the study, however, this is not the case.

Of the 571 people included in the study who survived a cardiac arrest and were admitted to hospital, 395 were sedated, 249 of them with midazolam. The chance that their blood oxygen saturation levels were in the optimal range following a cardiac arrest increased twofold when midazolam was administered. The chance that carbon dioxide was effectively exhaled increased by a factor of 1.6 with the drug. “Our statistical methods confirmed a correlation between these results and the administration of midazolam, without any indication of negative circulatory effects,” says Gerrit Jansen.

“The European guidelines of the European Resuscitation Council don’t yet set out any specific recommendations for possible anesthetic drugs,” explains Jansen. “The German guideline for pre-hospital anaesthesia for patients with cardiovascular risk doesn’t mention patients in cardiac arrest. We’ve therefore carried out pioneering research in this field, the results of which should be incorporated into the recommendations for the benefit of the patients.”

Source: Ruhr-University Bochum

Categories : Cardiovascular Disease Mental HealthTags :

Inflammation may Link Depression and Cardiomyopathy

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Coronary artery disease and major depression may be genetically linked via inflammatory pathways to an increased risk for cardiomyopathy, a degenerative heart muscle disease, researchers at Vanderbilt University Medical Center and Massachusetts General Hospital have found.

Their report, published in Nature Mental Health, suggests that drugs prescribed for coronary artery disease and depression, when used in combination, potentially may reduce inflammation and prevent the development of cardiomyopathy.

“This work suggests that chronic low-level inflammation may be a significant contributor to both depression and cardiovascular disease,” said the paper’s corresponding author, Lea Davis, PhD, associate professor of Medicine in the Division of Genetic Medicine and Vanderbilt Genetics Institute.

The connection between depression and other serious health conditions is well known. As many as 44% of patients with coronary artery disease (CAD), the most common form of cardiovascular disease, also have a diagnosis of major depression. Yet the biological relationship between the two conditions remains poorly understood.

A possible connection is inflammation. Changes in the levels of inflammatory markers have been observed in both conditions, suggesting that there may be a common biological pathway linking neuroinflammation in depression with atherosclerotic inflammation in CAD.

In the current study, the researchers used a technique called transcriptome-wide association scans to map single nucleotide polymorphisms (genetic variations) involved in regulating the expression of genes associated with both CAD and depression.

The technique identified 185 genes that were significantly associated with both depression and CAD, and which were “enriched” for biological roles in inflammation and cardiomyopathy.

This suggests that predisposition to both depression and CAD, which the researchers called (major) depressive CAD, or (m)dCAD, may further predispose individuals to cardiomyopathy.

However, when the researchers scanned large electronic health record databases at VUMC, Mass General, and the National Institutes of Health’s All of Us Research Program, they found the actual incidence of cardiomyopathy in patients with the enriched genes for (m)dCAD was lower than in patients with CAD alone.

One possible explanation is that medications prescribed for CAD and depression, such as statins and antidepressants, may prevent development of cardiomyopathy by reducing inflammation, the researchers concluded.

“More research is needed to investigate optimal treatment mechanisms,” Davis added, “but at a minimum this work suggests that patient heart and brain health should be considered together when developing management plans to treat depression or cardiovascular disease.”

Source: Vanderbilt University Medical Center

Categories : Cardiovascular Disease Environmental EffectsTags :

Hot Days may Drive Inflammation and Accelerate Cardiovascular Disease

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Photo by Fandy Much: https://www.pexels.com/photo/toshiba-outdoor-air-conditioner-unit-on-yellow-wall-14086132/

Short-term exposure to higher heat may increase inflammation and interfere with normal immune system functions in the body, which may, in turn, increase susceptibility to infections and accelerate the progression of cardiovascular disease, according to preliminary research be presented at the American Heart Association’s Epidemiology and Prevention – Lifestyle and Cardiometabolic Scientific Sessions 2024, March 18-21.

An inflammatory response that is longstanding (lasting weeks to months) or that occurs in healthy tissues is damaging and plays a key role in the build-up of plaque in the arteries. This may lead to atherosclerosis. Heat waves are known to promote inflammation, however, studies examining air temperature and biomarkers of inflammation have had mixed results.

“Most research only considers temperature as the exposure of interest, which may not be adequate to capture a person’s response to heat,” said lead study author Daniel W. Riggs, PhD, an assistant professor of medicine at the University of Louisville. “In our study, we used alternative measurements of heat in relation to multiple markers of inflammation and immune response in the body to investigate the short-term effects of heat exposure and produce a more complete picture of its health impact.”

Participants visited study sites in Louisville, during the summer months for a blood test, and researchers analysed the blood for multiple markers of immune system function. The researchers then examined associations between the markers of immune system function and heat levels, including temperature, net effective temperature (which factors in relative humidity, air temperature and windspeed) and the Universal Thermal Climate Index (UTCI) on that day. UTCI is a thermo-physiological model developed by the International Society of Biometeorology Commission that factors in temperature, humidity, wind speed and ultraviolet radiation levels, which was used to evaluate participant’s physical comfort.

The analysis found:

  • For every 5°F (2.8°C) increase in UTCI (in this study, the equivalent of going from a day with no thermal stress to a day with moderate thermal stress, Riggs said), there was an increase in blood levels of key inflammatory markers: monocytes (4.2%), eosinophils (9.5%), natural killer T-cells (9.9%) and tumour necrosis factor-alpha (7.0%). These immune molecules indicate activation of the body’s innate immune system, which spurs a fast and non-specific inflammatory response throughout the body to protect against pathogens and injury.
  • A decrease in B-cells (-6.8%), indicating the body’s adaptive immune system that remembers specific viruses and germs and creates antibodies to fight them, was lowered.
  • A lesser impact on the immune system was found when heat was measured by average 24-hour temperature or by net effective temperature, which incorporates humidity and wind but not sunshine.

“Our study participants only had minor exposure to high temperatures on the day of their blood test, however, even minor exposure may contribute to changes in immune markers,” Riggs said. “With rising global temperatures, the association between heat exposure and a temporarily weakened response from the immune system is a concern because temperature and humidity are known to be important environmental drivers of infectious, airborne disease transmission. Thus, during the hottest days of summer people may be at higher risk of heat exposure, they may also be more vulnerable to disease or inflammation.”

Adults over 60 years and adults with existing cardiovascular disease are particularly at risk for heat-related cardiovascular events and deaths, Riggs explained.

“It’s important for physicians to communicate with patients about the risk of adverse health effects from heat exposure. For example, cardiologists could conduct customised consultations and assessments to increase patient awareness about their susceptibility to the effects of high temperatures. Also, changes to treatment regimens may be important to consider to address other risks. For example, some medications could make people more susceptible to heat-related illness or some may not be as effective when the body is exposed to high temperatures,” Riggs said.

Source: American Heart Association

Categories : Cardiovascular DiseaseTags :

At-home Nasal Spray for Episodes of Arrhythmia

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A clinical trial led by Weill Cornell Medicine investigators showed that a nasal spray that patients administer at home, without a physician, successfully and safely treated recurrent episodes of a condition that causes arrythmia. The study, published in the Journal of the American College of Cardiology, provides real-world evidence that a wide range of patients can safely and effectively use the experimental drug etripamil to treat recurrent paroxysmal supraventricular tachycardia (PSVT) episodes at home. For many, this could spare the need for repeated hospital trips for more invasive treatments.

The study is the latest in a series of studies by lead author Dr James Ip, professor of clinical medicine at Weill Cornell Medicine and a cardiologist at New York-Presbyterian/Weill Cornell Medical Center, and colleagues to demonstrate the potential of nasal spray calcium-channel blocker etripamil as an at-home treatment for PSVT.

Patients with PSVT experience sudden and recurrent rapid heart rhythms triggered by abnormal electrical activity in the upper chambers of the heart.

Though the episodes are not commonly life-threatening, they can be frightening and cause shortness of breath, chest pain, dizziness or fainting and lead to frequent emergency department visits. Treatment for PSVT often requires hospitalisation to receive intravenous medication. Some patients undergo cardiac ablation.

Dr Ip and colleagues previously showed that almost two-thirds of patients with PSVT who took one or more doses of the calcium channel blocker etripamil without a physician present experienced symptom relief on average in 17 minutes.

The latest study builds on those findings, showing that etripamil is safe and effective under more real-world circumstances in a larger patient population, and could be safely used to treat multiple episodes of PSVT.

The new study enrolled 1116 patients at 148 sites in the United States, Canada and South America. It did not require a pretest dose supervised by a physician as the previous studies did. It also included patients with a history of atrial fibrillation or atrial flutter, who were excluded from the previous studies. Patients monitored their heart for one hour with a home electrocardiogram monitor after self-administering the first dose, took an additional dose if necessary, and were allowed to self-treat up to four PSVT episodes with etripamil. Two-thirds of the patients experienced relief within an hour, and the average time needed for symptom relief was 17 minutes. Mild, temporary nasal symptoms such as runny nose, nasal congestion or discomfort, and bloody nose were common after the first use of etripamil but became less common with subsequent use.

Source: Weill Cornell Medicine

Categories : Cardiovascular Disease Surgeries & ProceduresTags :

Stop Aspirin after Stent to Reduce Bleeding in MI Patients, Study Suggests

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Percutaneous coronary intervention.
Percutaneous coronary intervention. Credit: Scientific Animations CC4.0

Withdrawing aspirin one month after percutaneous coronary intervention (PCI) in high-risk heart patients and keeping them on ticagrelor alone safely improves outcomes and reduces major bleeding by more than half when compared to patients taking aspirin and ticagrelor combined (also known as dual antiplatelet therapy or DAPT), which is the current standard of care.

These are the results from the ULTIMATE-DAPT study announced during a late-breaking trial presentation at the American College of Cardiology Scientific Sessions on Sunday, April 7, and published in The Lancet.

This is the first and only trial to test high-risk patients with recent or threatened heart attack (acute coronary artery syndromes, or ACS) taking ticagrelor with a placebo starting one month after PCI, and compare them with ACS patients taking ticagrelor with aspirin over the same period. The significant findings could change the current guidelines for standard of care worldwide.

“Our study has demonstrated that withdrawing aspirin in patients with recent ACS one month after PCI is beneficial by reducing major and minor bleeding through one year by more than 50 percent. Moreover, there was no increase in adverse ischaemic events, meaning continuing aspirin was causing harm without providing any benefit,” says Gregg W. Stone, MD, the study co-chair of ULTIMATE-DAPT, who presented the trial results.

“It is my belief that it’s time to change the guidelines and standard clinical practice such that we no longer treat most ACS patients with dual antiplatelet therapy beyond one month after a successful PCI procedure. Treating these high-risk patients with a single potent platelet inhibitor such as ticagrelor will improve prognosis,” adds Dr Stone.

The study analysed 3400 patients with ACS at 58 centres in four countries between August 2019 and October 2022. All of the patients had undergone PCI, a non-surgical procedure in which interventional cardiologists use a catheter to place stents in the blocked coronary arteries to restore blood flow. The patients were stable one month after PCI and were on ticagrelor and aspirin. Researchers randomised the patients after one month, withdrawing aspirin in 1700 patients and putting them on ticagrelor and a placebo, while leaving the other 1700 patients on ticagrelor and aspirin. All patients were evaluated between 1 and 12 months after the procedure.

During the study period, 35 patients in the ticagrelor-placebo group had a major or minor bleeding event, compared to 78 patients in the ticagrelor-aspirin group, meaning that the incidence of overall bleeding incidents was reduced by 55 percent by withdrawing aspirin. The study also analysed major adverse cardiac and cerebrovascular events including death, heart attack, stroke, bypass graft surgery, or repeat PCI. These events occurred in 61 patients in the ticagrelor-placebo group compared to 63 patients in the ticagrelor-aspirin group, and were not statistically significant – further demonstrating that removing aspirin did no harm and improved outcomes.

“It was previously believed that discontinuing dual antiplatelet therapy within one year after PCI in patients with ACS would increase the risk of heart attack and other ischaemic complications, but the present study shows that is not the case, with contemporary drug-eluting stents now used in all PCI procedures. Discontinuing aspirin in patients with a recent or threatened heart attack who are stable one month after PCI is safe and, by decreasing serious bleeding, improves outcomes,” Dr Stone adds. “This study extends the results of prior work that showed similar results but without the quality of using a placebo, which eliminates bias from the study.”

Source: The Mount Sinai Hospital / Mount Sinai School of Medicine

Categories : Cardiovascular Disease GastrointestinalTags :

Certain Gut Bacteria Linked to Reduced Cardiovascular Disease Risk

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Gut Microbiome. Credit Darryl Leja National Human Genome Research Institute National Institutes Of Health

Changes in the gut microbiome have been implicated in a range of diseases including type 2 diabetes, obesity, and inflammatory bowel disease. Now, a team of researchers has found that microbes in the gut may affect cardiovascular disease as well. In a study published in Cell, the team has identified specific species of bacteria that consume cholesterol in the gut and may help lower cholesterol and heart disease risk in people.

Researchers at the Broad Institute of MIT and Harvard along with Massachusetts General Hospital analysed metabolites and microbial genomes from more than 1400 participants in the Framingham Heart Study, a decades-long project focused on risk factors for cardiovascular disease.

The team discovered that bacteria called Oscillibacter take up and metabolise cholesterol from their surroundings, and that people carrying higher levels of the microbe in their gut had lower levels of cholesterol. They also identified the mechanism the bacteria likely use to break down cholesterol. The results suggest that interventions that manipulate the microbiome in specific ways could one day help decrease cholesterol in people. The findings also lay the groundwork for more targeted investigations of how changes to the microbiome affect health and disease.

“Our research integrates findings from human subjects with experimental validation to ensure we achieve actionable mechanistic insight that will serve as starting points to improve cardiovascular health,” said Xavier, who is a core institute member and a professor at Harvard Medical School and Massachusetts General Hospital.

Postdoctoral researcher Chenhao Li and research scientist Martin Stražar, both in Xavier’s lab, were co-first authors on the study.

Cholesterol cues

In the past decade, other researchers have uncovered links between composition of the gut microbiome and elements of cardiovascular disease, such as a person’s triglycerides and blood sugar levels after a meal. But scientists haven’t been able to target those connections with therapies in part because they lack a complete understanding of metabolic pathways in the gut.

In the new study, the Broad team gained a more complete and detailed picture of the impact of gut microbes on metabolism. They combined shotgun metagenomic sequencing, which profiles all of the microbial DNA in a sample, with metabolomics, which measures the levels of hundreds of known and thousands of unknown metabolites. They used these tools to study stool samples from the Framingham Heart Study.

“The project outcomes underline the importance of high-quality, curated patient data,” Stražar said. “That allowed us to note effects that are really subtle and hard to measure and directly follow up on them.”

More than 16 000 associations between microbes and metabolic traits were found, one of them particularly strong: People with several species of bacteria from the Oscillibacter genus had lower cholesterol levels than those who lacked the bacteria. The researchers found that species in the Oscillibacter genus were surprisingly abundant in the gut, representing on average 1 in every 100 bacteria.

The researchers then wanted to figure out the biochemical pathway the microbes use to break down cholesterol. To do this, they first needed to grow the organism in the lab. Fortunately, the lab has spent years collecting bacteria from stool samples to create a unique library that also included Oscillibacter.

After successfully growing the bacteria, the team used mass spectrometry to identify the most likely byproducts of cholesterol metabolism in the bacteria. This allowed them to determine the pathways the bacteria uses to lower cholesterol levels. They found that the bacteria converted cholesterol into intermediate products that can then be broken down by other bacteria and excreted from the body. Next, the team used machine-learning models to identify the candidate enzymes responsible for this biochemical conversion, and then detected those enzymes and cholesterol breakdown products specifically in certain Oscillibacter in the lab.

The team found another gut bacterial species, Eubacterium coprostanoligenes, that also contributes to decreased cholesterol levels. This species carries a gene that the scientists had previously shown is involved in cholesterol metabolism. In the new work, the team discovered that Eubacterium might have a synergistic effect with Oscillibacter on cholesterol levels, which suggests that new experiments that study combinations of bacterial species could help shed light on how different microbial communities interact to affect human health.

Microbial messages

The human gut microbiome remains mostly unmapped, but the team believes they have paved the way for the discovery of other similar metabolic pathways impacted by gut microbes, which could be targeted therapeutically.

“There are many clinical studies trying to do faecal microbiome transfer studies without much understanding of how the microbes interact with each other and the gut,” Li said. “Hopefully stepping back by focusing on one particular bug or gene first, we’ll get a systematic understanding of gut ecology and come up with better therapeutic strategies like targeting one or a few bugs.”

“Because of the large number of genes of unknown function in the gut microbiome, there are gaps in our ability to predict metabolic functions,” Li added. “Our work highlights the possibility that additional sterol metabolism pathways may be modified by gut microbes. There are potentially a lot of new discoveries to be made that will bring us closer to a mechanistic understanding of how microbes interact with the host.”

Source: Broad Institute of MIT and Harvard

Categories : Cardiovascular Disease Diet and NutritionTags :

Eggs are not the Cholesterol Menace They were Thought to be

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Many people hesitate to eat eggs amid concerns that they may raise cholesterol levels, with negative cardiovascular consequences. However, results from a prospective, controlled trial presented at the American College of Cardiology’s Annual Scientific Session show that over a four-month period cholesterol levels and other cardiovascular markers were similar among people who ate fortified eggs most days of the week compared with a non-egg eating control group.

A total of 140 patients with or at high risk for cardiovascular disease were enrolled in the PROSPERITY trial, which aimed to assess the effects of eating 12 or more fortified eggs a week versus a non-egg diet (consuming less than two eggs a week) on HDL- and LDL-cholesterol, as well as other key markers of cardiovascular health over a four-month study period.

“We know that cardiovascular disease is, to some extent, mediated through risk factors like high blood pressure, high cholesterol and increased BMI and diabetes. Dietary patterns and habits can have a notable influence on these and there’s been a lot of conflicting information about whether or not eggs are safe to eat, especially for people who have or are at risk for heart disease,” said Nina Nouhravesh, MD, a research fellow at the Duke Clinical Research Institute in Durham, North Carolina, and the study’s lead author. “This is a small study, but it gives us reassurance that eating fortified eggs is OK with regard to lipid effects over four months, even among a more high-risk population.”

Eggs are a common and relatively inexpensive source of protein and dietary cholesterol. Nouhravesh and her team wanted to look specifically at fortified eggs as they contain less saturated fat and additional vitamins and minerals, such as iodine, vitamin D, selenium, vitamin B2, 5 and 12, and omega-3 fatty acids.

For this study, patients were randomly assigned to eat 12 fortified eggs a week (cooked in whatever manner they chose) or to eat fewer than two eggs of any kind (fortified or not) per week.  All patients were 50 years of age or older (the average age was 66 years), half were female and 27% were Black. All patients had experienced one prior cardiovascular event or had two cardiovascular risk factors, such as high blood pressure, high cholesterol, increased BMI or diabetes. The co-primary endpoint was LDL and HDL cholesterol at four months. Secondary endpoints included lipid, cardiometabolic and inflammatory biomarkers and levels of vitamin and minerals. 

Patients had in-person clinic visits at the start of the study and visits at one and four months to take vital signs and have bloodwork done. Phone check-ins occurred at two and three months and patients in the fortified egg group were asked about their weekly egg consumption. Those with low adherence were provided additional education materials.

Results showed a -0.64mg/dL and a -3.14mg/dL reduction in HDL-cholesterol and LDL cholesterol, respectively, in the fortified egg group. While these differences weren’t statistically significant, the researchers said the differences suggest that eating 12 fortified eggs each week had no adverse effect on blood cholesterol. In terms of secondary endpoints, researchers observed a numerical reduction in total cholesterol, LDL particle number, another lipid biomarker called apoB, high-sensitivity troponin (a marker of heart damage), and insulin resistance scores in the fortified egg group, while vitamin B increased.

“While this is a neutral study, we did not observe adverse effects on biomarkers of cardiovascular health and there were signals of potential benefits of eating fortified eggs that warrant further investigation in larger studies as they are more hypothesis generating here,” Nouhravesh said, explaining that subgroup analyses revealed numerical increases in HDL cholesterol and reductions in LDL cholesterol in patients 65 years or older and those with diabetes in the fortified egg group compared with those eating fewer than two eggs.

So why have eggs gotten a bad rap? Some of the confusion stems from the fact that egg yolks contain cholesterol. Experts said a more important consideration, especially in the context of these findings, might be what people are eating alongside their eggs, such as buttered toast, bacon and other processed meats, which are not heart healthy choices. As always, Nouhravesh said it’s a good idea for people with heart disease to talk with their doctor about a heart healthy diet.

This single-centre study is limited by its small size and reliance on patients’ self-reporting of their egg consumption and other dietary patterns. It was also an unblinded study, which means patients knew what study group they were in, which can influence their health behaviours.

The study was funded by Eggland’s Best.

Source: American College of Cardiology

Categories : Cardiovascular Disease Mental HealthTags :

ADHD Stimulants may Increase Risk of Cardiomyopathy in Young Adults, Study Finds

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Photo by Inzmam Khan

Young adults who were prescribed stimulant medications for attention-deficit/hyperactivity disorder (ADHD) were significantly more likely to develop cardiomyopathy compared with those who were not prescribed stimulants, in a study presented at the American College of Cardiology’s Annual Scientific Session.

The study found that people prescribed stimulants such as Adderall and Ritalin were 17% more likely to have cardiomyopathy at one year and 57% more likely to have cardiomyopathy at eight years compared with those who were not taking these medications. Cardiomyopathy involves structural changes in the heart muscle that weaken its pumping ability. It can cause a person to tire easily and limit their ability to perform daily tasks, and it often worsens over time.

However, researchers said that the overall risk of cardiomyopathy remained relatively low even when stimulants were used long-term. They said the findings do not necessarily point to a need for clinicians to change their approach to screening patients or prescribing stimulants.

“The longer you leave patients on these medications, the more likely they are to develop cardiomyopathy, but the risk of that is very low,” said Pauline Gerard, a second-year medical student at the University of Colorado School of Medicine in Aurora, Colorado, and the study’s lead author. “I don’t think this is a reason to stop prescribing these medications. There’s very little increased risk of these medications over the long term; it’s a real risk, but it’s small.”

ADHD is one of the most common neurodevelopmental disorders in children, affecting about 1 out of 10 American children aged 3 to 17, and can continue into adulthood. It is typically treated with behavioural therapy initially, which may be combined with stimulant or non-stimulant medications to help control behaviours that interfere with daily life and relationships. Stimulant medications can elevate blood pressure by causing the heart to beat faster and with greater force.

Most previous studies assessing the safety of stimulant medications have focused on the first year or two of use and found no evidence of harm to the heart. Since many patients are prescribed these medications in early childhood and continue taking them into adulthood, this new study was designed to assess their potential to cause harm over a longer period of time, Gerard said.

Using the TriNetX research database that includes information from about 80 hospitals across the U.S., researchers analysed data from people diagnosed with ADHD between 20–40 years of age. Individuals with the presence or absence of a prescription for stimulant medications along with rates of cardiomyopathy that could potentially be linked to stimulant use were included. Those with heart damage caused by other known factors, such as cancer treatments, were excluded.

For the analysis, the researchers paired each person who had been prescribed stimulants with an individual who had not been prescribed stimulants but was as similar as possible in all other respects, such as age, sex and other health conditions. Overall, 12 759 pairs were created and were followed for at least 10 years. Of these pairs, people prescribed stimulants were found to be significantly more likely to develop cardiomyopathy throughout the 10-year follow-up period, with the gap growing larger each year except the last two, when it narrowed slightly.

Despite the significant gap, the overall prevalence of cardiomyopathy was still quite low in both groups. After being prescribed stimulants for 10 years, 0.72% (less than three-quarters of one percent) of patients developed cardiomyopathy, compared with 0.53% (a little over half of one percent) among those who were not prescribed stimulants.

To put the numbers into context, Gerard said, “You can have almost 2000 patients on these medications for a year and you might only cause one of them to have a cardiomyopathy that they otherwise would not have had, but if you leave them on it for 10 years, 1 in 500 will have that happen.”

At these levels, researchers said the study does not suggest that aggressive testing for cardiovascular risk is warranted before prescribing stimulants, given that the potential benefits of testing must be balanced against the risks and costs. They suggest that further studies could help to identify subgroups of patients at greater risk who may benefit from future screening approaches.

Gerard said that it could also be helpful to study potential differences among different types of ADHD medications and different types of cardiomyopathies.

Source: American College of Cardiology

Categories : Cardiovascular DiseaseTags :

New Advance against Heart Failure Caused by Y Chromosome Loss

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Chromosomes. Credit: NIH

Researchers have discovered a gene on the Y chromosome that contributes to the greater incidence of heart failure in men when the Y chromosome is lost to ageing.

Y chromosome loss in men occurs progressively throughout life and can be detected in approximately 40% of 70-year-old men. In 2022, Kenneth Walsh, PhD, at University of Virginia discovered that this loss can contribute to heart muscle scarring and lead to heart failure. (That finding was the first to directly link Y chromosome loss to a specific harm to men’s health; Y chromosome loss is increasingly thought to play a role in diseases ranging from Alzheimer’s to cancer.)

In an important follow-up finding published in Nature Cardiovascular Research, Walsh and his team have discovered how Y chromosome loss triggers changes in heart immune cells that make the cells more likely to cause scarring and heart failure.

Further, the researchers found they could reverse the harmful heart changes by giving lab mice a drug that targets the process of fibrosis that leads to the heart scarring, which could lead to a similar treatment for men.

“Our previous work identified that it was loss of the entire Y chromosome that contributed to heart disease in men,” said Walsh, the director of UVA’s Hematovascular Biology Center. “This new work identified a single gene on the Y chromosome that can account for the disease-promoting effects of Y chromosome loss.”

About Y chromosome loss

Unlike women, who have two X chromosomes, men have an X and a Y. For a long time, the genes found on the Y chromosome were not thought to play important roles in disease. Sex hormones, scientists thought, explained the differences in certain diseases in men and women. But Walsh’s groundbreaking work has helped change that perception. It also suggested an explanation for why heart failure is more common in men than women. (Cardiovascular disease, which includes heart failure, is the leading cause of death worldwide.)

Y chromosome loss occurs in only a small percentage of affected men’s cells. This results in what is called “mosaicism,” where genetically different cells occur within one individual. Researchers aren’t entirely sure why this partial Y chromosome loss occurs, but predominantly it strikes elderly men and men who smoke compared to those who don’t.

To better understand the effects of Y chromosome loss, Walsh and his team examined genes found on the Y chromosome to determine which might be important to heart scarring. One gene they looked at, Uty, helps control the operating instructions for immune cells called macrophages and monocytes, the scientists determined. When the Uty gene was disrupted, either individually or through Y chromosome loss, that triggered changes in the immune cells in lab mice. Suddenly, the macrophages were much more “pro-fibrotic,” or prone to scarring. This accelerated heart failure as well, the scientists found.

“The identification of a single gene on the Y chromosome provides information about a new druggable target to treat fibrotic diseases,” said Walsh, of UVA’s Division of Cardiovascular Medicine and Robert M. Berne Cardiovascular Research Center.

Walsh and his team were able to prevent the harmful changes in the mice’s macrophages by giving them a specially designed monoclonal antibody. This halted the harmful changes in the heart, suggesting the approach might, with further research, lead to a way to treat or avoid heart failure and other fibrotic diseases in men with Y chromosome loss.

“Currently, we are working with our clinician colleagues in the Division of Cardiovascular Medicine at UVA to assess whether loss of the Y chromosome in men is associated with greater scarring in the heart,” Walsh said. “This research will provide new avenues for understanding the causes of heart disease.”

Based on their findings, Walsh and his team believe that a small group of genes found on the Y chromosome may have big effects on a wide array of diseases. Their new work identifies mechanisms that may lead to this, and they are hopeful that further research will provide a much better understanding of unknown causes of sickness and death in men.

“This research further documents the utility of studying the genetics of mutations that are acquired after conception and accumulate throughout life,” Walsh said. “These mutations appear to be as important to health and lifespan as the mutations that are inherited from one’s parents. The study of these age-acquired mutations represents a new field of human genetics.”

Source: University of Virginia Health System

Categories : Cardiovascular DiseaseTags :

Getting too Little Sleep Linked to High Blood Pressure

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Photo by Andrea Piacquadio

Sleeping fewer than seven hours is associated with a higher risk of developing hypertension over time, according to a study presented at the American College of Cardiology’s Annual Scientific Session.

While the association between sleep patterns and hypertension has been reported, evidence about the nature of this relationship has been inconsistent, according to researchers. The current analysis pools data from 16 studies conducted between January 2000 and May 2023, evaluating hypertension incidence in 1 044 035 people from six countries without a prior history of hypertension over a median follow-up of five years (follow-up ranged from 2.4 to 18 years). Short sleep duration was significantly associated with a higher risk of developing hypertension after adjusting for demographic and cardiovascular risk factors, including age, sex, education, BMI, blood pressure, smoking status etc. Furthermore, the association was found to be even stronger for those getting less than five hours of sleep.

“Based on the most updated data, the less you sleep – that is less than seven hours a day – the more likely you will develop high blood pressure in the future,” said Kaveh Hosseini, MD, assistant professor of cardiology at the Tehran Heart Center in Iran and principal investigator of the study. “We saw a trend between longer sleep durations and a greater occurrence of high blood pressure, but it was not statistically significant. Getting seven to eight hours of sleep, as is recommended by sleep experts, may be the best for your heart too.”

The study found that sleeping less than seven hours was associated with a 7% increased risk of developing hypertension, which spiked to 11% when reported sleep duration was less than five hours. By comparison, diabetes and smoking are known to heighten one’s risk of hypertension by at least 20%, Hosseini said.

While the study did not look at why this might be the case, Hosseini said that disrupted sleep could be to blame. For example, he said lifestyle habits or comorbid conditions such as overeating, alcohol use, nightshift work, certain medication use, anxiety, depression, sleep apnoea or other sleep disorders may be factors.

Researchers were surprised there were no age-based differences in the association between sleep duration and hypertension given that sleep patterns tend to shift with age. Participants ranged in age from 35.4 years to 60.9 years and 61% were female. When compared with men, females who reported less than seven hours of sleep had a 7% greater risk of developing hypertension.

“Getting too little sleep appears to be riskier in females,” Hosseini said. “The difference is statistically significant, though we are not sure it’s clinically significant and should be further studied. What we do see is that lack of good sleep patterns may increase the risk of high blood pressure, which we know can set the stage for heart disease and stroke.”

It’s important for people to talk with their health care team about their sleep patterns, especially if they have disrupted sleep that might be due to obstructive sleep apnoea. Sleep apnoea has been tied to higher rates of high blood pressure, stroke and coronary artery disease.

This study has several limitations, including that sleep duration was based on self-reported questionnaires, so changes in sleep duration over the follow-up period were not assessed. Moreover, there were variations in how short sleep duration was defined between the studies (fewer than five or six hours).

“Further research is required to evaluate the association between sleep duration and high blood pressure using more accurate methods like polysomnography, a method for evaluating sleep quality more precisely,” Hosseini said. “Moreover, the variations in reference sleep duration underline the need for standardised definition in sleep research to enhance the comparability and generalisability of findings across diverse studies.”

Source: American College of Cardiology