Tag: myocardial infarction

Categories : Cardiovascular Disease New Compounds and TreatmentsTags :

An Experimental Drug to Prevent Post-heart Attack Heart Failure

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Scientists at UCLA have developed a first-of-its-kind experimental therapy that has the potential to enhance heart repair following a heart attack, preventing the onset of heart failure. After a heart attack, the heart’s innate ability to regenerate is limited, causing the muscle to develop scars to maintain its structural integrity. This inflexible scar tissue, however, interferes with the heart’s ability to pump blood, leading to heart failure in many patients – 50% of whom do not survive beyond five years.

The new therapeutic approach aims to improve heart function after a heart attack by blocking a protein called ENPP1, which is responsible for increasing the inflammation and scar tissue formation that exacerbate heart damage. The findings, published in Cell Reports Medicine, could represent a major advance in post-heart attack treatment.

The research was led by senior author Dr Arjun Deb, a professor of medicine and molecular, cell and developmental biology at UCLA.

“Despite the prevalence of heart attacks, therapeutic options have stagnated over the last few decades,” said Deb, who is also a member of the UCLA Broad Stem Cell Research Center. “There are currently no medications specifically designed to make the heart heal or repair better after a heart attack.”

The experimental therapy uses a therapeutic monoclonal antibody engineered by Deb and his team. This targeted drug therapy is designed to mimic human antibodies and inhibit the activity of ENPP1, which Deb had previously established increases in the aftermath of a heart attack.

The researchers found that a single dose of the antibody significantly enhanced heart repair in mice, preventing extensive tissue damage, reducing scar tissue formation and improving cardiac function. Four weeks after a simulated heart attack, only 5% of animals that received the antibody developed severe heart failure, compared with 52% of animals in the control group.

This therapeutic approach could become the first to directly enhance tissue repair in the heart following a heart attack; an advantage over current therapies that focus on preventing further damage but not actively promoting healing. This can be attributed to the way the antibody is designed to target cellular cross-talk, benefitting multiple cell types in the heart, including heart muscle cells, the endothelial cells that form blood vessels, and fibroblasts, which contribute to scar formation. 

Initial findings from preclinical studies also show that the antibody therapy safely decreased scar tissue formation without increasing the risk of heart rupture – a common concern after a heart attack. However, Deb acknowledges that more work is needed to understand potential long-term effects of inhibiting ENPP1, including potential adverse effects on bone mass or bone calcification. 

Deb’s team is now preparing to move this therapy into clinical trials. The team plans to submit an Investigational New Drug, or IND, application to the U.S. Food and Drug Administration this winter with the goal of beginning first-in-human studies in early 2025. These studies will be designed to administer a single dose of the drug in eligible individuals soon after a heart attack, helping the heart repair itself in the critical initial days after the cardiac event.

While the current focus is on heart repair after heart attacks, Deb’s team is also exploring the potential for this therapy to aid in the repair of other vital organs.

“The mechanisms of tissue repair are broadly conserved across organs, so we are examining how this therapeutic might help in other instances of tissue injury,” said Deb, who is also the director of the UCLA Cardiovascular Research Theme at the David Geffen School of Medicine. “Based on its effect on heart repair, this could represent a new class of tissue repair-enhancing drugs.”

Categories : Cardiovascular Disease Emergency MedicineTags :

Two Types of Bloodstream Access in Heart Attacks are Equally Effective

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There is no difference in the effectiveness of the two most commonly used methods for administering medication during out-of-hospital cardiac arrest, according to a large new clinical study published in NEJM.

This is shown in a large new clinical study from Aarhus University and Prehospital Services, Region Midtjylland, which compared two ways of accessing the bloodstream: a standard needle in a vein (venous catheter) and a so-called intraosseous needle, which is inserted into the bone marrow.

“When a person suffers cardiac arrest outside the hospital, it is crucial to quickly access the bloodstream to administer life-saving medication. We investigated which method is best,” explains Lars Wiuff Andersen, professor and physician at the Department of Clinical Medicine, Aarhus University, Prehospital Services, Region Midtjylland, and Aarhus University Hospital.

Venous catheter or intraosseous needle?

Until now, healthcare professionals have preferred using a venous catheter, but it can be difficult to place as veins may collapse during cardiac arrest.

The intraosseous needle, inserted either into the shinbone or upper arm, can be faster and easier to use in an emergency.

Therefore, it’s interesting to investigate the effectiveness of both methods, explains Lars Wiuff Andersen.

The study, based on data from nearly 1500 cardiac arrest patients across Denmark, showed that about 30 percent of patients in both groups had their blood circulation restored.

“The two methods proved to be equally effective in restoring blood circulation and saving lives. There was no difference in the patients’ survival or quality of life,” explains Mikael Fink Vallentin, associate professor at the Department of Clinical Medicine and Prehospital Services, Region Midtjylland, and co-lead author of the study.

May change guidelines

According to the researchers behind the study, the results may impact future guidelines, which previously recommended venous catheters as the first choice.

However, Lars Wiuff Andersen notes that it is too early to say exactly how the guidelines will change.

“Our data must be considered alongside a large clinical trial from the UK, which is being published simultaneously with our study. Combined, these two trials will likely influence guidelines for cardiac arrest treatment, but a thorough review of the results will be needed,” he says.

More unanswered questions

There are still several unanswered questions, especially regarding whether specific groups of cardiac arrest patients benefit more from one method than the other.

The researchers are continuing to analyse and compare their own data with data from the UK trial.

The Danish research team has already planned a new, large clinical trial to investigate which method is best for delivering electric shocks during cardiac arrest.

“We hope to gain even more answers on how to best save lives in cardiac arrest in the future,” says Lars Wiuff Andersen.

Source: Aarhus University

Categories : Cardiovascular Disease NeurologyTags :

Heart Attacks Trigger a Greater Need for Sleep to Promote Healing

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A heart attack can trigger a desire to get more sleep, allowing the heart to heal and reduce inflammation as a result of the heart’s special signals to the brain, according to a new Mount Sinai study. This is the first study showing how the heart and brain communicate via the immune system to promote sleep and recovery after a major cardiovascular event.

The novel findings, published in Nature, highlight the importance of increased sleep after a heart attack, and suggest that sufficient sleep should be a focus of post-heart-attack clinical management and care, including in intensive care, where sleep is frequently disrupted, along with cardiac rehabilitation.

“This study is the first to demonstrate that the heart regulates sleep during cardiovascular injury by using the immune system to signal to the brain. Our data show that after a myocardial infarction (heart attack) the brain undergoes profound changes that augment sleep, and that in the weeks following a myocardial infarction, sleep abundance and drive is increased,” says senior author Cameron McAlpine, PhD, Assistant Professor of Medicine (Cardiology), and Neuroscience, at the Icahn School of Medicine at Mount Sinai. “We found that neuro-inflammation and the recruitment of immune cells called monocytes to the brain after a myocardial infarction is a beneficial and adaptive response that increases sleep to enable heart healing and the reduction of damaging cardiac inflammation.”

The researchers from the Cardiovascular Research Institute at Icahn Mount Sinai first used mouse models to discover this phenomenon. They induced heart attacks in half of the mice and performed high-resolution imaging and cell analysis, and used implantable wireless electroencephalogram devices to record electrical signals from their brains and analyse sleep patterns. After the heart attack, they found a three-fold increase in slow-wave sleep, a deep stage of sleep characterized by slow brain waves and reduced muscle activity. This increase in sleep occurred quickly after the heart attack and lasted one week.

When the researchers studied the brains of the mice with heart attacks, they found that immune cells called monocytes were recruited from the blood to the brain and used a protein called tumour necrosis factor (TNF) to activate neurons in an area of the brain called the thalamus, which caused the increase in sleep. This happened within hours after the cardiac event, and none of this occurred in the mice that did not have heart attacks.

The researchers then used sophisticated approaches to manipulate neuron TNF signaling in the thalamus and uncovered that the sleeping brain uses the nervous system to send signals back to the heart to reduce heart stress, promote healing, and decrease heart inflammation after a heart attack. To further identify the function of increased sleep after a heart attack, the researchers also interrupted the sleep of some of the mice. The mice with sleep disruption after a heart attack had an increase in heart sympathetic stress responses and inflammation, leading to slower recovery and healing when compared to mice with undisrupted sleep.

The research team also performed several human studies. The first studied the brains of patients 1–2 days after a heart attack and found an increase in monocytes compared to people without a heart attack or other CVD, mirroring the mice findings. The next analysed the sleep of more than 80 heart attack patients during the four weeks post-event and followed them for two years. The patients were divided into good sleepers and poor sleepers based on the quality of their sleep during the four weeks post-heart attack. The poor sleepers had a worse prognosis; their risk of having another cardiovascular event was twice as high as good sleepers. Additionally, the good sleepers had a significant improvement in heart function while poor sleepers had no or little improvement. 

In another human study, the researchers analysed the impact of five weeks of restricted sleep in 20 healthy adults. Sleep was monitored using electronic devices and the participants kept a sleep diary. During the five-week study period, half the participants slept for the recommended seven to eight hours a night uninterrupted, while the other half restricted their sleep by 1.5 hours each night – either delaying bedtime or waking up early. After the study period, researchers analysed blood monocytes and found similar sympathetic stress signaling and inflammatory responses in the sleep-restricted group as those that were identified in mice.

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

Categories : Cardiovascular Disease Lab Tests and ImagingTags :

New Blood Test on a Chip Rapidly Detects Earliest Signs of Heart Attack

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Peng Zheng shows off the heart of the blood test, chip with a groundbreaking nanostructured surface on which blood is tested. Image: Will Kirk / Johns Hopkins University

With heart attacks, every second counts. A newly developed blood test on a chip diagnoses them in minutes rather than hours and could be adapted as a tool for first responders and people at home.

“Heart attacks require immediate medical intervention in order to improve patient outcomes, but while early diagnosis is critical, it can also be very challenging – and near impossible outside of a clinical setting,” said lead author Peng Zheng, an assistant research scientist at Johns Hopkins University. “We were able to invent a new technology that can quickly and accurately establish if someone is having a heart attack.”

The proof-of-concept work, which can be modified to detect infectious diseases and cancer biomarkers, is described in Advanced Science.

Zheng and senior author Ishan Barman develop diagnostic tools through biophotonics, using laser light to detect biomarkers, which are bodily responses to conditions including disease. Here they used the technology to find the earliest signs in the blood that someone was having a heart attack. Heart attacks remain one of the trickiest conditions to diagnose, with symptoms that vary widely and biological signals that can be subtle and easy to miss in the early stages of an attack, when medical intervention can do the most good.

Will be like ‘ Star Trek tricorder’

People suspected of having heart attacks typically are given a combination of tests to confirm the diagnosis – usually starting with electrocardiograms to measure the electrical activity of the heart, a procedure that takes about five minutes, and blood tests to detect the hallmarks of a heart attack, where lab work can take at least an hour and often has to be repeated.

The stand-alone blood test the team created provides results in five to seven minutes. It’s also more accurate and more affordable than current methods, the researchers say.

Though created for speedy diagnostic work in a clinical setting, the test could be adapted as a hand-held tool that first responders could use in the field, or that people might even be able to use themselves at home.

“We’re talking about speed, we’re talking about accuracy, and we’re talking of the ability to perform measurements outside of a hospital,” said Barman, a bioengineer in JHU’s Department of Mechanical Engineering. “In the future we hope this could be made into a hand-held instrument like a Star Trek tricorder, where you have a drop of blood and then, voilà, in a few seconds you have detection.”

The heart of the invention is a tiny chip with a groundbreaking nanostructured surface on which blood is tested. The chip’s “metasurface” enhances electric and magnetic signals during Raman spectroscopy analysis, making heart attack biomarkers visible in seconds, even in ultra-low concentrations. The tool is sensitive enough to flag heart attack biomarkers that might not be detected at all with current tests, or not detected until much later in an attack.

Though designed to diagnose heart attacks, the tool could be adapted to detect cancer and infectious diseases, the researchers say.

“There is enormous commercial potential,” Barman said. “There’s nothing that limits this platform technology.”

Next the team plans to refine the blood test and explore larger clinical trials.

Source: John Hopkins University

Categories : Cardiovascular Disease COVIDTags :

COVID Infection Linked to MI & Stroke Risk Increases up to 3 Years Later

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An analysis of data in the UK Biobank has found that COVID infection may increase the risk of myocardial infarction (MI), stroke and death from any cause for up to three years for people with and without cardiovascular disease, according to new research published in the American Heart Association’s peer-reviewed journal Arteriosclerosis, Thrombosis and Vascular Biology (ATVB).

“We found a long-term cardiovascular health risk associated with COVID, especially among people with more severe COVID cases that required hospitalisation,” said lead study author James Hilser, M.P.H., Ph.D.-candidate at the University of Southern California Keck School of Medicine in Los Angeles. “This increased risk of heart attack and stroke continued three years after COVID infection. Remarkably, in some cases, the increased risk was almost as high as having a known cardiovascular risk factor such as Type 2 diabetes or peripheral artery disease.”

Previous research has shown that COVID increases the risk of serious cardiovascular complications within the first month after infection. This study examined how long the increased risk lasted and whether it subsided after recovering from COVID infection.

Researchers reviewed health and genetic data in the UK Biobank for more than 10 000 adults, including approximately 8000 who had tested positive for SARS-CoV-2 from February 1 to December 31, 2020 and about 2000 who tested positive for the virus in a hospital setting in 2020. A group of more than 200,000 adults who had no history of COVID infection during the same time frame in the UK Biobank were also reviewed for comparison. None of the participants were vaccinated at the time of infection because COVID vaccines were not yet available in 2020.

The analysis found:

  • During the nearly 3-year follow-up period, the risk of heart attack, stroke and death was more than two times higher among adults who had COVID, and nearly four times greater among adults hospitalized with COVID, compared with the group with no history of COVID infection.
  • People hospitalized with COVID, without cardiovascular disease or without Type 2 diabetes, had a 21% greater risk of heart attack, stroke and death compared to people with cardiovascular disease and without COVID infection.
  • There was a significant genetic interaction among the non-O blood types and hospitalisation for COVID. People with severe COVID infections had an increased risk of heart attack and stroke, however, that risk was even higher in people who had non-O blood types (those with blood types A, B or AB).
  • The risk of heart attack and stroke was about 65% higher in adults with non-O blood types compared to those who had type O blood. A preliminary analysis did not show that Rh (positive or negative) blood type interacted with severe COVID, the authors noted.

“Worldwide, over a billion people have already experienced COVID infection. The findings reported are not a small effect in a small subgroup,” said co-senior study author Stanley Hazen, M.D., Ph.D., chair of cardiovascular and metabolic sciences in Cleveland Clinic’s Lerner Research Institute and co-section head of preventive cardiology. “The results included nearly a quarter million people and point to a finding of global health care importance that may translate into an explanation for a rise in cardiovascular disease around the world.” 

Study details, background and design:

  • Health data was from the UK Biobank, a large-scale study of 503,325 adults living in the United Kingdom who were 40 to 69 years of age at enrollment between 2006 and 2010. The in-depth health and biomedical information was collected for participants registered in the UK National Health Service with a UK general practitioner (similar to a primary care physician in the U.S.).
  • This analysis included health data for 10,005 adults who tested positive for the COVID virus or were hospitalized with COVID between February 1, 2020, and December 31, 2020. An additional 217,730 peers enrolled in the UK Biobank who did not have COVID during the same time period were included. In the analysis, all participants were matched as closely as possible for demographics and similar health conditions.
  • Major adverse cardiovascular events (heart attack, stroke and all-cause death) were evaluated for long-term risk, through October 31, 2022, approximately 3 years later.

“This interesting paper is really two studies in one,” said Sandeep R. Das, M.D., M.P.H., MBA, FAHA, co-chair of the American Heart Association’s COVID-19 CVD Registry committee and director for quality and value in the cardiology division for UT Southwestern Medical Center in Dallas. “First, the authors show that having been hospitalized with COVID is a marker of increased cardiovascular risk, on par with having a pre-existing diagnosis of cardiovascular disease. Although proving direct cause and effect is very difficult to tease out in a study that only analyses past data collected for other purposes, this finding is important because it suggests a history of prior COVID hospitalization, even without a history of CVD, should be considered to initiate and possibly accelerate CVD prevention efforts. Whether severe COVID infection has a direct impact on the vascular system is an interesting area for study as well,” Das said.

“The second ‘study’ in this paper looks at the relationship between ABO blood type and COVID outcomes. They show that something located close to the genetic home of ABO blood type is associated with different degrees of susceptibility to COVID. This is really fascinating, and I look forward to seeing scientists tease out what the specific pathway may be.”

The study had several limitations, including that the data was from patients who had the original strain of the COVID virus before vaccines were widely available in 2021. Additionally, the researchers noted that UK Biobank information on medication use was not specific to the beginning of the pandemic in 2020 or the date that patients were infected with SARS-CoV-2. Also, because the majority of participants in the UK Biobank are white, additional research is needed to confirm that these results apply to people with diverse racial and ethnic backgrounds.

“The results of our study highlight the long-term cardiovascular effects of COVID infection. Given the increased risk of heart attack, stroke and death, the question is whether or not severe COVID should be considered as another risk factor for CVD, much like Type 2 diabetes or peripheral artery disease, where treatment focused on CVD prevention may be valuable,” said co-senior study author Hooman Allayee, Ph.D., a professor of population and public health sciences at the University of Southern California Keck School of Medicine in Los Angeles. “The results suggest that people with prior COVID infection may benefit from preventive care for cardiovascular disease.”

Source: American Heart Association

Categories : Cardiovascular DiseaseTags :

Is Long-term Beta-blocker Therapy Needed after a Heart Attack?

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For patients with a history of myocardial infarction (MI), cardiovascular safety of interrupting beta-blocker could not be shown in comparison to continuation and there was no benefit to the patients’ quality of life, according to late-breaking research presented in a Hot Line session today at ESC Congress 2024.1 

“Improvements in MI management and data from observational studies have led physicians to question whether continuing beta-blockers after one year post-MI is needed since unnecessary treatment may result in side effects.2-5 We conducted the ABYSS trial to provide conclusive randomised data on the effects of beta-blocker interruption vs. continuation on cardiovascular events and quality of life, but we were unable to show safety preservation in terms of clinical events nor any benefit on quality of life with beta-blocker interruption,” said Principal Investigator, Professor Johanne Silvain of the Sorbonne University, Paris, France. 

The open-label, non-inferiority, randomised ABYSS trial, conducted by the ACTION Group, included patients with a prior MI taking long-term beta-blockers, with a left ventricular ejection fraction of at least 40% and no cardiovascular events in the previous six months. Participants were randomised (1:1) to interrupting or continuing their β-blocker medication. 

The primary endpoint was a composite of death, non-fatal MI, non-fatal stroke or hospitalisation for cardiovascular reasons at the longest follow-up (minimum, one year), according to an analysis of non-inferiority (defined as a between-group absolute difference of < 3 percentage points for the upper boundary of the two-sided 95% confidence interval [CI]). The main secondary endpoint was the change in quality of life as measured by the European Quality of Life–5 Dimensions questionnaire. 

In total 3698 patients were randomised from 49 sites in France. The mean age was 64 years and 17% were female. The median time between last MI and randomisation was 2.9 years (interquartile range 1.2–6.4 years). 

Over median follow-up of 3 years, interruption of long-term beta-blocker treatment was not shown to be non-inferior to beta-blocker continuation. A primary-outcome event occurred in 23.8% of patients in the interruption group and in 21.1% in the continuation group (risk difference 2.8 percentage points; 95% CI <0.1–5.5), with a hazard ratio of 1.16 (95% CI 1.01–1.33; p = 0.44 for non-inferiority).  

Death occurred in 4.1% in the interruption group and 4.0% in the continuation group, while MI occurred in 2.5% and 2.4%, respectively. Of note, hospitalisation for cardiovascular causes occurred in 18.9% in the interruption group and 16.6% in the continuation group. Beta-blocker interruption was also associated with increases in systolic and diastolic blood pressure and heart rate at 6 months (all p<0.001 vs. beta-blocker continuation) and during the study follow up. Beta-blocker interruption did not improve the patients’ quality of life.  

Summing up the evidence from the ABYSS trial, Professor Silvain concluded: “Differences between the groups with respect to hospitalisation for cardiovascular reasons and the negative effect on blood pressure levels, together with the absence of quality-of-life improvement do not support interruption of a chronic beta-blocker treatment in post-MI patients. These results must be put into context with recent findings from the open-label REDUCE-MI6 trial and ongoing trials to provide additional evidence on the optimal use of beta-blockers after MI.”  

References

  1. ‘Beta blocker interruption in patients with prior myocardial infarction: results of the ABYSS trial and effect on blood pressure and heart rate control’ will be discussed during Hot Line 1 on Friday 30 August in room London. 
  2. Holt A, Blanche P, Zareini B, et al. Effect of long-term beta-blocker treatment following myocardial infarction among stable, optimally treated patients without heart failure in the reperfusion era: a Danish, nationwide cohort study. Eur Heart J. 2021;42:907–914. 
  3. Park CS, Yang H-M, Ki Y-J, et al. Left ventricular ejection fraction 1 year after acute myocardial infarction identifies the benefits of the long-term use of beta-blockers: analysis of data from the KAMIR-NIH Registry. Circ Cardiovasc Interv. 2021;14:e010159.  
  4. Puymirat E, Riant E, Aissaoui N, et al. β Blockers and mortality after myocardial infarction in patients without heart failure: multicentre prospective cohort study. BMJ. 2016;354:i4801. 
  5. Kim J, Kang D, Park H, et al. Long-term β-blocker therapy and clinical outcomes after acute myocardial infarction in patients without heart failure: nationwide cohort study. Eur Heart J. 2020;41:3521–3529. 
  6. Yndigegn T, Lindahl B, Mars K, et al. Beta-blockers after myocardial infarction and preserved ejection fraction. N Engl J Med. 2024;390:1372–1381.  

Source: European Society of Cardiology

Categories : Cardiovascular Disease Obstetrics & GynaecologyTags :

Women Lose More Years of Life After a Heart Attack Than Men

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A new study shows that women lose more years of life after a heart attack than men. A 50-year-old woman with a large heart attack loses an average of 11 years, while an 80-year-old man with a small heart attack loses an average of 5 months of life. The results of the study, led by researchers at Karolinska Institutet and Danderyd Hospital, are published in the journal Circulation.

The new study examined 335 000 individuals with first-time myocardial infarction registered in the SWEDEHEART quality registry during the period 1991-2022. The individuals with myocardial infarction were compared with 1.6 million individuals without myocardial infarction using data from Statistics Sweden and the National Board of Health and Welfare. Using the comparator population and new statistical methods, the difference in life expectancy between heart attack individuals and comparison individuals could be calculated, providing a measure of how much life expectancy was shortened due to the disease. 

“We found that there were large differences between groups. Women and young individuals lost the most life expectancy when they had a heart attack. If the cardiac function was impaired after the infarction, the effects were even greater. For example, a 50-year-old woman with impaired cardiac function loses an average of 11 years in 2022 compared to an 80-year-old man with normal cardiac function who loses an average of 5 months in life expectancy,” says first author Christian Reitan, researcher at the Department of Clinical Sciences, Danderyd Hospital, Karolinska Institut. 

Parameters affecting heart attack risk

The researchers were also able to take into account differences in income, education, other illnesses and medication at the time of the illness – which helped to measure the effect of the heart attack itself when everything else was taken into account.

“The results showed that a fairly large part of the reduction in life expectancy disappeared, that is, much of the reduction in life expectancy is explained by factors other than the heart attack itself, but which may still be associated with heart attack, such as socioeconomics or other diseases such as hypertension and diabetes. Provided that the patient had preserved cardiac function, we saw that the gender difference had disappeared. We interpret this to mean that the effect of the heart attack, and thus also the care for heart attacks, is similar between the sexes and that the large reduction in life expectancy we see in women is due to differences in risk factors, other diseases and socioeconomics,” says Christian Reitan. 

According to the researchers, there is a lack of individualized heart attack care in Sweden for women. The study shows that women who have a heart attack lose more years of life than men of the same age.

“If a woman had impaired cardiac function, the gender difference was large. We don’t have the data to answer why, but it raises questions about whether women get as good follow-up and treatment for heart failure as men, or whether it is simply a more serious condition for a woman. Our findings are important because they challenge existing guidelines for heart attack treatment today. By identifying high-risk groups, we can hopefully better tailor treatment to the individual. We believe that ‘years of life lost’ is a good and easy-to-understand measure of risk for both doctors and patients. It makes it easier for us to assess and communicate the seriousness of the disease,” concludes Christian Reitan. 

Source: Karolinska Institutet

Categories : Cardiovascular DiseaseTags :

Cannabis Use Linked to Increase in Heart Attack and Stroke Risk

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An analysis of 430 000 adults in the U.S. found that using cannabis, most commonly through smoking, eating or vaporising it, was significantly associated with a higher risk of heart attack and stroke, even after controlling for tobacco use (combustible cigarettes and other tobacco products) and other cardiovascular risk factors, according to new research published today in the Journal of the American Heart Association.

Although cannabis, or marijuana, is illegal at the federal level, 24 states and Washington, D.C., have legalized the use of recreational cannabis. Additionally, the number of people in the U.S. who use cannabis has increased significantly in recent decades, according to the 2019 National Survey on Drug Use and Health from the Substance Abuse and Mental Health Services Administration of the U.S. Department of Health and Human Services.

The annual survey found that in 2019, 48.2 million people ages 12 or older reported using cannabis at least once, compared to 25.8 million people ages 12 or older in 2002, an increase to 17% from 11%.

“Despite common use, little is known about the risks of cannabis use and, in particular, the cardiovascular disease risks,” said lead study author Abra Jeffers, PhD, a data analyst at Massachusetts General Hospital in Boston. “The perceptions of the harmfulness of smoking cannabis are decreasing, and people have not considered cannabis use dangerous to their health. However, previous research suggested that cannabis could be associated with cardiovascular disease. In addition, smoking cannabis – the predominant method of use – may pose additional risks because particulate matter is inhaled.”

In this study, researchers reviewed survey data collected for 430 000 adults from 2016 through 2020 to examine the association between cannabis use and adverse cardiovascular outcomes including heart disease, heart attack and stroke. The survey data was collected through the Behavioral Risk Factor Surveillance System, a national, cross-sectional survey performed annually by the U.S. Centers for Disease Control and Prevention.

The researchers specifically investigated whether cannabis use was associated with adverse cardiovascular outcomes among the general adult population, among people who had never smoked tobacco or used e-cigarettes, and among younger adults (defined as men under age 55 and women under age 65) at risk for heart disease. They also factored in the number of days per month that people used cannabis.

The analyses of found:

  • Any cannabis use (smoked, eaten or vaporized) was independently associated with a higher number of adverse cardiovascular outcomes (coronary heart disease, myocardial infarction and stroke) and with more frequent use (more days per month), the odds of adverse outcomes were even higher. The results were similar after controlling for other cardiovascular risk factors, including tobacco and/or e-cigarette use, alcohol consumption, body mass index, Type 2 diabetes and physical activity.
  • Both daily and non-daily cannabis users had an increased risk of heart attack compared to non-users; daily cannabis users had 25% higher odds of heart attack compared to non-users.
  • The odds of stroke for daily cannabis users were 42% higher compared to non-users, with lower risk among those who used cannabis less than daily.
  • Among younger adults at risk for premature cardiovascular disease (defined as men younger than 55 years old and women younger than 65 years old) cannabis use was significantly associated with 36% higher combined odds of coronary heart disease, heart attack and stroke, regardless of whether or not they also used traditional tobacco products. A separate analysis of a smaller subgroup of these adults who had never smoked tobacco cigarettes or used nicotine e-cigarettes also found a significant association between cannabis use and an increase in the combined odds of coronary heart disease, heart attack and stroke.

“Our sample was large enough that we could investigate the association of cannabis use with cardiovascular outcomes among adults who had never used tobacco cigarettes or e-cigarettes,” Jeffers said. “Cannabis smoke is not all that different from tobacco smoke, except for the psychoactive drug: THC vs. nicotine. Our study shows that smoking cannabis has significant cardiovascular risk risks, just like smoking tobacco. This is particularly important because cannabis use is increasing, and conventional tobacco use is decreasing.”

Study background and details:

  • Survey participants were ages 18-74, with an average age of 45 years.
  • About half of the participants self-identified as female. 60.2% self-identified as white adults, 11.6 self-identified as Black adults, 19.3 self-identified as Hispanic adults and 8.9% self-identified as other.
  • Nearly 90% of adults did not use cannabis at all; 7% used it less than daily; and 4% were daily users. Among current cannabis users, 73.8% reported smoking as the most common form of cannabis consumption. More than 60% of total respondents had never used tobacco cigarettes; 28.6% of daily cannabis users had never used tobacco cigarettes; 44.6% of non-daily cannabis users had never used tobacco cigarettes and 63.9% of participants who did not use cannabis had never used tobacco cigarettes.

The study had several limitations, including that cardiovascular conditions and cannabis use were self-reported, making them potentially subject to recall bias (potential errors in memory); that the authors did not have health data measuring participants’ baseline lipid profile or blood pressure; and the study captured data for only a single point in time for the participants. The authors note that there is a need for prospective cohort studies to examine the association of cannabis use and cardiovascular outcomes while accounting for frequency of cannabis use.

“The findings of this study have very important implications for population health and should be a call to action for all practitioners, as this study adds to the growing literature that cannabis use and cardiovascular disease may be a potentially hazardous combination,” said Robert L. Page II, PharmD, MSPH, FAHA, chair of the volunteer writing group for the 2020 American Heart Association Scientific Statement: Medical Marijuana, Recreational Cannabis, and Cardiovascular Health. Page is professor of clinical pharmacy, medicine and physical medicine at the Skaggs School of Pharmacy and Pharmaceutical Sciences at the University of Colorado School of Medicine in Aurora, Colorado. Page was not involved in this study.

“In the overall population, the study findings are consistent with other studies indicating that daily cannabis use was associated with an increase in heart attack, stroke and the combined endpoint of coronary heart disease, heart attack and stroke,” he said. “As cannabis use continues to grow in legality and access across the U.S., practitioners and clinicians need to remember to assess cannabis use at each patient encounter in order to have a non-judgmental, shared decision conversation about potential cardiovascular risks and ways to reduce those risks.”

Source: American Heart Association

Categories : Cardiovascular Disease Obstetrics & GynaecologyTags :

New Findings on Cardiovascular Risk, Menopause and Migraines Ease Concerns

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Research suggesting a link between migraines and menopause symptoms and cardiovascular disease has gotten a lot of attention. But a pair of new studies in the journal Menopause suggest that most women experiencing these symptoms can rest easier, especially if they don’t have both migraines and long-term hot flashes and night sweats.

Instead, they should focus on tackling the other factors that can raise their cardiovascular risk by getting more sleep, exercise and healthy foods, quitting tobacco, and minding their blood pressure, blood sugar, cholesterol and weight.

For women who have experienced both migraines and hot flashes or night sweats over many years, one of the new studies does suggest an extra level of cardiovascular risk.

That makes heart disease and stroke prevention even more important in this group, says study leader Catherine Kim, MD, MPH, of the University of Michigan.

And for women currently in their 20s and 30s who experience migraines, the new research suggests that they might be heading for a higher risk of long-term menopause-related symptoms when they get older.

Long-term study yields important insights

Kim and her colleagues at Michigan Medicine, U-M’s academic medical centre, published the new pair of studies based on an in-depth analysis of data from a long-term study of more than 1900 women who volunteered to have regular physical exams and blood tests, and to take yearly health surveys, when they were in their late teens to early 30s.

Those women, now in their 50s and 60s, have provided researchers with a priceless view of what factors shape health in the years leading up to menopause and beyond, through their continued participation in the CARDIA study.

“The anxiety and dread that women with migraines and menopausal symptoms feel about cardiovascular risk is real – but these findings suggest that focusing on prevention, and correcting unhealthy habits and risk factors, could help most women,” said Kim, who is an associate professor of internal medicine at U-M and a primary care physician.

“For the subgroup with both migraines and early persistent hot flashes and night sweats, and for those currently experiencing migraines in their early adulthood, these findings point to an added need to control risks, and address symptoms early,” she adds.

Just over 30% of the middle-aged women in the study reported they had persistent hot flashes and night sweats, which together are called vasomotor symptoms or VMS because they relate to changes in the diameter of blood vessels.

Of them, 23% had reported also having migraines. This was the only group for whom Kim and her colleagues found extra risk of stroke, heart attack or other cardiovascular events that couldn’t be explained by other risk factors that have long been known to be linked to cardiovascular problems.

In addition to those with persistent vasomotor symptoms starting in their 40s or before, 43% of the women in the study had minimal levels of such symptoms in their 50s, and 27% experienced an increase in VMS over time into their 50s and early 60s.

The latter two groups had no excess cardiovascular risk once their other risk factors were taken into account, whether or not they had migraines.

Use of hormone-based birth control and estrogen to address medical issues did not affect this risk.

Controlling destiny

In the study of data from the same women in their earlier stages of life, the researchers found that the biggest factors in predicting which ones would go on to have persistent hot flashes and night sweats were having migraines, having depression, and smoking cigarettes, as well as being Black or having less than a high school education.

“These two studies, taken together, underscore that not all women have the same experiences as they grow older, and that many can control the risk factors that might raise their chances of heart disease and stroke later in life,” said Kim.

“In other words, women can do a lot to control their destiny when it comes to both menopause symptoms and cardiovascular diseases.”

She notes that the American Heart Association calls these risk factors the “Essential 8” and offers guides for what women, men and even children and teens can do to address them.

Evolving knowledge and treatment

The long-term study that the two new findings come from was specifically designed to look at cardiovascular risks when it launched in the mid-1980s. CARDIA stands for Coronary Artery Risk Development in Young Adults.

Back in the 80s, knowledge about the biology of blood vessels, down to the cellular and molecular level, was nowhere near where it is today. Both vasomotor symptoms in menopause and migraines have to do with blood vessel contraction and dilation.

But decades of research has shown the microscopic impacts on blood vessels of years of smoking, poor sleep, poor eating habits and lack of activity, as well as a person’s genetic inheritance, life experiences and hormonal history.

Newer injectable migraine medications called calcitonin gene-related peptide (CGRP) antagonists have reached the market in recent years. Using monoclonal antibodies, they target a key receptor on the surface of blood vessel cells to prevent migraines and cluster headaches. But they are expensive and not covered by insurance for all people with migraines.

While the new study is based on data from years before these medications became available, Kim said she recommends them to her patients with persistent migraines, as well as working with them to understand what triggers their migraines and how to use other medications including pain relievers and antiseizure medications to prevent them.

She also notes that the paper on future risk of persistent hot flashes and night sweats echoes the recent trend of using antidepressant medications to try to ease these menopause effects.

Kim also says that evidence has grown about the importance of healthy sleep habits for reducing hot flashes, as well the short-term use of oestradiol-based hormone therapy patches, which have not been shown to have a link to cardiovascular risk. And, she notes that research has not shown any over-the-counter supplement or herbal remedy to be effective, and that these are far less regulated than medications.

Source: Michigan Medicine – University of Michigan

Categories : Cardiovascular Disease Metabolic DisordersTags :

Semaglutide Cuts CVD Events by 20% in People with Obesity or Overweight but not Diabetes

On By ModernMedia
By HualinXMN – Own work, CC BY-SA 4.0

In a large, international clinical trial, people with obesity or overweight but not diabetes taking semaglutide for more than three years had a 20% lower risk of cardiovascular disease outcomes and lost an average of 9.4% of their body weight.

Semaglutide, a GLP-1 medication primarily prescribed for people with Type 2 diabetes, is also FDA-approved for weight loss in people with obesity.

These results were shared in a late-breaking science presentation at the American Heart Association’s Scientific Sessions 2023 and the full manuscript was also published in The New England Journal of Medicine.

“This news is very encouraging for people with overweight or obesity because no treatment specifically directed at the management of obesity and overweight in people without Type 1 or Type 2 diabetes has been tested in a randomised trial and been shown to influence cardiovascular outcomes,” said lead study author A. Michael Lincoff, MD.

While prior research has confirmed the benefits of semaglutide in managing blood sugar, decreasing cardiovascular disease events and reducing weight in people with Type 2 diabetes, this study specifically investigated the potential impact of semaglutide on cardiovascular disease in people with overweight or obesity and cardiovascular disease who did not have either Type 1 or Type 2 diabetes.

In this randomised, controlled, double-blind trial, participants were assigned to take either 2.4mg of semaglutide (the FDA-approved semaglutide dose for weight management) or a placebo once a week, which is higher than the FDA-approved semaglutide dose limit for Type 2 diabetes of 2.0mg/week. Each person in the study used a ‘pen’ to inject the medicine or placebo into a skin fold in their stomach, thigh or upper arm each week on the same day, and the dose started at 0.24mg and gradually increased every four weeks up to 2.4mg, and mean follow-up for all participants was 40 months.

In addition to taking either semaglutide or placebo for the trial, all participants also received standard of care treatment for cardiovascular disease, such as cholesterol modifying medications, antiplatelet therapies, beta blockers or other treatments. The authors note that heart disease diagnoses varied among the participants, therefore, treatment was adjusted to meet each individual’s diagnosis and needs, as well as the treatment guidelines in their country of residence.

The study, which ran from October 2018 through June 2023, indicated the following:

  • There was a 20% reduction in the risk of heart attacks, strokes or death due to cardiovascular disease in the participants who took semaglutide, compared to the participants in the placebo group.
  • In the semaglutide group, the participants’ body weight was reduced, on average, by 9.4% compared to a reduction of 0.9% among the adults in the placebo group.
  • There were no new safety concerns found in the study, which researchers note is encouraging since the SELECT trial is the largest and longest (4.5 years) trial of semaglutide in adults without Type 1 or Type 2 diabetes.
  • The number of serious adverse events was lower in the semaglutide group. Previous studies of medications of the GLP-1 receptor agonist class have shown an association with gallbladder disorders, and in SELECT, there was a slightly higher rate of gallbladder disorders in the semaglutide vs placebo group (2.8% vs 2.3%, respectively).
  • Semaglutide was stopped more frequently than placebo for gastrointestinal intolerance, a known side effect of this class of medications; however, there was no higher rate of serious gastrointestinal events.
  • The researchers noted that this medication did not lead to an increased rate of pancreatitis, which has been a concern with prior medications of this type.
  • Of note, other weight-loss medications that are not GLP-1 receptor agonists have been associated with increased risks of psychiatric disorders or cancer; these risks were not elevated with semaglutide in the SELECT trial.

“It’s been estimated that within about ten years, over half of the world’s population will have overweight or obesity,” said Dr Lincoff. “And while GLP-1 medications are frequently prescribed for patients with vascular disease and Type 2 diabetes, there is a significant number of people who do not have Type 1 or Type 2 diabetes but do have vascular disease and overweight or obesity for whom these medications are often not available due to access to care issues, insurance coverage or other factors. This population may now potentially benefit from semaglutide, and importantly, our results indicate the magnitude of cardiovascular risk reduction with semaglutide among people without Type 1 or Type 2 diabetes is the same as what we have seen in people with Type 2 diabetes. Our findings expand the opportunity to treat patients who have overweight or obesity and existing heart disease without Type 1 or Type 2 diabetes, and we have a chance to significantly reduce their risk of a secondary cardiovascular event including death.”

Among the study limitations were including adults with prior cardiovascular disease, thereby not investigating primary prevention of cardiovascular disease (people with no history of a heart attack, stroke and/or peripheral artery disease). In addition, 28% of the study participants were female, which is not proportionate to the number of women with cardiovascular disease and overweight or obesity in the general population.

Additional analyses will include identifying the mediators of the cardiovascular benefit to determine to what extent the results were driven by reduction of metabolically unhealthy body fat, positive impacts on inflammation or blood sugar, direct effects of the medication itself on plaque build-up in the arteries, or a combination of one or more variables.

Source: American Heart Association